Science.gov

Sample records for heart injuries

  1. Iodide Protects Heart Tissue from Reperfusion Injury

    PubMed Central

    Iwata, Akiko; Morrison, Michael L.; Roth, Mark B.

    2014-01-01

    Iodine is an elemental nutrient that is essential for mammals. Here we provide evidence for an acute therapeutic role for iodine in ischemia reperfusion injury. Infusion of the reduced form, iodide, but not the oxidized form iodate, reduces heart damage by as much as 75% when delivered intravenously following temporary loss of blood flow but prior to reperfusion of the heart in a mouse model of acute myocardial infarction. Normal thyroid function may be required because loss of thyroid activity abrogates the iodide benefit. Given the high degree of protection and the high degree of safety, iodide should be explored further as a therapy for reperfusion injury. PMID:25379708

  2. [Heart injury following closed thoracic injury].

    PubMed

    Bourguignon, N; Godier, S; Genevois, A; Kaeffer, N; Dureuil, B

    1996-01-01

    A 60-year-old man, was admitted in the emergency ward, following a motor vehicle accident. At the time of arrival his clinical state was stable. The initial investigations showed a moderate left haemopneumothorax and fractured ribs. After insertion of a thoracostomy tube into the left pleural cavity he had to undergo surgery for an open fracture of the left arm. Following induction of anaesthesia, a cardiovascular collapse occurred rapidly. An emergency thoracotomy was performed which showed a right ventricular perforation by a rib fragment. The authors discuss the role of possible changes in heart position produced by induction of general anaesthesia. Indeed the decrease in functional residual capacity following induction of anaesthesia with a cephalad diaphragmatic shift may have secondarily exposed the right ventricle to the bevel of a fractured rib. PMID:9180985

  3. Penetrating Heart Injury due to Screwdriver Assault

    PubMed Central

    Dieng, P. A.; Diop, M. S.; Ciss, A. G.; Ba, P. S.; Diatta, S.; Gaye, M.; Fall, M. L.; Ndiaye, A.; Ndiaye, M.

    2015-01-01

    Penetrating heart injuries cause wounds in the cardiac chambers. Most of them are due to gunshot or stabbing by knives. Screwdriver is an uncommon weapon. Authors report a case of stab wound by screwdriver, treated at cardiovascular center in Dakar. This is a 16-year-old boy who experienced physical aggression. He was assaulted with a screwdriver and had stab wound on the anterior wall of the chest. Physical examination showed a screwdriver penetrating the sternum bone over a right angle. He had a mild pericardial blood effusion and a right ventricle wound 5 mm in diameter with transection of the right coronary vein. The screwdriver was removed without cardiopulmonary bypass (CPB) and the ventricle wound repaired by direct suture of stitches reinforced with Teflon pledgets. The right coronary artery was ligated. Postoperative period was free of events. Screwdriver is uncommonly used as a weapon. It is a dangerous device because of its rigid structure and narrow tip. PMID:25945263

  4. Penetrating injuries of the heart and the great vessels.

    PubMed

    Slim, M; Yacoubian, H D; Dagher, I K

    1983-01-01

    Twenty eight patients with penetrating injuries to the heart and/or the great vessels are presented. These constituted 9% of all penetrating chest injuries during the period between April 1975 and November 1976. The injuries were confined to the cardio-vascular system in 3 patients only. Twelve patients presented with signs of cardiac tamponade, of whom 2 succumbed intra-operatively due to ventricular fibrillation. Eight patients required respiratory support immediately after operation, of whom one died eventually due to extra-cardiac injuries. The mortality rate in this series was 11%. The remaining 25 survivors have resumed their regular life activities after discharge from the hospital. In none of the cases was the heart-lung machine used for repair. PMID:6672552

  5. [Injuries of the heart--diagnosis and therapy].

    PubMed

    Kaiser, M E; Birnbaum, D E

    2001-01-01

    Injuries of the heart are present in 7-12% of all thoracic trauma cases. Most of these (80%) are polytrauma patients. The mechanism of the accident, the localisation of injuries, the physical condition of the patients and the skills of the hospital stuff are determinant factors for the outcome. Hemodynamic instability needs an urgent echocardiography, signs of an obstructive pericardial hematoma and/or progressive bleeding require an urgent operation using a left lateral or mediosternal approach. ECC and cell saving should be available. The contusion of the heart is monitored by ECG and Troponin tests. The application of a "mini" heart-lung machine in difficult situations could be very useful. PMID:11824316

  6. Conditioning the heart to prevent myocardial reperfusion injury during PPCI

    PubMed Central

    2012-01-01

    For patients presenting with a ST-segment elevation myocardial infarction (STEMI), early myocardial reperfusion by primary percutaneous coronary intervention (PPCI) remains the most effective treatment strategy for limiting myocardial infarct size, preserving left ventricular systolic function, and preventing the onset of heart failure. Recent advances in PCI technology to improve myocardial reperfusion and the introduction of novel anti-platelet and anti-thrombotic agents to maintain the patency of the infarct-related coronary artery continue to optimize PPCI procedure. However, despite these improvements, STEMI patients still experience significant major adverse cardiovascular events. One major contributing factor has been the inability to protect the heart against the lethal myocardial reperfusion injury, which accompanies PPCI. Past attempts to translate cardioprotective strategies, discovered in experimental studies to prevent lethal myocardial reperfusion injury, into the clinical setting of PPCI have been disappointing. However, a number of recent proof-of-concept clinical studies suggest that the heart can be ‘conditioned’ to protect itself against lethal myocardial reperfusion injury, as evidenced by a reduction in myocardial infarct size. This can be achieved using either mechanical (such as ischaemic postconditioning, remote ischaemic preconditioning, therapeutic hypothermia, or hyperoxaemia) or pharmacological (such as cyclosporin-A, natriuretic peptide, exenatide) ‘conditioning’ strategies as adjuncts to PPCI. Furthermore, recent developments in cardiac magnetic resonance (CMR) imaging can provide a non-invasive imaging strategy for assessing the efficacy of these novel adjunctive therapies to PPCI in terms of key surrogate clinical endpoints such as myocardial infarct size, myocardial salvage, left ventricular ejection fraction, and the presence of microvascular obstruction or intramyocardial haemorrhage. In this article, we review the

  7. Cardiopulmonary Circuit Models for Predicting Injury to the Heart

    NASA Astrophysics Data System (ADS)

    Ward, Richard; Wing, Sarah; Bassingthwaighte, James; Neal, Maxwell

    2004-11-01

    Circuit models have been used extensively in physiology to describe cardiopulmonary function. Such models are being used in the DARPA Virtual Soldier (VS) Project* to predict the response to injury or physiological stress. The most complex model consists of systemic circulation, pulmonary circulation, and a four-chamber heart sub-model. This model also includes baroreceptor feedback, airway mechanics, gas exchange, and pleural pressure influence on the circulation. As part of the VS Project, Oak Ridge National Laboratory has been evaluating various cardiopulmonary circuit models for predicting the effects of injury to the heart. We describe, from a physicist's perspective, the concept of building circuit models, discuss both unstressed and stressed models, and show how the stressed models are used to predict effects of specific wounds. *This work was supported by a grant from the DARPA, executed by the U.S. Army Medical Research and Materiel Command/TATRC Cooperative Agreement, Contract # W81XWH-04-2-0012. The submitted manuscript has been authored by the U.S. Department of Energy, Office of Science of the Oak Ridge National Laboratory, managed for the U.S. DOE by UT-Battelle, LLC, under contract No. DE-AC05-00OR22725. Accordingly, the U.S. Government retains a non-exclusive, royalty-free license to publish or reproduce the published form of this contribution, or allow others to do so, for U.S. Government purpose.

  8. Remote skin injury: a protean complication of open heart surgery.

    PubMed

    LoCicero, J; Fisher, E; Atlas, P L; Shanks, C; Wade, R J; Michaelis, L L

    1986-02-01

    In the 12-month period ending August, 1984, 14 adult patients (2.9%) developed within 24 hr following open heart surgery skin defects of varying magnitude remote from the incision site. Electrical injury secondary to a grounding defect was documented in two patients and suspected in one. Four patients' injuries were caused by the roller device when transfering from operating room table to intensive care unit bed. The remaining eight patients all had skin loss at sites of pressure on either the head, back, buttocks, or arm. Retrospective analysis showed no correlation with mean pressure during cardiopulmonary bypass (CPB), depth of cooling, length of time to rewarm, or the use vasoactive drugs. Subsequently, core temperature plus ten surface temperatures were monitored during and following CPB in ten patients. The data showed that during active cooling and rewarming, skin temperature actually lagged behind the core temperature (4 C). Thus, the skin appears to develop a relative oxygen debt during CPB which may decrease the threshold for skin injury particularly in older patients who may have other predisposing factors, such as obesity, generalized atherosclerosis, diabetes, or friable skin. Pressure points during positioning and subsequent skin trauma must be meticulously avoided in any patient undergoing CPB. PMID:3946942

  9. SIRT3 deficiency exacerbates ischemia-reperfusion injury: implication for aged hearts

    PubMed Central

    Porter, George A.; Urciuoli, William R.; Brookes, Paul S.

    2014-01-01

    Ischemia-reperfusion (IR) injury is significantly worse in aged hearts, but the underlying mechanisms are poorly understood. Age-related damage to mitochondria may be a critical feature, which manifests in an exacerbation of IR injury. Silent information regulator of transcription 3 (SIRT3), the major mitochondrial NAD+-dependent lysine deacetylase, regulates a variety of functions, and its inhibition may disrupt mitochondrial function to impact recovery from IR injury. In this study, the role of SIRT3 in mediating the response to cardiac IR injury was examined using an in vitro model of SIRT3 knockdown (SIRT3kd) in H9c2 cardiac-derived cells and in Langendorff preparations from adult (7 mo old) wild-type (WT) and SIRT3+/− hearts and aged (18 mo old) WT hearts. SIRT3kd cells were more vulnerable to simulated IR injury and exhibited a 46% decrease in mitochondrial complex I (Cx I) activity with low O2 consumption rates compared with controls. In the Langendorff model, SIRT3+/− adult hearts showed less functional recovery and greater infarct vs. WT, which recapitulates the in vitro results. In WT aged hearts, recovery from IR injury was similar to SIRT3+/− adult hearts. Mitochondrial protein acetylation was increased in both SIRT3+/− adult and WT aged hearts (relative to WT adult), suggesting similar activities of SIRT3. Also, enzymatic activities of two SIRT3 targets, Cx I and MnSOD, were similarly and significantly inhibited in SIRT3+/− adult and WT aged cardiac mitochondria. In conclusion, decreased SIRT3 may increase the susceptibility of cardiac-derived cells and adult hearts to IR injury and may contribute to a greater level of IR injury in the aged heart. PMID:24748594

  10. GATA4 regulates Fgf16 to promote heart repair after injury.

    PubMed

    Yu, Wei; Huang, Xiuzhen; Tian, Xueying; Zhang, Hui; He, Lingjuan; Wang, Yue; Nie, Yu; Hu, Shengshou; Lin, Zhiqiang; Zhou, Bin; Pu, William; Lui, Kathy O; Zhou, Bin

    2016-03-15

    Although the mammalian heart can regenerate during the neonatal stage, this endogenous regenerative capacity is lost with age. Importantly, replication of cardiomyocytes has been found to be the key mechanism responsible for neonatal cardiac regeneration. Unraveling the transcriptional regulatory network for inducing cardiomyocyte replication will, therefore, be crucial for the development of novel therapies to drive cardiac repair after injury. Here, we investigated whether the key cardiac transcription factor GATA4 is required for neonatal mouse heart regeneration. Using the neonatal mouse heart cryoinjury and apical resection models with an inducible loss of GATA4 specifically in cardiomyocytes, we found severely depressed ventricular function in the Gata4-ablated mice (mutant) after injury. This was accompanied by reduced cardiomyocyte replication. In addition, the mutant hearts displayed impaired coronary angiogenesis and increased hypertrophy and fibrosis after injury. Mechanistically, we found that the paracrine factor FGF16 was significantly reduced in the mutant hearts after injury compared with littermate controls and was directly regulated by GATA4. Cardiac-specific overexpression of FGF16 via adeno-associated virus subtype 9 (AAV9) in the mutant hearts partially rescued the cryoinjury-induced cardiac hypertrophy, promoted cardiomyocyte replication and improved heart function after injury. Altogether, our data demonstrate that GATA4 is required for neonatal heart regeneration through regulation of Fgf16, suggesting that paracrine factors could be of potential use in promoting myocardial repair. PMID:26893347

  11. DJ-1 protects the heart against ischemia-reperfusion injury by regulating mitochondrial fission.

    PubMed

    Shimizu, Yuuki; Lambert, Jonathan P; Nicholson, Chad K; Kim, Joshua J; Wolfson, David W; Cho, Hee Cheol; Husain, Ahsan; Naqvi, Nawazish; Chin, Li-Shen; Li, Lian; Calvert, John W

    2016-08-01

    Recent data indicates that DJ-1 plays a role in the cellular response to stress. Here, we aimed to examine the underlying molecular mechanisms mediating the actions of DJ-1 in the heart following myocardial ischemia-reperfusion (I/R) injury. In response to I/R injury, DJ-1 KO mice displayed increased areas of infarction and worsened left ventricular function when compared to WT mice, confirming a protective role for DJ-1 in the heart. In an effort to evaluate the potential mechanism(s) responsible for the increased injury in DJ-1 KO mice, we focused on SUMOylation, a post-translational modification process that regulates various aspects of protein function. DJ-1 KO hearts after I/R injury were found to display enhanced accumulation of SUMO-1 modified proteins and reduced SUMO-2/3 modified proteins. Further analysis, revealed that the protein expression of the de-SUMOylation enzyme SENP1 was reduced, whereas the expression of SENP5 was enhanced in DJ-1 KO hearts after I/R injury. Finally, DJ-1 KO hearts were found to display enhanced SUMO-1 modification of dynamin-related protein 1, excessive mitochondrial fission, and dysfunctional mitochondria. Our data demonstrates that the activation of DJ-1 in response to myocardial I/R injury protects the heart by regulating the SUMOylation status of Drp1 and attenuating excessive mitochondrial fission. PMID:27108530

  12. Prenatal methamphetamine differentially alters myocardial sensitivity to ischemic injury in male and female adult hearts.

    PubMed

    Rorabaugh, Boyd R; Seeley, Sarah L; Bui, Albert D; Sprague, Lisanne; D'Souza, Manoranjan S

    2016-02-15

    Methamphetamine is one of the most common illicit drugs abused during pregnancy. The neurological effects of prenatal methamphetamine are well known. However, few studies have investigated the potential effects of prenatal methamphetamine on adult cardiovascular function. Previous work demonstrated that prenatal cocaine exposure increases sensitivity of the adult heart to ischemic injury. Methamphetamine and cocaine have different mechanisms of action, but both drugs exert their effects by increasing dopaminergic and adrenergic receptor stimulation. Thus the goal of this study was to determine whether prenatal methamphetamine also worsens ischemic injury in the adult heart. Pregnant rats were injected with methamphetamine (5 mg·kg(-1)·day(-1)) or saline throughout pregnancy. When pups reached 8 wk of age, their hearts were subjected to ischemia and reperfusion by means of a Langendorff isolated heart system. Prenatal methamphetamine had no significant effect on infarct size, preischemic contractile function, or postischemic recovery of contractile function in male hearts. However, methamphetamine-treated female hearts exhibited significantly larger infarcts and significantly elevated end-diastolic pressure during recovery from ischemia. Methamphetamine significantly reduced protein kinase Cε expression and Akt phosphorylation in female hearts but had no effect on these cardioprotective proteins in male hearts. These data indicate that prenatal methamphetamine differentially affects male and female sensitivity to myocardial ischemic injury and alters cardioprotective signaling proteins in the adult heart. PMID:26683901

  13. Oxygen surrounding the heart during ischemic conservation determines the myocardial injury during reperfusion.

    PubMed

    Feng, Yansheng; Bopassa, Jean Chrisostome

    2015-01-01

    There is discrepancy regarding the duration of reperfusion required using 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) staining to assess myocardial infarction in an isolated, perfused heart model. Several investigators prefer long-term reperfusion (120 minutes) to determine myocardial injury, while others have used a shorter duration (30-40 minutes). We investigated whether oxygen surrounding the myocardium during ischemia plays a critical role in the installation of myocardial infarction during reperfusion. Mice hearts were perfused with a Langendorff apparatus using Krebs Henseleit (KH) buffer oxygenated with 95% O2 plus 5% CO2 at 37°C. Hearts were either immersed in KH or suspended in air during 18 minutes of global ischemia in a normothermic, water-jacketed chamber. Hearts then were reperfused for 40, 60, or 90 minutes. We found that hearts immersed in KH had decreased recovery of function and increased myocardial infarct size, reaching a steady-state level after 40 minutes of reperfusion. In contrast, hearts suspended in air approached steady-state after 90 minutes of reperfusion. Thus, mitochondrial reactive oxygen species (ROS) production was much lower in air-maintained hearts than in KH-immersed hearts. To investigate whether an increase in oxygen surrounding the myocardium during ischemia might cause further damage, we bubbled the KH solution with nitrogen (KH+N2) rather than oxygen (KH+O2). With this alteration, recovery of cardiac function was improved and myocardial infarct size and mitochondrial ROS production were reduced compared with hearts immersed in KH+O2. In conclusion, short-term (40 minutes) reperfusion is sufficient to reach steady-state myocardial infarct size when hearts are immersed in physiologic solution during ischemia; however, a longer duration of reperfusion (90 minutes) is required if hearts are suspended in air. Thus, oxygen surrounding the heart during ischemia determines the extent of myocardium injury during reperfusion

  14. Pericardiocentesis followed by thoracotomy and repair of penetrating cardiac injury caused by nail gun injury to the heart

    PubMed Central

    Chirumamilla, Vasu; Prabhakaran, Kartik; Patrizio, Petrone; Savino, John A.; Marini, Corrado P.; Zoha, Zobair

    2016-01-01

    Introduction Work site injuries involving high projectile tools such as nail guns can lead to catastrophic injuries. Generally, penetrating cardiac injuries are associated with a high mortality rate. Presentation of case A construction worker was brought to the emergency room having sustained a nail gun injury to the chest. The patient was hypotensive, tachycardic with prominent jugular venous distention, and had a profound lactic acidosis. Bedside ultrasound confirmed the presence of pericardial fluid. Pericardiocentesis was performed twice using a central venous catheter inserted into the pericardial space, resulting in improvement in the patient’s hemodynamics. Thereafter he underwent left anterolateral thoracotomy and repair of a right atrial laceration. He recovered uneventfully. Discussion Penetrating cardiac injuries caused by nail guns, although rare, have been previously described. However, pericardiocentesis, while retaining a role in the management of medical causes of cardiac tamponade, has been reported only sporadically in the setting of trauma. We report a rare case of penetrating nail gun injury to the heart where pericardiocentesis was used as a temporizing measure to stabilize the patient in preparation for definitive but timely operative intervention. Conclusion We propose awareness that percardiocentesis can serve as a temporary life saving measure in the setting of trauma, particularly as a bridge to definitive therapy. To our knowledge, this represents the first reported case of catheter pericardiocentesis used to stabilize a patient until definitive repair of a penetrating cardiac injury caused by a nail gun. PMID:27107304

  15. Analysis of Heart Rate and Self-Injury with and without Restraint in an Individual with Autism

    ERIC Educational Resources Information Center

    Jennett, Heather; Hagopian, Louis P.; Beaulieu, Lauren

    2011-01-01

    The relation between self-injury and heart rate was analyzed for an individual who appeared anxious while engaging in self-injury. The analysis involved manipulating the presence or absence of restraint while simultaneously measuring heart rate. The following findings were obtained and replicated: (a) when some form of restraint was applied, heart…

  16. Moderate exercise training attenuates aging-induced cardiac inflammation, hypertrophy and fibrosis injuries of rat hearts

    PubMed Central

    Liao, Po-Hsiang; Hsieh, Dennis Jine-Yuan; Kuo, Chia-Hua; Day, Cecilia-Hsuan; Shen, Chia-Yao; Lai, Chao-Hung; Chen, Ray-Jade; Padma, V. Vijaya

    2015-01-01

    Aging is the most important risk factor in cardiovascular disease (CVD), which is the leading causes of death worldwide and the second major cause of death in Taiwan. The major factor in heart failure during aging is heart remodeling, including long-term stress-induced cardiac hypertrophy and fibrosis. Exercise is good for aging heart health, but the impact of exercise training on aging is not defined. This study used 3-, 12- and 18-month-old rats and randomly divided each age group into no exercise training control groups (C3, A12 and A18) and moderate gentle swimming exercise training groups (E3, AE12 and AE18). The protocol of exercise training was swimming five times weekly with gradual increases from the first week from 20 to 60 min for 12 weeks. Analyses of protein from rat heart tissues and sections revealed cardiac inflammation, hypertrophy and fibrosis pathway increases in aged rat groups (A12 and A18), which were improved in exercise training groups (AE12 and AE18). There were no heart injuries in young rat hearts in exercise group E3. These data suggest that moderate swimming exercise training attenuated aging-induced cardiac inflammation, hypertrophy and fibrosis injuries of rat hearts. PMID:26496028

  17. Loss of PINK1 Increases the Heart's Vulnerability to Ischemia-Reperfusion Injury

    PubMed Central

    Siddall, Hilary K.; Yellon, Derek M.; Ong, Sang-Bing; Mukherjee, Uma A.; Burke, Niall; Hall, Andrew R.; Angelova, Plamena R.; Ludtmann, Marthe H. R.; Deas, Emma; Davidson, Sean M.; Mocanu, Mihaela M.; Hausenloy, Derek J.

    2013-01-01

    Objectives Mutations in PTEN inducible kinase-1 (PINK1) induce mitochondrial dysfunction in dopaminergic neurons resulting in an inherited form of Parkinson’s disease. Although PINK1 is present in the heart its exact role there is unclear. We hypothesized that PINK1 protects the heart against acute ischemia reperfusion injury (IRI) by preventing mitochondrial dysfunction. Methods and Results Over-expressing PINK1 in HL-1 cardiac cells reduced cell death following simulated IRI (29.2±5.2% PINK1 versus 49.0±2.4% control; N = 320 cells/group P<0.05), and delayed the onset of mitochondrial permeability transition pore (MPTP) opening (by 1.3 fold; P<0.05). Hearts excised from PINK1+/+, PINK1+/− and PINK1−/− mice were subjected to 35 minutes regional ischemia followed by 30 minutes reperfusion. Interestingly, myocardial infarct size was increased in PINK1−/− hearts compared to PINK1+/+ hearts with an intermediate infarct size in PINK1+/− hearts (25.1±2.0% PINK1+/+, 38.9±3.4% PINK1+/− versus 51.5±4.3% PINK1−/− hearts; N>5 animals/group; P<0.05). Cardiomyocytes isolated from PINK1−/− hearts had a lower resting mitochondrial membrane potential, had inhibited mitochondrial respiration, generated more oxidative stress during simulated IRI, and underwent rigor contracture more rapidly in response to an uncoupler when compared to PINK1+/+ cells suggesting mitochondrial dysfunction in hearts deficient in PINK1. Conclusions We show that the loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury. This may be due, in part, to increased mitochondrial dysfunction. These findings implicate PINK1 as a novel target for cardioprotection. PMID:23638067

  18. Low Frequency Electromagnetic Field Conditioning Protects against I/R Injury and Contractile Dysfunction in the Isolated Rat Heart

    PubMed Central

    Bialy, Dariusz; Wawrzynska, Magdalena; Bil-Lula, Iwona; Krzywonos-Zawadzka, Anna; Wozniak, Mieczyslaw; Cadete, Virgilio J. J.

    2015-01-01

    Low frequency electromagnetic field (LF-EMF) decreases the formation of reactive oxygen species, which are key mediators of ischemia/reperfusion (I/R) injury. Therefore, we hypothesized that the LF-EMF protects contractility of hearts subjected to I/R injury. Isolated rat hearts were subjected to 20 min of global no-flow ischemia, followed by 30 min reperfusion, in the presence or absence of LF-EMF. Coronary flow, heart rate, left ventricular developed pressure (LVDP), and rate pressure product (RPP) were determined for evaluation of heart mechanical function. The activity of cardiac matrix metalloproteinase-2 (MMP-2) and the contents of coronary effluent troponin I (TnI) and interleukin-6 (IL-6) were measured as markers of heart injury. LF-EMF prevented decreased RPP in I/R hearts, while having no effect on coronary flow. In addition, hearts subjected to I/R exhibited significantly increased LVDP when subjected to LF-EMF. Although TnI and IL-6 levels were increased in I/R hearts, their levels returned to baseline aerobic levels in I/R hearts subjected to LF-EMF. The reduced activity of MMP-2 in I/R hearts was reversed in hearts subjected to LF-EMF. The data presented here indicate that acute exposure to LF-EMF protects mechanical function of I/R hearts and reduces I/R injury. PMID:25961016

  19. Musculoskeletal overuse injuries and heart rate variability: Is there a link?

    PubMed

    Gisselman, Angela Spontelli; Baxter, G David; Wright, Alexis; Hegedus, Eric; Tumilty, Steve

    2016-02-01

    Accurate detection and prevention of overuse musculoskeletal injuries is limited by the nature of somatic tissue injury. In the pathogenesis of overuse injuries, it is well recognized that an abnormal inflammatory response occurs within somatic tissue before pain is perceived which can disrupt the normal remodeling process and lead to subsequent degeneration. Current overuse injury prevention methods focused on biomechanical faults or performance standards lack the sensitivity needed to identify the status of tissue injury or repair. Recent evidence has revealed an apparent increase in the prevalence and impact of overuse musculoskeletal injuries in athletics. When compared to acute injuries, overuse injuries have a potentially greater negative impact on athletes' overall health burden. Further, return to sport rehabilitation following overuse injury is complicated by the fact that the absence of pain does not equate to complete physiological healing of the injured tissue. Together, this highlights the need for exercise monitoring and injury prevention methods which incorporate assessment of somatic tissue response to loading. One system primarily involved in the activation of pathways and neuromediators responsible for somatic tissue repair is the autonomic nervous system (ANS). Although not completely understood, emerging research supports the critical importance of peripheral ANS activity in the health and repair of somatic tissue injury. Due to its significant contributions to cardiac function, ANS activity can be measured indirectly with heart rate monitoring. Heart rate variability (HRV) is one index of ANS activity that has been used to investigate the relationship between athletes' physiological response to accumulating training load. Research findings indicated that HRV may provide a reflection of ANS homeostasis, or the body's stress-recovery status. This noninvasive marker of the body's primary driver of recovery has the potential to incorporate

  20. Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation

    PubMed Central

    Vassalli, Giuseppe; Milano, Giuseppina; Moccetti, Tiziano

    2012-01-01

    In solid organ transplantation, ischemia/reperfusion (IR) injury during organ procurement, storage and reperfusion is an unavoidable detrimental event for the graft, as it amplifies graft inflammation and rejection. Intracellular mitogen-activated protein kinase (MAPK) signaling pathways regulate inflammation and cell survival during IR injury. The four best-characterized MAPK subfamilies are the c-Jun NH2-terminal kinase (JNK), extracellular signal- regulated kinase-1/2 (ERK1/2), p38 MAPK, and big MAPK-1 (BMK1/ERK5). Here, we review the role of MAPK activation during myocardial IR injury as it occurs during heart transplantation. Most of our current knowledge regarding MAPK activation and cardioprotection comes from studies of preconditioning and postconditioning in nontransplanted hearts. JNK and p38 MAPK activation contributes to myocardial IR injury after prolonged hypothermic storage. p38 MAPK inhibition improves cardiac function after cold storage, rewarming and reperfusion. Small-molecule p38 MAPK inhibitors have been tested clinically in patients with chronic inflammatory diseases, but not in transplanted patients, so far. Organ transplantation offers the opportunity of starting a preconditioning treatment before organ procurement or during cold storage, thus modulating early events in IR injury. Future studies will need to evaluate combined strategies including p38 MAPK and/or JNK inhibition, ERK1/2 activation, pre- or postconditioning protocols, new storage solutions, and gentle reperfusion. PMID:22530110

  1. Curcumin ameliorates streptozotocin-induced heart injury in rats.

    PubMed

    Abo-Salem, Osama M; Harisa, Gamaleldin I; Ali, Tarek M; El-Sayed, El-Sayed M; Abou-Elnour, Fatma M

    2014-06-01

    Heart failure (HF) is one of diabetic complications. This work was designed to investigate the possible modulatory effect of curcumin against streptozotocin-induced diabetes and consequently HF in rats. Rats were divided into control, vehicle-treated, curcumin-treated, diabetic-untreated, diabetic curcumin-treated, and diabetic glibenclamide-treated groups. Animal treatment was started 5 days after induction of diabetes and extended for 6 weeks. Diabetic rats showed significant increase in serum glucose, triglycerides, total cholesterol, low-density lipoprotein-cholesterol, very low density lipoprotein-cholesterol, nitric oxide, lactate dehydrogenase, cardiac malondialdehyde, plasma levels of interleukin-6, and tumor necrosis factor-alpha, and also showed marked decrease in serum high-density lipoprotein-cholesterol, cardiac reduced glutathione, and cardiac antioxidant enzymes (catalase, superoxide dismutase, and glutathione-S-transferase). However, curcumin or glibenclamide treatment significantly mitigated such changes. In conclusion, curcumin has a beneficial therapeutic effect in diabetes-induced HF, an effect that might be attributable to its antioxidant and suppressive activity on cytokines. PMID:24760747

  2. Hyperamylinemia Increases IL-1β Synthesis in the Heart via Peroxidative Sarcolemmal Injury.

    PubMed

    Liu, Miao; Verma, Nirmal; Peng, Xiaoli; Srodulski, Sarah; Morris, Andrew; Chow, Martin; Hersh, Louis B; Chen, Jing; Zhu, Haining; Netea, Mihai G; Margulies, Kenneth B; Despa, Sanda; Despa, Florin

    2016-09-01

    Hypersecretion of amylin is common in individuals with prediabetes, causes amylin deposition and proteotoxicity in pancreatic islets, and contributes to the development of type 2 diabetes. Recent studies also identified amylin deposits in failing hearts from patients with obesity or type 2 diabetes and demonstrated that hyperamylinemia accelerates the development of heart dysfunction in rats expressing human amylin in pancreatic β-cells (HIP rats). To further determine the impact of hyperamylinemia on cardiac myocytes, we investigated human myocardium, compared diabetic HIP rats with diabetic rats expressing endogenous (nonamyloidogenic) rat amylin, studied normal mice injected with aggregated human amylin, and developed in vitro cell models. We found that amylin deposition negatively affects cardiac myocytes by inducing sarcolemmal injury, generating reactive aldehydes, forming amylin-based adducts with reactive aldehydes, and increasing synthesis of the proinflammatory cytokine interleukin-1β (IL-1β) independently of hyperglycemia. These results are consistent with the pathological role of amylin deposition in the pancreas, uncover a novel contributing mechanism to cardiac myocyte injury in type 2 diabetes, and suggest a potentially treatable link of type 2 diabetes with diabetic heart disease. Although further studies are necessary, these data also suggest that IL-1β might function as a sensor of myocyte amylin uptake and a potential mediator of myocyte injury. PMID:27335231

  3. Effects of caffeine on ischemia-reperfusion injury in isolated rat hearts.

    PubMed

    Yamahara, Y; Asayama, J; Matsumoto, T; Miyazaki, H; Tatsumi, T; Ohta, B; Sakai, R; Inoue, M; Inoue, D; Nakagawa, M

    1993-07-01

    Cardiac sarcoplasmic reticulum (SR) plays an important role in regulation of the intracellular Ca2+ concentration. It is well known that intracellular Ca2+ overload is one cause of reperfusion injury. Thus, it is predicted that reperfusion injury of myocardium can be prevented by eliminating the Ca2+ overload. This study examined the effects of caffeine, a SR blocker, on reperfusion injury in isolated perfused rat hearts. Working hearts were reperfused for 25 min after 30 or 50 min of ischemia. Caffeine (10(-4) M) was administered during the period of ischemia or the initial 5 min of reperfusion. The left ventricular pressure and the electrocardiogram were recorded. Rate-pressure products were calculated as an index of cardiac function. Adenine nucleotides were measured by high-performance liquid chromatography to assess energy charge. The administration of caffeine for a short period during the initial reperfusion significantly improved cardiac function in the hearts. Caffeine pretreatment during 50 min of ischemia, though, resulted in deterioration of both energy charge and cardiac function. Caffeine did not affect the incidence of either ventricular fibrillation or reversion to sinus rhythm. The energy charges were lower in the preparations with sustained ventricular fibrillation. PMID:8246349

  4. Heart Rate Response During Underwater Treadmill Training in Adults with Incomplete Spinal Cord Injury

    PubMed Central

    Morgan, Don W.

    2015-01-01

    Background: Walking on a submerged treadmill can improve mobility in persons displaying lower limb muscle weakness and balance deficits. Little is known, however, regarding the effect of water treadmill exercise on cardiac performance in persons with incomplete spinal cord injury (iSCI). Objective: To assess heart rate response during underwater treadmill training (UTT) in adults with iSCI. Methods: Seven males and 4 females with iSCI (age = 48 ± 13 years; 5 ± 8 years after injury) completed 8 weeks of UTT (3 sessions per week; 3 walks per session) incorporating individually determined walking speeds, personalized levels of body weight unloading, and gradual, alternating increases in speed and duration. Heart rate was monitored during the last 15 seconds of the final 2 minutes of each walk. Results: Over the course of 3 biweekly periods in which walking speed remained constant, heart rate fell by 7% (7 ± 1 b•min-1; P < .001) in weeks 2 and 3, 14% (17 ± 6 b•min-1; P < .001) in weeks 4 and 5, and 17% (21 ± 11 b•min-1; P < .001) in weeks 6 and 7. Conclusion: In adults with iSCI, progressively greater absolute and relative reductions in submaximal exercise heart rate occurred after 2 months of UTT featuring a systematic increase in training volume. PMID:25762859

  5. Hydrogen sulfide post-conditioning preserves interfibrillar mitochondria of rat heart during ischemia reperfusion injury.

    PubMed

    Banu, Shakila A; Ravindran, Sriram; Kurian, Gino A

    2016-07-01

    Cardiac mitochondrial dysfunction is considered to be the main manifestation in the pathology of ischemia reperfusion injury, and by restoring its functional activity, hydrogen sulfide (H2S), a novel endogenous gaseotransmitter renders cardioprotection. Given that interfibrillar (IFM) and subsarcolemmal (SSM) mitochondria are the two main types in the heart, the present study investigates the specific H2S-mediated action on IFM and SSM during ischemic reperfusion in the Langendorff rat heart model. Rats were randomly divided into five groups, namely normal, ischemic control, reperfusion control (I/R), ischemic post-conditioning (POC), and H2S post-conditioning (POC_H2S). In reperfusion control, cardiac contractility decreased, and lactate dehydrogenase, creatine kinase, and infracted size increased compared to both normal and ischemic group. In hearts post-conditioned with H2S and the classical method improved cardiac mechanical function and decreased cardiac markers in the perfusate and infarct size significantly. Both POC and POC_H2S exerts its cardioprotective effect of preserving the IFM, as evident by significant improvement in electron transport chain enzyme activities and mitochondrial respiration. The in vitro action of H2S on IFM and SSM from normal and I/R rat heart supports H2S and mediates cardioprotection via IFM preservation. Our study indicates that IFM play an important role in POC_H2S mediated cardioprotection from reperfusion injury. PMID:26951457

  6. Hyperoxic preconditioning fails to confer additional protection against ischemia-reperfusion injury in acute diabetic rat heart

    PubMed Central

    Pourkhalili, Khalil; Hajizadeh, Sohrab; Akbari, Zahra; Dehaj, Mansour Esmaili; Akbarzadeh, Samad; Alizadeh, Alimohammad

    2012-01-01

    Experimental studies show that detrimental effects of ischemia-reperfusion (I/R) injury can be attenuated by hyperoxic preconditioning in normal hearts, however, there are few studies about hyperoxia effects in diseased myocardium. The present study was designed to assess the cardioprotective effects of hyperoxia pretreatment (≥ 95 % O2) in acute diabetic rat hearts. Normal and one week acute diabetic rats were either exposed to 60 (H60) and 180 (H180) min of hyperoxia or exposed to normal atmospheric air (21 % O2). Then hearts were isolated immediately and subjected to 30 min of regional ischemia followed by 120 min of reperfusion. Infarct size, cardiomyocyte apoptosis, enzymes release and ischemia induced arrhythmias were determined. Heart of diabetic control rats had less infarct size and decreased LDH and CK-MB release compared to normal hearts. 60 and 180 min of hyperoxia reduced myocardial infarct size and enzymes release in normal hearts. 180 min of hyperoxia also decreased cardiomyocytes apoptosis in normal state. On the other hand, protective values of hyperoxia were not significantly different in diabetic hearts. Moreover, hyperoxia reduced severity of ventricular arrhythmias in normal rat hearts whereas; it did not confer any additional antiarrhythmic protection in diabetic hearts. These findings suggest that diabetic hearts are less susceptible to ischemia-induced arrhythmias and infarction. Hyperoxia greatly protects rat hearts against I/R injury in normal hearts, however, it could not provide added cardioprotective effects in acute phase of diabetes.

  7. [Penetrating knife injury to the heart treated with emergency department thoracotomy--case report].

    PubMed

    Sigurðardóttir, Anna; Stefánsson, Sigurjón Örn; Jóhannesdóttir, Bergrós Kristín; Guðbjartsson, Tómas

    2015-12-01

    Penetrating cardiac injuries usually result in an excessive bleeding and a cardiac tamponade with a very high mortality. If patients reach hospital alive, or within 15 minutes after no signs of life are found, an emergency department thoracotomy (EDT) can be indicated. However, the indications and outcome of this procedure have been debated. We report a 40 year old male that sustained a cardiac stab injury, causing a cardiac tamponade and a circulatory arrest. By performing an EDT with a pericardiotomy and direct cardiac massage, his circulation could be restored and the perforation of the heart sutured. Twelve months later the patient is in good health. This case shows that an EDT can be life saving in patients with penetrating cardiac injuries. PMID:26656399

  8. A Retained Bullet in Pericardial Sac: Penetrating Gunshot Injury of the Heart

    PubMed Central

    Kaya, Adnan; Caliskan, Emine; Tatlisu, Mustafa Adem; Hayiroglu, Mert Ilker; Tekessin, Ahmet Ilker; Cakilli, Yasin; Avsar, Sahin; Oz, Ahmet; Uzman, Osman

    2016-01-01

    Penetrating cardiac trauma is rarely seen but when present there is a short time lag to keep the patients alive. Cardiac gunshot injuries are exceptional and it occurs mostly during interpersonal disagreements casualties or a mistakenly fired gun nowadays. Here we present a case of cardiac gunshot injury from the war of Kobani, Syria. The patient was mistakenly diagnosed to have a sole bullet in the left shoulder while he had a penetrating cardiac trauma with a bullet in the heart and pericardial effusion possibly giving rise to pericardial tamponade. Luckily the cardiac gunshot injury was noticed one day later and the patient was referred to a tertiary hospital. Intrapericardial bullet was conservatively followed up. The patient was discharged one week later after resection of the bullet in the shoulder. PMID:26977324

  9. Early biomarkers of doxorubicin-induced heart injury in a mouse model

    SciTech Connect

    Desai, Varsha G.; Kwekel, Joshua C.; Vijay, Vikrant; Moland, Carrie L.; Herman, Eugene H.; Lee, Taewon; Han, Tao; Lewis, Sherry M.; Davis, Kelly J.; Muskhelishvili, Levan; Kerr, Susan; Fuscoe, James C.

    2014-12-01

    Cardiac troponins, which are used as myocardial injury markers, are released in plasma only after tissue damage has occurred. Therefore, there is a need for identification of biomarkers of earlier events in cardiac injury to limit the extent of damage. To accomplish this, expression profiling of 1179 unique microRNAs (miRNAs) was performed in a chronic cardiotoxicity mouse model developed in our laboratory. Male B6C3F{sub 1} mice were injected intravenously with 3 mg/kg doxorubicin (DOX; an anti-cancer drug), or saline once a week for 2, 3, 4, 6, and 8 weeks, resulting in cumulative DOX doses of 6, 9, 12, 18, and 24 mg/kg, respectively. Mice were euthanized a week after the last dose. Cardiac injury was evidenced in mice exposed to 18 mg/kg and higher cumulative DOX dose whereas examination of hearts by light microscopy revealed cardiac lesions at 24 mg/kg DOX. Also, 24 miRNAs were differentially expressed in mouse hearts, with the expression of 1, 1, 2, 8, and 21 miRNAs altered at 6, 9, 12, 18, and 24 mg/kg DOX, respectively. A pro-apoptotic miR-34a was the only miRNA that was up-regulated at all cumulative DOX doses and showed a significant dose-related response. Up-regulation of miR-34a at 6 mg/kg DOX may suggest apoptosis as an early molecular change in the hearts of DOX-treated mice. At 12 mg/kg DOX, up-regulation of miR-34a was associated with down-regulation of hypertrophy-related miR-150; changes observed before cardiac injury. These findings may lead to the development of biomarkers of earlier events in DOX-induced cardiotoxicity that occur before the release of cardiac troponins. - Highlights: • Upregulation of miR-34a before doxorubicin-induced cardiac tissue injury • Apoptosis might be an early event in mouse heart during doxorubicin treatment. • Expression of miR-150 declined before doxorubicin-induced cardiac tissue injury.

  10. Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts.

    PubMed

    Rodríguez-Sinovas, Antonio; García-Dorado, David; Ruiz-Meana, Marisol; Soler-Soler, Jordi

    2006-02-01

    It has been shown that cell-to-cell chemical coupling may persist during severe myocardial hypoxia or ischemia. We aimed to analyze the effects of different, chemically unrelated gap junction uncouplers on the progression of ischemic injury in hypoxic myocardium. First, we analyzed the effects of heptanol, 18alpha-glycyrrhetinic acid, and palmitoleic acid on intracellular Ca2+ concentration during simulated hypoxia (2 mM NaCN) in isolated cardiomyocytes. Next, we analyzed their effects on developed and diastolic tension and electrical impedance in 47 isolated rat hearts submitted to 40 min of hypoxia and reoxygenation. All treatments were applied only during the hypoxic period. Cell injury was determined by lactate dehydrogenase (LDH) release. Heptanol, but not 18alpha-glycyrrhetinic acid nor palmitoleic acid, attenuated the increase in cytosolic Ca2+ concentration induced by simulated ischemia in cardiomyocytes and delayed rigor development (rigor onset at 7.31 +/- 0.71 min in controls vs. 14.76 +/- 1.44 in heptanol-treated hearts, P < 0.001) and the onset of the marked changes in electrical impedance (tissue resistivity: 4.02 +/- 0.29 vs. 7.75 +/- 1.84 min, P = 0.016) in hypoxic rat hearts. LDH release from hypoxic hearts was minimal and was not significantly modified by drugs. However, all gap junction uncouplers, given during hypoxia, attenuated LDH release during subsequent reoxygenation. Dose-response analysis showed that increasing heptanol concentration beyond the level associated with maximal effects on cell coupling resulted in further protection against hypoxic injury. In conclusion, gap junction uncoupling during hypoxia has a protective effect on cell death occurring upon subsequent reoxygenation, and heptanol has, in addition, a marked protective effect independent of its uncoupling actions. PMID:16183732

  11. Brain in Congenital Heart Disease Across the Lifespan: The Cumulative Burden of Injury.

    PubMed

    Marelli, Ariane; Miller, Steven P; Marino, Bradley Scott; Jefferson, Angela L; Newburger, Jane W

    2016-05-17

    The number of patients surviving with congenital heart disease (CHD) has soared over the last 3 decades. Adults constitute the fastest-growing segment of the CHD population, now outnumbering children. Research to date on the heart-brain intersection in this population has been focused largely on neurodevelopmental outcomes in childhood and adolescence. Mutations in genes that are highly expressed in heart and brain may cause cerebral dysgenesis. Together with altered cerebral perfusion in utero, these factors are associated with abnormalities of brain structure and brain immaturity in a significant portion of neonates with critical CHD even before they undergo cardiac surgery. In infancy and childhood, the brain may be affected by risk factors related to heart disease itself or to its interventional treatments. As children with CHD become adults, they increasingly develop heart failure, atrial fibrillation, hypertension, diabetes mellitus, and coronary disease. These acquired cardiovascular comorbidities can be expected to have effects similar to those in the general population on cerebral blood flow, brain volumes, and dementia. In both children and adults, cardiovascular disease may have adverse effects on achievement, executive function, memory, language, social interactions, and quality of life. Against the backdrop of shifting demographics, risk factors for brain injury in the CHD population are cumulative and synergistic. As neurodevelopmental sequelae in children with CHD evolve to cognitive decline or dementia during adulthood, a growing population of CHD can be expected to require support services. We highlight evidence gaps and future research directions. PMID:27185022

  12. Protective effects of fluvoxamine against ischemia/reperfusion injury in isolated, perfused guinea-pig hearts.

    PubMed

    Muto, Tatsuya; Usuda, Haruki; Yamamura, Aya; Yoshida, Koji; Ohashi, Ai; Mitsui-Saitoh, Kumiko; Sakai, Junichi; Sugimoto, Yumi; Mizutani, Hideki; Nonogaki, Tsunemasa; Hotta, Yoshihiro

    2014-01-01

    Serotonin (5-hydroxytryptamine; 5-HT) is known to be activated during ischemia-reperfusion and triggers contractile dysfunction and pathological apoptosis. Here, the beneficial effects of the selective serotonin reuptake inhibitor (SSRI) fluvoxamine was demonstrated on ischemia-reperfusion injury in guinea-pig hearts perfused using the Langendorff technique. The recovery (%) of left ventricular developed pressure (LVDP) by fluvoxamine (5×10(-8) M) was 95.4% (control: 32%), which was consistent with the inhibition of mitochondrial Ca(2+)([Ca(2+)]m) uptake induced by changes in the Ca(2+) content and acidification of the perfusate, and similar to reperfusion following global ischemia in Langendorff-perfused hearts. Fluvoxamine inhibited the increase in [Ca(2+)]m induced by changes in the Ca(2+) content of the perfusate in perfused preparations of mitochondria, which was similar to the results obtained with the mitochondrial permeability transition pore (MPTP) opener atractyroside. The terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL)-positive cells were significantly less in fluvoxamine-treated hearts than in control hearts, with decreases in caspase-3 activity. These results suggest that SSRI inhibits opening of the MPTP by preventing [Ca(2+)]m overload-induced apoptosis related to the endogenous accumulation of 5-HT in ischemia-reperfusion hearts. PMID:24789996

  13. CTGF/CCN2 Postconditioning Increases Tolerance of Murine Hearts towards Ischemia-Reperfusion Injury

    PubMed Central

    Kaasbøll, Ole Jørgen; Moe, Ingvild Tronstad; Ahmed, Mohammad Shakil; Stang, Espen; Hagelin, Else Marie Valbjørn; Attramadal, Håvard

    2016-01-01

    Background and Purpose Previous studies of ischemia-reperfusion injury (IRI) in hearts from mice with cardiac-restricted overexpression of CCN2 have shown that CCN2 increases tolerance towards IRI. The objectives of this study were to investigate to what extent post-ischemic administration of recombinant human CCN2 (rhCCN2) would limit infarct size and improve functional recovery and what signaling pathways are involved. Experimental Approach Isolated mice hearts were perfused ad modum Langendorff, subjected to no-flow, global ischemia, and subsequently, exposed to mammalian cell derived, full-length (38-40kDa) rhCCN2 (250 nM) or vehicle during the first 15 min of a 60 min reperfusion period. Key Results Post-ischemic administration of rhCCN2 resulted in attenuation of infarct size from 58 ± 4% to 34 ± 2% (p < 0.001) which was abrogated by concomitant administration of the PI3 kinase inhibitor LY294002 (45 ± 3% vs. 50 ± 3%, ns). In congruence with reduction of infarct size rhCCN2 also improved recovery of left ventricular developed pressure (p < 0.05). Western blot analyses of extracts of ex vivo-perfused murine hearts also revealed that rhCCN2 evoked concentration-dependent increase of cardiac phospho-GSK3β (serine-9) contents. Conclusions and Implications We demonstrate that post-ischemic administration of rhCCN2 increases the tolerance of ex vivo-perfused murine hearts to IRI. Mechanistically, this postconditioning effect of rhCCN2 appeared to be mediated by activation of the reperfusion injury salvage kinase pathway as demonstrated by sensitivity to PI3 kinase inhibition and increased CCN2-induced phosphorylation of GSK3β (Ser-9). Thus, the rationale for testing rhCCN2-mediated post-ischemic conditioning of the heart in more complex models is established. PMID:26872261

  14. Protective effects of drag-reducing polymers on ischemic reperfusion injury of isolated rat heart.

    PubMed

    Hu, Feng; Wang, Yali; Gong, Kaizheng; Ge, Gaoyuan; Cao, Mingqiang; Zhao, Pei; Sun, Xiaoning; Zhang, Zhengang

    2016-01-01

    Drag-reducing polymers (DRPs) are blood-soluble macromolecules that can increase blood flow and reduce vascular resistance. The purpose of the present study was to observe the effect of DRPs on ischemic reperfusion (I/R) injury of isolated rat hearts. Experiments were performed on isolated rat hearts subjected to 30 min of ischemia followed by 90 min of reperfusion in Langendorff preparations. Adult Wistar rats were divided into the following five groups: control group, I/R group, group III (I/R and 2×10(-7)  g/ml PEO reperfusion), group IV (I/R and 1×10(-6)  g/ml PEO reperfusion), and group V (I/R and 5×10(-6)  g/ml PEO reperfusion). Left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), maximum rate of ventricular pressure increase and decrease ( ± dp/dtmax), heart rate (HR) and coronary flow were measured. Lactate dehydrogenase (LDH) and creatine kinase (CK) activity and coronary flow, myocardial infarction size and cardiomyocytes apoptosis were also assayed. Our results showed that PEO decreased LVEDP and increased LVSP, ± dP/dtmax in group IV and group V compared with the I/R group (all P <  0.05). The coronary flow significantly increased and the activities of LDH and CK in the coronary flow significantly decreased in group IV and group V compared with those in the I/R group (all P <  0.05). Cell apoptosis and myocardial infarction size were reduced in group IV and group V compared with the I/R group (all P <  0.05). Collectively, these results suggested that DRPs had a protective effect on cardiac I/R injury of isolated rat hearts and it may offer a new potential approach for the treatment of acute ischemic heart diseases. PMID:25633566

  15. Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

    PubMed Central

    Qu, Daoxu; Ren, Huanhuan; Yang, Wenxiao; Zhang, Xinjie; Zheng, Qiusheng; Wang, Dong

    2016-01-01

    This study aims to evaluate the cardioprotective effects of astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague-Dawley rats were randomly divided into five groups. The results showed that astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) decreased in astragalin-treated groups. The infarct size (IS) and apoptosis rate in hearts from astragalin-treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that astragalin preconditioning significantly reduced Bax level, whereas Bcl-2 was increased in the myocardium. Therefore, astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti-inflammatory activities. PMID:26788251

  16. Long range correlations in the heart rate variability following the injury of cardiac arrest

    NASA Astrophysics Data System (ADS)

    Tong, Shanbao; Jiang, Dineng; Wang, Ziming; Zhu, Yisheng; Geocadin, Romeryko G.; Thakor, Nitish V.

    2007-07-01

    Cardiovascular and neurological recovery following cardiac arrest (CA) largely influence the morbidity and mortality of the patients. Monitoring the cardiovascular system has been an important clinical issue in intensive care unit (ICU). On the other hand, the rhythms of the heart rate variability following CA are still not fully understood, and there are limited number of literatures reporting the cardiovascular function recovery following CA. In this paper, we studied the scaling properties of heart rate variability (HRV) after CA by centered-moving-average-based detrended fluctuation analysis (DFA). Our results showed that the scaling factor of the baseline HRV is close to that of Brownian motion, and after a CA event it shifts to a 1/f noise-like rhythm. DFA could be a promising tool in evaluating the cardiovascular long term recovery following CA injury.

  17. Protective effect of apigenin on ischemia/reperfusion injury of the isolated rat heart.

    PubMed

    Hu, Jing; Li, Zilin; Xu, Li-ting; Sun, Ai-jun; Fu, Xiao-yan; Zhang, Li; Jing, Lin-lin; Lu, An-dong; Dong, Yi-fei; Jia, Zheng-ping

    2015-07-01

    Apigenin (Api), a mainly bioactive component of Apium graveolens L. var. dulce DC. (a traditional Chinese medicinal herb), possesses a wide range of biological activities, including antioxidant effects. It also has been shown to associate with lower prevalence of cardiovascular diseases, but its mechanisms of action remain unclear. The aim of the present study is to investigate the role of Api in isolated rat heart model of ischemia/reperfusion (I/R). Langendorff-perfused isolated rat hearts were used in our study. Api was added to the perfusate before ischemia and during reperfusion in the isolated pulsed rat heart exposed to 30-min ischemia followed by 50-min reperfusion. The treatment with Api conferred a cardioprotective effect, and the treated hearts demonstrated an improved ischemic cardiac functional recovery, a decreased myocardial infarct size, a reduced activities of creatine kinase isoenzyme and lactate dehydrogenase in the coronary flow, a reduced number of apoptotic cardiomyocytes, a reduced activity of caspase-3, up-regulation of the anti-apoptotic protein Bcl-2 and down-regulation of the pro-apoptotic protein Bax. In addition, Api inhibited the phosphorylation of p38 MAPKS during I/R. In conclusion, these observations provide preliminary evidence that Api can protect cardiomyocytes from I-/R-induced injury, at least partially, through the inhibition of p38 MAPKS signaling pathway. PMID:25377428

  18. [Heart injury secondary to carbon monoxide poisoning--the use of imaging techniques].

    PubMed

    Kołodziej, Małgorzata; Zaleski, Kamil; Majewska, Magdalena; Górska, Agnieszka; Kwiecień-Obara, Ewelina; Szponar, Jarosław

    2013-01-01

    The heart muscle is particularly sensitive to the toxic effects of carbon monoxide. Cardiovascular complications are present in 30-40% poisoned patients. Currently, multiple ECG records and at least two-time determination of cardiac markers' concentration (mainly troponin I) are known as the gold standard practice in the diagnosis of cardiac injury especially with regard to medium and severe poisoning. So far there have not been any recommendations for further diagnostic steps in case of abnormalities in these examinations. This paper presents a review of cardiac imaging techniques as well as the analysis of their usefulness in carbon monoxide poisoning. According to the authors echocardiography is considered to be an extremely important examination which, thanks to its accessibility and non-invasive nature, should be performed on all patients with myocardium injury suspicion made on the basis of clinical image, ECG records and biochemical markers. PMID:24466706

  19. Protease-activated receptor-2 modulates myocardial ischemia-reperfusion injury in the rat heart

    PubMed Central

    Napoli, Claudio; Cicala, Carla; Wallace, John L.; de Nigris, Filomena; Santagada, Vincenzo; Caliendo, Giuseppe; Franconi, Flavia; Ignarro, Louis J.; Cirino, Giuseppe

    2000-01-01

    Protease-activated receptor-2 (PAR-2) is a member of seven transmembrane domain G protein-coupled receptors activated by proteolytic cleavage whose better known member is the thrombin receptor. The pathophysiological role of PAR-2 remains poorly understood. Because PAR-2 is involved in inflammatory and injury response events, we investigated the role of PAR-2 in experimental myocardial ischemia-reperfusion injury. We show for the first time that PAR-2 activation protects against reperfusion-injury. After PAR-2-activating peptide (2AP) infusion, we found a significant recovery of myocardial function and decrease in oxidation at reflow. Indeed, the glutathione cycle (glutathione and oxidized glutathione) and lipid peroxidation analysis showed a reduced oxidative reperfusion-injury. Moreover, ischemic risk zone and creatine kinase release were decreased after PAR-2AP treatment. These events were coupled to elevation of PAR-2 and tumor necrosis factor α (TNFα) expression in both nuclear extracts and whole heart homogenates. The recovery of coronary flow was not reverted by L-nitroarginine methylester, indicating a NO-independent pathway for this effect. Genistein, a tyrosine kinase inhibitor, did not revert the PAR-2AP effect. During early reperfusion injury in vivo not only oxygen radicals are produced but also numerous proinflammatory mediators promoting neutrophil and monocyte targeting. In this context, we show that TNFα and PAR-2 are involved in signaling in pathophysiological conditions, such as myocardial ischemia-reperfusion. At the same time, because TNFα may exert pro-inflammatory actions and PAR-2 may constitute one of the first protective mechanisms that signals a primary inflammatory response, our data support the concept that this network may regulate body responses to tissue injury. PMID:10737808

  20. Protease-activated receptor-2 modulates myocardial ischemia-reperfusion injury in the rat heart.

    PubMed

    Napoli, C; Cicala, C; Wallace, J L; de Nigris, F; Santagada, V; Caliendo, G; Franconi, F; Ignarro, L J; Cirino, G

    2000-03-28

    Protease-activated receptor-2 (PAR-2) is a member of seven transmembrane domain G protein-coupled receptors activated by proteolytic cleavage whose better known member is the thrombin receptor. The pathophysiological role of PAR-2 remains poorly understood. Because PAR-2 is involved in inflammatory and injury response events, we investigated the role of PAR-2 in experimental myocardial ischemia-reperfusion injury. We show for the first time that PAR-2 activation protects against reperfusion-injury. After PAR-2-activating peptide (2AP) infusion, we found a significant recovery of myocardial function and decrease in oxidation at reflow. Indeed, the glutathione cycle (glutathione and oxidized glutathione) and lipid peroxidation analysis showed a reduced oxidative reperfusion-injury. Moreover, ischemic risk zone and creatine kinase release were decreased after PAR-2AP treatment. These events were coupled to elevation of PAR-2 and tumor necrosis factor alpha (TNFalpha) expression in both nuclear extracts and whole heart homogenates. The recovery of coronary flow was not reverted by L-nitroarginine methylester, indicating a NO-independent pathway for this effect. Genistein, a tyrosine kinase inhibitor, did not revert the PAR-2AP effect. During early reperfusion injury in vivo not only oxygen radicals are produced but also numerous proinflammatory mediators promoting neutrophil and monocyte targeting. In this context, we show that TNFalpha and PAR-2 are involved in signaling in pathophysiological conditions, such as myocardial ischemia-reperfusion. At the same time, because TNFalpha may exert pro-inflammatory actions and PAR-2 may constitute one of the first protective mechanisms that signals a primary inflammatory response, our data support the concept that this network may regulate body responses to tissue injury. PMID:10737808

  1. Outcomes of recurrent laryngeal nerve injury following congenital heart surgery: A contemporary experience

    PubMed Central

    Alfares, Fahad A.; Hynes, Conor F.; Ansari, Ghedak; Chounoune, Reginald; Ramadan, Manelle; Shaughnessy, Conner; Reilly, Brian K.; Zurakowski, David; Jonas, Richard A.; Nath, Dilip S.

    2015-01-01

    Objective Injury to the recurrent laryngeal nerve can lead to significant morbidity during congenital cardiac surgery. The objective is to expand on the limited understanding of the severity and recovery of this iatrogenic condition. Design A six-year retrospective review of all congenital heart operations at a single institution from January 1, 2008 to December 31, 2013 was performed. All patients with documented vocal cord paralysis on laryngoscopic examination comprised the study cohort. Evaluation of time to vocal cord recovery and need for further surgical intervention was the primary focus. Results The incidence of post-operative vocal cord paralysis was 1.1% (32 out of 3036 patients; 95% confidence interval: 0.7–1.5%). The majority were left-sided injuries (71%). Overall rate of recovery was 61% with a median time of 10 months in those who recovered, and a total follow up of 46 months. Due to feeding complications, 45% of patients required gastrostomy tube after the injury, and these patients were found to have longer duration of post-operative days of intubation (median 10 vs. 5 days, p = 0.03), ICU length of stay (50 vs. 8 days, p = 0.002), and hospital length of stay (92 vs. 41 days, p = 0.01). No pre-operative variables were identified as predictive of recovery or need for gastrostomy placement. Conclusion Recurrent laryngeal nerve injury is a serious complication of congenital heart surgery that impacts post-operative morbidity, in some cases leading to a need for further intervention, in particular, gastrostomy tube placement. A prospective, multi-center study is needed to fully evaluate factors that influence severity and time to recovery. PMID:26778899

  2. High carbohydrate and high fat diets protect the heart against ischaemia/reperfusion injury

    PubMed Central

    2014-01-01

    Background Although obesity is still considered a risk factor in the development of cardiovascular disorders, recent studies suggested that it may also be associated with reduced morbidity and mortality, the so-called “obesity paradox”. Experimental data on the impact of diabetes, obesity and insulin resistance on myocardial ischaemia/reperfusion injury are controversial. Similar conflicting data have been reported regarding the effects of ischaemic preconditioning on ischaemia/reperfusion injury in hearts from such animals. The aim of the present study was to evaluate the susceptibility to myocardial ischaemia/reperfusion damage in two models of diet-induced obesity as well as the effect of ischaemic and pharmacological preconditioning on such hearts. Methods Three groups of rats were fed with: (i) normal rat chow (controls) (ii) a sucrose-supplemented diet (DIO) (iii) a high fat diet (HFD). After 16 weeks, rats were sacrificed and isolated hearts perfused in the working mode and subjected to 35 min regional ischaemia/60 min reperfusion. Endpoints were infarct size and functional recovery. Infarct size was determined, using tetrazolium staining. Activation of PKB/Akt and ERKp44/p42 (RISK pathway) during early reperfusion was determined using Western blot. Statistical evaluation was done using ANOVA and the Bonferroni correction. Results Infarct sizes of non-preconditioned hearts from the two obese groups were significantly smaller than those of the age-matched controls. Ischaemic as well as pharmacological (beta-adrenergic) preconditioning with a beta2-adrenergic receptor agonist, formoterol, caused a significant reduction in infarct size of the controls, but were without effect on infarct size of hearts from the obese groups. However, ischaemic as well as beta-preconditioning caused an improvement in functional performance during reperfusion in all three groups. A clear-cut correlation between the reduction in infarct size and activation of ERKp44/p42 and

  3. Hypercholesterolemia abrogates an increased resistance of diabetic rat hearts to ischemia-reperfusion injury.

    PubMed

    Adameová, A; Kuzelová, M; Andelová, E; Faberová, V; Pancza, D; Svec, P; Ziegelhöffer, A; Ravingerová, T

    2007-01-01

    Both, diabetes mellitus (DM) and hypercholesterolemia (HCH) are known as risk factors of ischemic heart disease, however, the effects of experimental DM, as well as of HCH alone, on ischemia/reperfusion-induced myocardial injury are not unequivocal. We have previously demonstrated an enhanced resistance to ischemia-induced arrhythmias in rat hearts in the acute phase of DM. Our objectives were thus to extend our knowledge on how DM in combination with HCH, a model that is relevant to diabetic patients with altered lipid metabolism, may affect the size of myocardial infarction and susceptibility to arrhythmias. A combination of streptozotocin (STZ; 80 mg/kg, i.p.) and the fat-cholesterol diet (1% cholesterol, 1% coconut oil; FCHD) was used as a double-disease model mimicking DM and HCH simultaneosly occurring in humans. Following 5 days after STZ injection and FCHD leading to increased blood glucose and cholesterol levels, anesthetized open-chest diabetic, diabetic-hypercholesterolemic (DM-HCH) and age-matched control rats were subjected to 6-min ischemia (occlusion of LAD coronary artery) followed by 10 reperfusion to test susceptibility to ventricular arrhythmias in the in vivo experiments and to 30-min ischemia and subsequent 2-h reperfusion for the evaluation of the infarct size (IS) in the Langendorff-perfused hearts. The incidence of the most life-threatening ventricular arrhythmia, ventricular fibrillation, was significantly increased in the DM-HCH rats as compared with non-diabetic control animals (100% vs. 50%; p<0.05). Likewise, arrhythmia severity score (AS) was significantly higher in the DM-HCH rats than in the controls (4.9+/-0.2 vs. 3.5+/-0.5; p<0.05), but was not increased in the diabetic animals (AS 3.7+/-0.9; p>0.05 vs. controls). Diabetic hearts exhibited a reduced IS (15.1+/-3.0% of the area at risk vs. 37.6+/-2.8% in the control hearts; p<0.05), however, a combination of DM and HCH increased the size of myocardial infarction to that observed in

  4. The cardioprotective effect of danshen and gegen decoction on rat hearts and cardiomyocytes with post-ischemia reperfusion injury

    PubMed Central

    2012-01-01

    Background Danshen (Salviae Miltiorrhizae Radix) and Gegen (Puerariae Lobatae Radix) have been used for treating heart disease for several thousand years in China. It has been found that a Danshen and Gegen decoction (DG) exhibiting an anti-atherosclerosis effect, which improves the patients’ heart function recovery. Pre-treatment with DG was reported to have protective effects on myocardium against ischemia/reperfusion injury. In the present study, we aim to investigate the post-treatment effect of DG on ischemic-reperfusion injuries ex vivo or in vitro and the underlying mechanisms involved. Methods The rat heart function in an ischemia and reperfusion (I/R) model was explored by examining three parameters including contractile force, coronary flow rate and the release of heart specific enzymes within the heart perfusate. In vitro model of hypoxia and reoxygenation (H/R), the protective effect of DG on damaged cardiomyocytes was investigated by examining the cell structure integrity, the apoptosis and the functionality of mitochondria. Results Our results showed that DG significantly improved rat heart function after I/R challenge and suppressed the release of enzymes by damaged heart muscles in a dose-dependent manner. DG also significantly inhibited the death of cardiomyocytes, H9c2 cells, with a H/R challenge. It obviously decreased cell apoptosis, protected the mitochondrial function and cell membrane skeleton integrity on H9c2 cells. The cardio-protection was also found to be related to a decrease in intracellular calcium accumulation within H9c2 cells after I/R challenge. Conclusion The potential application of DG in treating rat hearts with an I/R injury has been implied in this study. Our results suggested that DG decoction could act as an anti-apoptotic and anti-ion stunning agent to protect hearts against an I/R injury. PMID:23228089

  5. Acute kidney injury after using contrast during cardiac catheterization in children with heart disease.

    PubMed

    Hwang, Young Ju; Hyun, Myung Chul; Choi, Bong Seok; Chun, So Young; Cho, Min Hyun

    2014-08-01

    Acute kidney injury (AKI) is closely associated with the mortality of hospitalized patients and long-term development of chronic kidney disease, especially in children. The purpose of our study was to assess the evidence of contrast-induced AKI after cardiac catheterization in children with heart disease and evaluate the clinical usefulness of candidate biomarkers in AKI. A total of 26 children undergoing cardiac catheterization due to various heart diseases were selected and urine and blood samples were taken at 0 hr, 6 hr, 24 hr, and 48 hr after cardiac catheterization. Until 48 hr after cardiac catheterization, there was no significant increase in serum creatinine level in all patients. Unlike urine kidney injury molecule-1, IL-18 and neutrophil gelatinase-associated lipocalin, urine liver-type fatty acid-binding protein (L-FABP) level showed biphasic pattern and the significant difference in the levels of urine L-FABP between 24 and 48 hr. We suggest that urine L-FABP can be one of the useful biomarkers to detect subclinical AKI developed by the contrast before cardiac surgery. PMID:25120320

  6. S1P lyase: a novel therapeutic target for ischemia-reperfusion injury of the heart

    PubMed Central

    Bandhuvula, Padmavathi; Honbo, Norman; Wang, Guan-Ying; Jin, Zhu-Qiu; Fyrst, Henrik; Zhang, Meng; Borowsky, Alexander D.; Dillard, Lisa; Karliner, Joel S.

    2011-01-01

    Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid that promotes cardiomyocyte survival and contributes to ischemic preconditioning. S1P lyase (SPL) is a stress-activated enzyme responsible for irreversible S1P catabolism. We hypothesized that SPL contributes to oxidative stress by depleting S1P pools available for cardioprotective signaling. Accordingly, we evaluated SPL inhibition as a strategy for reducing cardiac ischemia-reperfusion (I/R) injury. We measured SPL expression and enzyme activity in murine hearts. Basal SPL activity was low in wild-type cardiac tissue but was activated in response to 50 min of ischemia (n = 5, P < 0.01). Hearts of heterozygous SPL knockout mice exhibited reduced SPL activity, elevated S1P levels, smaller infarct size, and increased functional recovery after I/R compared with littermate controls (n = 5, P < 0.01). The small molecule tetrahydroxybutylimidazole (THI) is a Federal Drug Administration-approved food additive that inhibits SPL. When given overnight at 25 mg/l in drinking water, THI raised S1P levels and reduced SPL activity (n = 5, P < 0.01). THI reduced infarct size and enhanced hemodynamic recovery in response to 50 min of ischemia and to 40 min of reperfusion in ex vivo hearts (n = 7, P < .01). These data correlated with an increase in MAP kinase-interacting serine/threonine kinase 1, eukaryotic translation initiation factor 4E, and ribosomal protein S6 phosphorylation levels after I/R, suggesting that SPL inhibition enhances protein translation. Pretreatment with an S1P1 and S1P3 receptor antagonist partially reversed the effects of THI. These results reveal, for the first time, that SPL is an ischemia-induced enzyme that can be targeted as a novel strategy for preventing cardiac I/R injury. PMID:21335477

  7. Effects of Glucose Concentration on Propofol Cardioprotection against Myocardial Ischemia Reperfusion Injury in Isolated Rat Hearts.

    PubMed

    Yao, Xinhua; Li, Yalan; Tao, Mingzhe; Wang, Shuang; Zhang, Liangqing; Lin, Jiefu; Xia, Zhengyuan; Liu, Hui-Min

    2015-01-01

    The anesthetic propofol confers cardioprotection against myocardial ischemia-reperfusion injury (IRI) by reducing reactive oxygen species (ROS). However, its cardioprotection on patients is inconsistent. Similarly, the beneficial effect of tight glycemic control during cardiac surgery in patients has recently been questioned. We postulated that low glucose (LG) may promote ROS formation through enhancing fatty acid (FA) oxidation and unmask propofol cardioprotection during IRI. Rat hearts were isolated and randomly assigned to be perfused with Krebs-Henseleit solution with glucose at 5.5 mM (LG) or 8 mM (G) in the absence or presence of propofol (5 μg/mL) or propofol plus trimetazidine (TMZ). Hearts were subjected to 35 minutes of ischemia followed by 60 minutes of reperfusion. Myocardial infarct size (IS) and cardiac CK-MB were significantly higher in LG than in G group (P < 0.05), associated with reduced left ventricular developed pressure and increases in postischemic cardiac contracture. Cardiac 15-F2t-isoprostane was higher, accompanied with higher cardiac lipid transporter CD36 protein expression in LG. Propofol reduced IS, improved cardiac function, and reduced CD36 in G but not in LG. TMZ facilitated propofol cardioprotection in LG. Therefore, isolated heart with low glucose lost sensitivity to propofol treatment through enhancing FA oxidation and TMZ supplementation restored the sensitivity to propofol. PMID:26491698

  8. Effects of Glucose Concentration on Propofol Cardioprotection against Myocardial Ischemia Reperfusion Injury in Isolated Rat Hearts

    PubMed Central

    Yao, Xinhua; Li, Yalan; Tao, Mingzhe; Wang, Shuang; Zhang, Liangqing; Lin, Jiefu; Xia, Zhengyuan; Liu, Hui-min

    2015-01-01

    The anesthetic propofol confers cardioprotection against myocardial ischemia-reperfusion injury (IRI) by reducing reactive oxygen species (ROS). However, its cardioprotection on patients is inconsistent. Similarly, the beneficial effect of tight glycemic control during cardiac surgery in patients has recently been questioned. We postulated that low glucose (LG) may promote ROS formation through enhancing fatty acid (FA) oxidation and unmask propofol cardioprotection during IRI. Rat hearts were isolated and randomly assigned to be perfused with Krebs-Henseleit solution with glucose at 5.5 mM (LG) or 8 mM (G) in the absence or presence of propofol (5 μg/mL) or propofol plus trimetazidine (TMZ). Hearts were subjected to 35 minutes of ischemia followed by 60 minutes of reperfusion. Myocardial infarct size (IS) and cardiac CK-MB were significantly higher in LG than in G group (P < 0.05), associated with reduced left ventricular developed pressure and increases in postischemic cardiac contracture. Cardiac 15-F2t-isoprostane was higher, accompanied with higher cardiac lipid transporter CD36 protein expression in LG. Propofol reduced IS, improved cardiac function, and reduced CD36 in G but not in LG. TMZ facilitated propofol cardioprotection in LG. Therefore, isolated heart with low glucose lost sensitivity to propofol treatment through enhancing FA oxidation and TMZ supplementation restored the sensitivity to propofol. PMID:26491698

  9. Hypoxia/Reoxygenation Cardiac Injury and Regeneration in Zebrafish Adult Heart

    PubMed Central

    Pompilio, Giulio; Verduci, Lorena; Colombo, Gualtiero I.; Milano, Giuseppina; Guerrini, Uliano; Squadroni, Lidia; Cotelli, Franco; Pozzoli, Ombretta; Capogrossi, Maurizio C.

    2013-01-01

    Aims the adult zebrafish heart regenerates spontaneously after injury and has been used to study the mechanisms of cardiac repair. However, no zebrafish model is available that mimics ischemic injury in mammalian heart. We developed and characterized zebrafish cardiac injury induced by hypoxia/reoxygenation (H/R) and the regeneration that followed it. Methods and Results adult zebrafish were kept either in hypoxic (H) or normoxic control (C) water for 15 min; thereafter fishes were returned to C water. Within 2–6 hours (h) after reoxygenation there was evidence of cardiac oxidative stress by dihydroethidium fluorescence and protein nitrosylation, as well as of inflammation. We used Tg(cmlc2:nucDsRed) transgenic zebrafish to identify myocardial cell nuclei. Cardiomyocyte apoptosis and necrosis were evidenced by TUNEL and Acridine Orange (AO) staining, respectively; 18 h after H/R, 9.9±2.6% of myocardial cell nuclei were TUNEL+ and 15.0±2.5% were AO+. At the 30-day (d) time point myocardial cell death was back to baseline (n = 3 at each time point). We evaluated cardiomyocyte proliferation by Phospho Histone H3 (pHH3) or Proliferating Cell Nuclear Antigen (PCNA) expression. Cardiomyocyte proliferation was apparent 18–24 h after H/R, it achieved its peak 3–7d later, and was back to baseline at 30d. 7d after H/R 17.4±2.3% of all cardiomyocytes were pHH3+ and 7.4±0.6% were PCNA+ (n = 3 at each time point). Cardiac function was assessed by 2D-echocardiography and Ventricular Diastolic and Systolic Areas were used to compute Fractional Area Change (FAC). FAC decreased from 29.3±2.0% in normoxia to 16.4±1.8% at 18 h after H/R; one month later ventricular function was back to baseline (n = 12 at each time point). Conclusions zebrafish exposed to H/R exhibit evidence of cardiac oxidative stress and inflammation, myocardial cell death and proliferation. The initial decrease in ventricular function is followed by full recovery. This model more closely

  10. Ramiprilat prevents PAF-induced myocellular and endothelial injury in a neutrophil-perfused heart preparation.

    PubMed

    Schrör, K; Felsch, A

    1992-01-01

    This study investigates the action of PAF-stimulated human polymorphonuclear leukocytes (PMN) on myocardial integrity and function in Langendorff-perfused guinea-pig hearts. Infusion of 10(6) PMN/ml resulted in a negative inotropic effect without larger biochemical evidence for myocardial tissue injury while infusion of PAF (1 microM) did not cause any permanent effect at all. However, the combined administration of PAF-stimulated PMN resulted in severely depressed myocardial contractile function and biochemical evidence for myocardial tissue injury. This was probably due to an enhanced uptake of PMN from the coronary perfusate and accumulation within the myocardial tissue. Ramiprilat, (10 microM) significantly improved left ventricular function and myocardial cell integrity. Similar results were obtained with bradykinin (1 nM). The data suggest a PAF-induced, PMN-mediated myocardial tissue injury as well as cardioprotective actions of ACE inhibition which are possibly related to stimulation of the kinin/prostacyclin axis. PMID:1334351

  11. Prenatal cocaine exposure increases heart susceptibility to ischaemia–reperfusion injury in adult male but not female rats

    PubMed Central

    Bae, Soochan; Gilbert, Raymond D; Ducsay, Charles A; Zhang, Lubo

    2005-01-01

    The present study tested the hypothesis that prenatal cocaine exposure differentially regulates heart susceptibility to ischaemia–reperfusion (I/R) injury in adult offspring male and female rats. Pregnant rats were administered intraperitoneally either saline or cocaine (15 mg kg−1) twice daily from day 15 to day 21 of gestational age. There were no differences in maternal weight gain and birth weight between the two groups. Hearts were isolated from 2-month-old male and female offspring and were subjected to I/R (25 min/60 min) in a Langendorff preparation. Preischaemic values of left ventricular (LV) function were the same between the saline control and cocaine-treated hearts for both male and female rats. Prenatal cocaine exposure significantly increased I/R-induced myocardial apoptosis and infarct size, and significantly attenuated the postischaemic recovery of LV function in adult male offspring. In contrast, cocaine did not affect I/R-induced injury and postischaemic recovery of LV function in the female hearts. There was a significant decrease in PKCɛ and phospho-PKCɛ levels in LV in the male, but not female, offspring exposed to cocaine before birth. These results suggest that prenatal cocaine exposure causes a sex-specific increase in heart susceptibility to I/R injury in adult male offspring, and the decreased PKCɛ gene expression in the male heart may play an important role. PMID:15677681

  12. Transplantation of autologously derived mitochondria protects the heart from ischemia-reperfusion injury.

    PubMed

    Masuzawa, Akihiro; Black, Kendra M; Pacak, Christina A; Ericsson, Maria; Barnett, Reanne J; Drumm, Ciara; Seth, Pankaj; Bloch, Donald B; Levitsky, Sidney; Cowan, Douglas B; McCully, James D

    2013-04-01

    Mitochondrial damage and dysfunction occur during ischemia and modulate cardiac function and cell survival significantly during reperfusion. We hypothesized that transplantation of autologously derived mitochondria immediately prior to reperfusion would ameliorate these effects. New Zealand White rabbits were used for regional ischemia (RI), which was achieved by temporarily snaring the left anterior descending artery for 30 min. Following 29 min of RI, autologously derived mitochondria (RI-mitochondria; 9.7 ± 1.7 × 10(6)/ml) or vehicle alone (RI-vehicle) were injected directly into the RI zone, and the hearts were allowed to recover for 4 wk. Mitochondrial transplantation decreased (P < 0.05) creatine kinase MB, cardiac troponin-I, and apoptosis significantly in the RI zone. Infarct size following 4 wk of recovery was decreased significantly in RI-mitochondria (7.9 ± 2.9%) compared with RI-vehicle (34.2 ± 3.3%, P < 0.05). Serial echocardiograms showed that RI-mitochondria hearts returned to normal contraction within 10 min after reperfusion was started; however, RI-vehicle hearts showed persistent hypokinesia in the RI zone at 4 wk of recovery. Electrocardiogram and optical mapping studies showed that no arrhythmia was associated with autologously derived mitochondrial transplantation. In vivo and in vitro studies show that the transplanted mitochondria are evident in the interstitial spaces and are internalized by cardiomyocytes 2-8 h after transplantation. The transplanted mitochondria enhanced oxygen consumption, high-energy phosphate synthesis, and the induction of cytokine mediators and proteomic pathways that are important in preserving myocardial energetics, cell viability, and enhanced post-infarct cardiac function. Transplantation of autologously derived mitochondria provides a novel technique to protect the heart from ischemia-reperfusion injury. PMID:23355340

  13. Activated c-Kit receptor in the heart promotes cardiac repair and regeneration after injury

    PubMed Central

    Di Siena, S; Gimmelli, R; Nori, S L; Barbagallo, F; Campolo, F; Dolci, S; Rossi, P; Venneri, M A; Giannetta, E; Gianfrilli, D; Feigenbaum, L; Lenzi, A; Naro, F; Cianflone, E; Mancuso, T; Torella, D; Isidori, A M; Pellegrini, M

    2016-01-01

    The role of endogenous c-Kit receptor activation on cardiac cell homeostasis and repair remains largely unexplored. Transgenic mice carrying an activating point mutation (TgD814Y) in the kinase domain of the c-Kit gene were generated. c-KitTgD814Y receptor was expressed in the heart during embryonic development and postnatal life, in a similar timing and expression pattern to that of the endogenous gene, but not in the hematopoietic compartment allowing the study of a cardiac-specific phenotype. c-KitTgD814Y mutation produced a constitutive active c-Kit receptor in cardiac tissue and cells from transgenic mice as demonstrated by the increased phosphorylation of ERK1/2 and AKT, which are the main downstream molecular effectors of c-Kit receptor signaling. In adult transgenic hearts, cardiac morphology, size and total c-Kit+ cardiac cell number was not different compared with wt mice. However, when c-KitTgD814Y mice were subjected to transmural necrotic heart damage by cryoinjury (CI), all transgenic survived, compared with half of wt mice. In the sub-acute phase after CI, transgenic and wt mice showed similar heart damage. However, 9 days after CI, transgenic mice exhibited an increased number of c-Kit+CD31+ endothelial progenitor cells surrounding the necrotic area. At later follow-up, a consistent reduction of fibrotic area, increased capillary density and increased cardiomyocyte replenishment rate (as established by BrdU incorporation) were observed in transgenic compared with wt mice. Consistently, CD45−c-Kit+ cardiac stem cells isolated from transgenic c-KitTgD814Y mice showed an enhanced endothelial and cardiomyocyte differentiation potential compared with cells isolated from the wt. Constitutive activation of c-Kit receptor in mice is associated with an increased cardiac myogenic and vasculogenic reparative potential after injury, with a significant improvement of survival. PMID:27468693

  14. Eprosartan improves cardiac function in swine working heart model of ischemia-reperfusion injury

    PubMed Central

    Weymann, Alexander; Sabashnikov, Anton; Patil, Nikhil P.; Konertz, Wolfgang; Modersohn, Diethelm; Dohmen, Pascal M.

    2014-01-01

    Background Eprosartan is an angiotensin II receptor antagonist used as an antihypertensive. We sought to evaluate the regional effect of Eprosartan on postinfarct ventricular remodeling and myocardial function in an isolated swine working heart model of ischemia-reperfusion injury. Material/Methods 22 swine hearts were perfused with the Langendorff perfusion apparatus under standard experimental conditions. Myocardial ischemia was induced by a 10-min left anterior descending artery ligation. Hearts were reperfused with either saline (control group, n=11), or Eprosartan (treatment group, n=11). Left ventricular pressure (LVP) and regional heart parameters such as intramyocardial pressure (IMP), wall thickening rate (WTh), and pressure-length-loops (PLL) were measured at baseline and after 30 min of reperfusion. Results Measured parameters were statistically similar between the 2 groups at baseline. The administration of Eprosartan led to a significantly better recovery of IMP and WTh: 44.4±2.5 mmHg vs. 51.2±3.3 mmHg, p<0.001 and 3.8±0.4 μm vs. 4.4±0.3 μm, p=0.001, respectively. PLL were also significantly higher in the treatment group following reperfusion (21694±3259 units vs. 31267±3429 units, p<0.01). There was no difference in the LVP response to Eprosartan versus controls (63.6±3.0 mmHg vs. 62.5±3.1 mmHg, p=0.400). Conclusions Pre-treatment with Eprosartan is associated with a significant improvement in regional cardiac function under ischemic conditions. Pharmacological treatment with eprosartan may exert a direct cardioprotective effect on ischemic myocardium. PMID:24762635

  15. Protection from ischemic heart injury by a vigilant heme oxygenase-1 plasmid system.

    PubMed

    Tang, Yao Liang; Tang, Yi; Zhang, Y Clare; Qian, Keping; Shen, Leping; Phillips, M Ian

    2004-04-01

    Although human heme oxygenase-1 (hHO-1) could provide a useful approach for cellular protection in the ischemic heart, constitutive overexpression of hHO-1 may lead to unwanted side effects. To avoid this, we designed a hypoxia-regulated hHO-1 gene therapy system that can be switched on and off. This vigilant plasmid system is composed of myosin light chain-2v promoter and a gene switch that is based on an oxygen-dependent degradation domain from the hypoxia inducible factor-1-alpha. The vector can sense ischemia and switch on the hHO-1 gene system, specifically in the heart. In an in vivo experiment, the vigilant hHO-1 plasmid or saline was injected intramyocardially into myocardial infarction mice or sham operation mice. After gene transfer, expression of hHO-1 was only detected in the ischemic heart treated with vigilant hHO-1 plasmids. Masson trichrome staining showed significantly fewer fibrotic areas in vigilant hHO-1 plasmids-treated mice compared with saline control (43.0%+/-4.8% versus 62.5%+/-3.3%, P<0.01). The reduction of interstitial fibrosis is accompanied by an increase in myocardial hHO-1 expression in peri-infarct border areas, concomitant with higher Bcl-2 levels and lower Bax, Bak, and caspase 3 levels in the ischemic myocardium compared with saline control. By use of a cardiac catheter, heart from vigilant hHO-1 plasmids-treated mice showed improved recovery of contractile and diastolic performance after myocardial infarction compared with saline control. This study documents the beneficial regulation and therapeutic potential of vigilant plasmid-mediated hHO-1 gene transfer. This novel gene transfer strategy can provide cardiac-specific protection from future repeated bouts of ischemic injury. PMID:14981066

  16. Heart Rate and the Role of the Active Receiver during Contingent Electric Shock for Severe Self-Injurious Behavior

    ERIC Educational Resources Information Center

    Duker, Pieter C.; Van den Munckhof, Marcia

    2007-01-01

    Five individuals, who were treated for severe self-injurious behaviors (SIB) with contingent electric shock, participated. Hereby, each occurrence of the target response was followed by a remotely administered aversive consequence. Participants' heart rates were compared at times when the active device of the equipment for the above procedure was…

  17. Emergency room thoracotomy for the resuscitation of patients with "fatal" penetrating injuries of the heart.

    PubMed

    Ivatury, R R; Shah, P M; Ito, K; Ramirez-Schon, G; Suarez, F; Rohman, M

    1981-10-01

    A total of 75 patients with penetrating cardiac injuries were treated at Lincoln Medical and Mental Health Center from January, 1974, to November, 1980. Twenty-two patients (29.3%) were unconscious on arrival and had no detectable vital signs, cardiac activity, or spontaneous respirations. Their last physical movement was observed in the ambulance. Immediate resuscitation of these patients employing intercostal or sternal splitting incisions in the emergency room revealed arrested hearts and permitted relief of tamponade, finger occlusion of the cardiac wound or wounds, and temporary suturing of the defect. Restoration of cardiac function was accomplished in 16 patients (72.7%). After transfer to the operating room for more definitive cardiorrhaphy and repair of other major wounds, 8 patients (36.4%) recovered without objective neurological disability. Our experience clearly supports the value of immediate emergency room thoracotomy in this group of patients. PMID:7305523

  18. Prenatal cocaine exposure increases apoptosis of neonatal rat heart and heart susceptibility to ischemia–reperfusion injury in 1-month-old rat

    PubMed Central

    Bae, Soochan; Zhang, Lubo

    2005-01-01

    Maternal cocaine administration during pregnancy increased apoptosis in near-term fetal rat heart. The present study tested the hypothesis that prenatal cocaine exposure increases the heart susceptibility to ischemia/reperfusion injury in the offspring. Pregnant Sprague–Dawley rats received cocaine (30 mg kg−1 day−1) or saline from days 15 to 21 of gestational age. Maternal body weights were not significantly different at the end of cocaine treatment, but body weights of offspring were decreased slightly at ages of 1, 3, and 7 days. Although heart-to-body weight ratio was not affected at all ages examined, prenatal cocaine significantly increased left ventricular myocyte size at an age of 30 days. Additionally, prenatal cocaine increased DNA fragmentation measured in the hearts isolated from offspring of 1, 3, 7, and 21 days, but not of 30 days, with the peak at 3-day neonates. Antiapoptotic (Bcl-2 and Bcl-XL) and proapoptotic (Bax and Bad) proteins were expressed in neonatal rat hearts of both groups. Prenatal cocaine exposure decreased levels of Bcl-2 in 21-day and increased Bax in 21- and 30-day rat hearts. In addition, hearts of 30-day-old male progeny were studied using the Langendorff preparation, and were subjected to 25 min of ischemia and 60 min of reperfusion. Preischemic baseline values of left ventricular (LV) function were the same between the two groups. However, prenatal cocaine exposure significantly attenuated postischemic recovery of LV function, and significantly increased elevated LV end diastolic pressure during reperfusion. This was associated with a significant increase in ischemia/reperfusion-induced LV myocardial infarct size. The results suggest that prenatal cocaine exposure induces abnormal apoptosis and myocyte hypertrophy in postnatal heart, leading to an increased heart susceptibility to ischemic insults in postnatal life. PMID:15685203

  19. Differential expression of embryonic epicardial progenitor markers and localization of cardiac fibrosis in adult ischemic injury and hypertensive heart disease.

    PubMed

    Braitsch, Caitlin M; Kanisicak, Onur; van Berlo, Jop H; Molkentin, Jeffery D; Yutzey, Katherine E

    2013-12-01

    During embryonic heart development, the transcription factors Tcf21, Wt1, and Tbx18 regulate activation and differentiation of epicardium-derived cells, including fibroblast lineages. Expression of these epicardial progenitor factors and localization of cardiac fibrosis were examined in mouse models of cardiovascular disease and in human diseased hearts. Following ischemic injury in mice, epicardial fibrosis is apparent in the thickened layer of subepicardial cells that express Wt1, Tbx18, and Tcf21. Perivascular fibrosis with predominant expression of Tcf21, but not Wt1 or Tbx18, occurs in mouse models of pressure overload or hypertensive heart disease, but not following ischemic injury. Areas of interstitial fibrosis in ischemic and hypertensive hearts actively express Tcf21, Wt1, and Tbx18. In all areas of fibrosis, cells that express epicardial progenitor factors are distinct from CD45-positive immune cells. In human diseased hearts, differential expression of Tcf21, Wt1, and Tbx18 also is detected with epicardial, perivascular, and interstitial fibrosis, indicating conservation of reactivated developmental mechanisms in cardiac fibrosis in mice and humans. Together, these data provide evidence for distinct fibrogenic mechanisms that include Tcf21, separate from Wt1 and Tbx18, in different fibroblast populations in response to specific types of cardiac injury. PMID:24140724

  20. Inhibition of KV7 Channels Protects the Rat Heart against Myocardial Ischemia and Reperfusion Injury.

    PubMed

    Hedegaard, Elise R; Johnsen, Jacob; Povlsen, Jonas A; Jespersen, Nichlas R; Shanmuganathan, Jeffrey A; Laursen, Mia R; Kristiansen, Steen B; Simonsen, Ulf; Bøtker, Hans Erik

    2016-04-01

    The voltage-gated KV7 (KCNQ) potassium channels are activated by ischemia and involved in hypoxic vasodilatation. We investigated the effect of KV7 channel modulation on cardiac ischemia and reperfusion injury and its interaction with cardioprotection by ischemic preconditioning (IPC). Reverse-transcription polymerase chain reaction revealed expression of KV7.1, KV7.4, and KV7.5 in the left anterior descending rat coronary artery and all KV7 subtypes (KV7.1-KV7.5) in the left and right ventricles of the heart. Isolated hearts were subjected to no-flow global ischemia and reperfusion with and without IPC. Infarct size was quantified by 2,3,5-triphenyltetrazolium chloride staining. Two blockers of KV7 channels, XE991 [10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone] (10 µM) and linopirdine (10 µM), reduced infarct size and exerted additive infarct reduction to IPC. An opener of KV7 channels, flupirtine (10 µM) abolished infarct size reduction by IPC. Hemodynamics were measured using a catheter inserted in the left ventricle and postischemic left ventricular recovery improved in accordance with reduction of infarct size and deteriorated with increased infarct size. XE991 (10 µM) reduced coronary flow in the reperfusion phase and inhibited vasodilatation in isolated small branches of the left anterior descending coronary artery during both simulated ischemia and reoxygenation. KV7 channels are expressed in rat coronary arteries and myocardium. Inhibition of KV7 channels exerts cardioprotection and opening of KV7 channels abrogates cardioprotection by IPC. Although safety issues should be further addressed, our findings suggest a potential role for KV7 blockers in the treatment of ischemia-reperfusion injury. PMID:26869667

  1. Increased fibrosis and progression to heart failure in MRL mice following ischemia/reperfusion injury.

    PubMed

    Smiley, Dia; Smith, Margaret A; Carreira, Vinicius; Jiang, Min; Koch, Sheryl E; Kelley, Melissa; Rubinstein, Jack; Jones, W Keith; Tranter, Michael

    2014-01-01

    The cardiac regenerative capacity of MRL/MpJ mouse remains a controversy. Although the MRL mouse has been reported to exhibit minimal scarring and subsequent cardiac regeneration after cryoinjury of the right ventricle, multiple studies have been unable to replicate this cardiac regenerative capacity after both cryogenic and coronary ligation cardiac injury. Therefore, we evaluated the cardiac regenerative wound-healing response and functional recovery of MRL mice compared to C57 mice, in response to a clinically relevant left ventricular (LV) coronary ligation. Male MRL/MpJ+/+ and C57BL/6 mice underwent left coronary artery ligation followed by reperfusion. Cardiac function was evaluated by echocardiography [LV ejection fraction (LVEF), LV end-diastolic volume (LVEDV), LV mass, wall thickness] at 24 hours post-ischemia and weekly for 13 weeks thereafter. Hearts were also analyzed histologically for individual cardiomyocyte hypertrophy and cardiac fibrosis. Our results show that contrary to prior reports of cardiac regenerations, MRL mice progress to heart failure more rapidly following I/R injury as marked by a significant decrease in LVEF, increase in LVEDV, LV mass, individual myocyte size, and fibrosis in the post-ischemic myocardium. Therefore, we conclude that MRL mice do not exhibit regeneration of the LV or enhanced functional improvement in response to coronary ligation. However, unlike prior studies, we matched initial infarct size in MRL and C57 mice, used high frequency echocardiography, and histological analysis to reach this conclusion. The prospect of cardiac regeneration after ischemia in MRL mice seems to have attenuated interest, given the multiple negative studies and the promise of stem cell cardiac regeneration. However, our novel observation that MRL may possess an impaired compensated hypertrophy response makes the MRL mouse strain an interesting model in the study of cardiac hypertrophy. PMID:25035060

  2. Profile of acute kidney injury after open heart surgeries in a tertiary care hospital.

    PubMed

    Rather, Fayaz A; Najar, Saleem M; Malla, Hilal A; Ahangar, A G; Bhat, Hilal M; Wani, Imtiyaz A

    2015-11-01

    Our objective is to determine the incidence, etiology, risk factors and outcome of acute kidney injury (AKI) after open heart surgery. A prospective study was conducted on 62 patients who underwent open heart surgery and were followed-up for the development of AKI and to determine its incidence, etiology and outcome. Post-operative AKI was considered when the post-operative serum creatinine was >1.5 mg/dL or there was doubling of serum creatinine above the baseline (pre-operative) with a prior normal renal function. The incidence of AKI in the post-operative period in our study was 17.7%. The common etiological factors for AKI in our study were sepsis, hypotension, prolonged need for ventilator and inotropic support and drugs given in the post-operative period. The important risk factors for the development of AKI in the post-operative period were hypertension, diabetes mellitus, gout, prolonged total bypass time and prolonged aortic cross-clamp time. The overall mortality in our study subjects was 11.3% (seven of 62 died) and the mortality in the patients who developed post-operative AKI was 71.4%. PMID:26586056

  3. Predictive Potential of Heart Rate Complexity Measurement: An Indication for Laparotomy Following Solid Organ Injury

    PubMed Central

    Foroutan, Ali; Paydar, Shahram; Heydari, Seyed Taghi; Erjaee, Gholamhussian; Bagheri Lankarani, Kamran; Nowroozi, Abbas; Moslemi, Sam

    2015-01-01

    Background: Nonlinear analysis of heart rate variability (HRV) has been recently used as a predictor of prognosis in trauma patients. Objectives: We applied nonlinear analysis of HRV in patients with blunt trauma and intraperitoneal bleeding to assess our ability to predict the outcome of conservative management. Patients and Methods: An analysis of electrocardiography (ECG) from 120 patients with blunt trauma was conducted at the onset of admission to the emergency department. ECGs of 65 patients were excluded due to inadequacy of noise-free length. Of the remaining 55 patients, 47 survived (S group) and eight patients died in the hospital (Non-S group). Nineteen patients were found to have intra-abdominal bleeding, eight of which ultimately underwent laparotomy to control bleeding (Op group) and 11 underwent successful non-operative management (non-Op). Demographic data including vital signs, glasgow coma scale (GCS), arterial blood gas and injury severity scores (ISS) were recorded. Heart rate complexity (HRC) methods, including entropy, were used to analyze the ECG. Results: There were no differences in age, gender, heart rate (HR) and blood pressure between the S and Non-S groups. However, approximate entropy, used as a method of HRC measurement, and GCS were significantly higher in S group, compared to the Non-S group. The base deficit and ISS were significantly higher in the Non-S group. Regarding age, sex, ISS, base deficit, vital signs and GCS, no difference was found between Op and Non-Op groups. Approximate entropy was significantly lower in the Op group, compared to the Non-Op group. Conclusions: The loss of HRC at the onset of admission may predict mortality in patients with blunt trauma. Lower entropy, in recently admitted patients with intra-abdominal bleeding, may indicate laparotomy when the vital signs are stable. PMID:26839850

  4. Severe Calorie Restriction Reduces Cardiometabolic Risk Factors and Protects Rat Hearts from Ischemia/Reperfusion Injury

    PubMed Central

    Melo, Dirceu S.; Costa-Pereira, Liliane V.; Santos, Carina S.; Mendes, Bruno F.; Costa, Karine B.; Santos, Cynthia Fernandes F.; Rocha-Vieira, Etel; Magalhães, Flávio C.; Esteves, Elizabethe A.; Ferreira, Anderson J.; Guatimosim, Sílvia; Dias-Peixoto, Marco F.

    2016-01-01

    Background and Aims: Recent studies have proposed that if a severe caloric restriction (SCR) is initiated at the earliest period of postnatal life, it can lead to beneficial cardiac adaptations later on. We investigated the effects of SCR in Wistar rats from birth to adult age on risk factors for cardiac diseases (CD), as well as cardiac function, redox status, and HSP72 content in response to ischemia/reperfusion (I/R) injury. Methods and Results: From birth to the age of 3 months, CR50 rats were fed 50% of the food that the ad libitum group (AL) was fed. Food intake was assessed daily and body weight were assessed weekly. In the last week of the SCR protocol, systolic blood pressure and heart rate were measured and the double product index was calculated. Also, oral glucose and intraperitoneal insulin tolerance tests were performed. Thereafter, rats were decapitated, visceral fat was weighed, and blood and hearts were harvested for biochemical, functional, tissue redox status, and western blot analyzes. Compared to AL, CR50 rats had reduced the main risk factors for CD. Moreover, the FR50 rats showed increased cardiac function both at baseline conditions (45% > AL rats) and during the post-ischemic period (60% > AL rats) which may be explained by a decreased cardiac oxidative stress and increased HSP72 content. Conclusion: SCR from birth to adult age reduced risk factors for CD, increased basal cardiac function and protected hearts from the I/R, possibly by a mechanism involving ROS. PMID:27092082

  5. Heme oxygenase-1 expression protects the heart from acute injury caused by inducible Cre recombinase

    PubMed Central

    Hull, Travis D.; Bolisetty, Subashini; DeAlmeida, Angela; Litovsky, Silvio H.; Prabhu, Sumanth D.; Agarwal, Anupam; George, James F.

    2013-01-01

    The protective effect of heme oxygenase-1 (HO-1) expression in cardiovascular disease has been previously demonstrated using transgenic animal models in which HO-1 is constitutively overexpressed in the heart. However, the temporal requirements for protection by HO-1 induction relative to injury have not been investigated, but are essential to employ HO-1 as a therapeutic strategy in human cardiovascular disease states. Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (MHC-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice) with mice containing an hHO-1 transgene preceded by a floxed stop signal (CBA-flox mice). MHC-HO-1 overexpress the HO-1 gene and enzymatically protein following TAM administration (40 mg/kg body weight on two consecutive days). In MHC-Cre controls, TAM administration leads to severe, acute cardiac toxicity, cardiomyocyte necrosis, and 80% mortality by day 3. This cardiac toxicity is accompanied by a significant increase in inflammatory cells in the heart that are predominantly neutrophils. In MHC-HO-1 mice, HO-1 overexpression ameliorates the depression of cardiac function and high mortality rate observed in MHC-Cre mice following TAM administration and attenuates cardiomyocyte necrosis and neutrophil infiltration. These results highlight that HO-1 induction is sufficient to prevent the depression of cardiac function observed in mice with TAM-inducible Cre recombinase expression by protecting the heart from necrosis and neutrophil infiltration. These findings are important because MHC-Cre mice are widely used in cardiovascular research despite the limitations imposed by Cre-induced cardiac toxicity and also because inflammation is an important pathological component of many human cardiovascular diseases. PMID:23732814

  6. Heme oxygenase-1 expression protects the heart from acute injury caused by inducible Cre recombinase.

    PubMed

    Hull, Travis D; Bolisetty, Subhashini; DeAlmeida, Angela C; Litovsky, Silvio H; Prabhu, Sumanth D; Agarwal, Anupam; George, James F

    2013-08-01

    The protective effect of heme oxygenase-1 (HO-1) expression in cardiovascular disease has been previously demonstrated using transgenic animal models in which HO-1 is constitutively overexpressed in the heart. However, the temporal requirements for protection by HO-1 induction relative to injury have not been investigated, but are essential to employ HO-1 as a therapeutic strategy in human cardiovascular disease states. Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (myosin heavy chain (MHC)-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice), with mice containing an hHO-1 transgene preceded by a floxed-stop signal. MHC-HO-1 mice overexpress HO-1 mRNA and the enzymatically active protein following TAM administration (40 mg/kg body weight on 2 consecutive days). In MHC-Cre controls, TAM administration leads to severe, acute cardiac toxicity, cardiomyocyte necrosis, and 80% mortality by day 3. This cardiac toxicity is accompanied by a significant increase in inflammatory cells in the heart that are predominantly neutrophils. In MHC-HO-1 mice, HO-1 overexpression ameliorates the depression of cardiac function and high mortality rate observed in MHC-Cre mice following TAM administration and attenuates cardiomyocyte necrosis and neutrophil infiltration. These results highlight that HO-1 induction is sufficient to prevent the depression of cardiac function observed in mice with TAM-inducible Cre recombinase expression by protecting the heart from necrosis and neutrophil infiltration. These findings are important because MHC-Cre mice are widely used in cardiovascular research despite the limitations imposed by Cre-induced cardiac toxicity, and also because inflammation is an important pathological component of many human cardiovascular diseases. PMID:23732814

  7. Donor Heart Treatment With COMP-Ang1 Limits Ischemia-Reperfusion Injury and Rejection of Cardiac Allografts.

    PubMed

    Syrjälä, S O; Nykänen, A I; Tuuminen, R; Raissadati, A; Keränen, M A I; Arnaudova, R; Krebs, R; Koh, G Y; Alitalo, K; Lemström, K B

    2015-08-01

    The major cause of death during the first year after heart transplantation is primary graft dysfunction due to preservation and ischemia-reperfusion injury (IRI). Angiopoietin-1 is a Tie2 receptor-binding paracrine growth factor with anti-inflammatory properties and indispensable roles in vascular development and stability. We used a stable variant of angiopoietin-1 (COMP-Ang1) to test whether ex vivo intracoronary treatment with a single dose of COMP-Ang1 in donor Dark Agouti rat heart subjected to 4-h cold ischemia would prevent microvascular dysfunction and inflammatory responses in the fully allogeneic recipient Wistar Furth rat. COMP-Ang1 reduced endothelial cell-cell junction disruption of the donor heart in transmission electron microscopy during 4-h cold ischemia, improved myocardial reflow, and reduced microvascular leakage and cardiomyocyte injury of transplanted allografts during IRI. Concurrently, the treatment reduced expression of danger signals, dendritic cell maturation markers, endothelial cell adhesion molecule VCAM-1 and RhoA/Rho-associated protein kinase activation and the influx of macrophages and neutrophils. Furthermore, COMP-Ang1 treatment provided sustained anti-inflammatory effects during acute rejection and prevented the development of cardiac fibrosis and allograft vasculopathy. These results suggest donor heart treatment with COMP-Ang1 having important clinical implications in the prevention of primary and subsequent long-term injury and dysfunction in cardiac allografts. PMID:25932532

  8. Estrogen Regulates Angiotensin II Receptor Expression Patterns and Protects the Heart from Ischemic Injury in Female Rats.

    PubMed

    Xue, Qin; Xiao, Daliao; Zhang, Lubo

    2015-07-01

    Previous studies have shown that female offspring are resistant to fetal stress-induced programming of ischemic-sensitive phenotype in the heart; however, the mechanisms responsible remain unclear. The present study tested the hypothesis that estrogen plays a role in protecting females in fetal programming of increased heart vulnerability. Pregnant rats were divided into normoxic and hypoxic (10.5% O2 from Day 15 to 21 of gestation) groups. Ovariectomy (OVX) and estrogen (E2) replacement were performed in 8-wk-old female offspring. Hearts of 4-mo-old females were subjected to ischemia and reperfusion injury in a Langendorff preparation. OVX significantly decreased postischemic recovery of left ventricular function and increased myocardial infarction, and no difference was observed between normoxic and hypoxic groups. The effect of OVX was rescued by E2 replacement. OVX decreased the binding of glucocorticoid receptor (GR) to glucocorticoid response elements at angiotensin II type 1 (Agtr1) and type 2 (Agtr2) receptor promoters, resulting in a decrease in Agtr1 and an increase in Agtr2 in the heart. Additionally, OVX decreased estrogen receptor (ER) expression in the heart and inhibited ER/GR interaction in binding to glucocorticoid response elements at the promoters. Consistent with the changes in Agtrs, OVX significantly decreased Prkce abundance in the heart. These OVX-induced changes were abrogated by E2 replacement. The results indicate that estrogen is not directly responsible for the sex dimorphism in fetal programming of heart ischemic vulnerability but suggest a novel mechanism of estrogen in regulating cardiac Agtr1/Agtr2 expression patterns and protecting female hearts against ischemia and reperfusion injury. PMID:25972014

  9. MMP-12 Deficiency Attenuates Angiotensin II-Induced Vascular Injury, M2 Macrophage Accumulation, and Skin and Heart Fibrosis

    PubMed Central

    Stawski, Lukasz; Haines, Paul; Fine, Alan; Rudnicka, Lidia; Trojanowska, Maria

    2014-01-01

    MMP-12, a macrophage-secreted elastase, is elevated in fibrotic diseases, including systemic sclerosis (SSc) and correlates with vasculopathy and fibrosis. The goal of this study was to investigate the role of MMP-12 in cardiac and cutaneous fibrosis induced by angiotensin II infusion. Ang II-induced heart and skin fibrosis was accompanied by a marked increase of vascular injury markers, including vWF, Thrombospondin-1 (TSP-1) and MMP-12, as well as increased number of PDGFRβ+ cells. Furthermore Ang II infusion led to an accumulation of macrophages (Mac3+) in the skin and in the perivascular and interstitial fibrotic regions of the heart. However, alternatively activated (Arg 1+) macrophages were mainly present in the Ang II infused mice and were localized to the perivascular heart regions and to the skin, but were not detected in the interstitial heart regions. Elevated expression of MMP-12 was primarily found in macrophages and endothelial cells (CD31+) cells, but MMP-12 was not expressed in the collagen producing cells. MMP-12 deficient mice (MMP12KO) showed markedly reduced expression of vWF, TSP1, and PDGFRβ around vessels and attenuation of dermal fibrosis, as well as the perivascular fibrosis in the heart. However, MMP-12 deficiency did not affect interstitial heart fibrosis, suggesting a heterogeneous nature of the fibrotic response in the heart. Furthermore, MMP-12 deficiency almost completely prevented accumulation of Arg 1+ cells, whereas the number of Mac3+ cells was partially reduced. Moreover production of profibrotic mediators such as PDGFBB, TGFβ1 and pSMAD2 in the skin and perivascular regions of the heart was also inhibited. Together, the results of this study show a close correlation between vascular injury markers, Arg 1+ macrophage accumulation and fibrosis and suggest an important role of MMP-12 in regulating these processes. PMID:25302498

  10. Estrogen Regulates Angiotensin II Receptor Expression Patterns and Protects the Heart from Ischemic Injury in Female Rats1

    PubMed Central

    Xue, Qin; Xiao, Daliao; Zhang, Lubo

    2015-01-01

    Previous studies have shown that female offspring are resistant to fetal stress-induced programming of ischemic-sensitive phenotype in the heart; however, the mechanisms responsible remain unclear. The present study tested the hypothesis that estrogen plays a role in protecting females in fetal programming of increased heart vulnerability. Pregnant rats were divided into normoxic and hypoxic (10.5% O2 from Day 15 to 21 of gestation) groups. Ovariectomy (OVX) and estrogen (E2) replacement were performed in 8-wk-old female offspring. Hearts of 4-mo-old females were subjected to ischemia and reperfusion injury in a Langendorff preparation. OVX significantly decreased postischemic recovery of left ventricular function and increased myocardial infarction, and no difference was observed between normoxic and hypoxic groups. The effect of OVX was rescued by E2 replacement. OVX decreased the binding of glucocorticoid receptor (GR) to glucocorticoid response elements at angiotensin II type 1 (Agtr1) and type 2 (Agtr2) receptor promoters, resulting in a decrease in Agtr1 and an increase in Agtr2 in the heart. Additionally, OVX decreased estrogen receptor (ER) expression in the heart and inhibited ER/GR interaction in binding to glucocorticoid response elements at the promoters. Consistent with the changes in Agtrs, OVX significantly decreased Prkce abundance in the heart. These OVX-induced changes were abrogated by E2 replacement. The results indicate that estrogen is not directly responsible for the sex dimorphism in fetal programming of heart ischemic vulnerability but suggest a novel mechanism of estrogen in regulating cardiac Agtr1/Agtr2 expression patterns and protecting female hearts against ischemia and reperfusion injury. PMID:25972014

  11. Cardioprotective effect of aqueous extract of Chichorium intybus on ischemia-reperfusion injury in isolated rat heart

    PubMed Central

    Sadeghi, Najmeh; Dianat, Mahin; Badavi, Mohammad; Malekzadeh, Ahad

    2015-01-01

    Objective: Several studies have shown that Chichorium intybus (C. intybus) which possesses flavonoid compounds has an effective role in treatment of cardiovascular diseases. Contractile dysfunction mostly occurs after acute myocardial infarction, cardiac bypass surgery, heart transplantation and coronary angioplasty. The aim of the present study was to investigate the effect of aqueous extract of C. intybus on ischemia- reperfusion injury in isolated rat heart. Materials and Methods: The animals were divided into four groups (Sham, Control, 1 mg/ml and 3 mg/ml of extract) of 8 rats. The aorta was cannulated, and then the heart was mounted on a Langendorff apparatus. Next, a balloon was inserted into the left ventricle (LV) and peak positive value of time derivate of LV pressure (+dp/dt), coronary flow (CF), and left ventricular systolic pressure (LVSP) in pre-ischemia and reperfusion period were calculated by a Power Lab system. All groups underwent a 30-minute global ischemia followed by a 60-minute reperfusion. Results: The results showed that heart rate (HR), coronary flow, and left ventricular developed pressure (LVDP) and rate of pressure product (RPP) significantly decreased in the control group during reperfusion, while these values in the groups receiving the extract (3mg/ml) improved significantly during reperfusion (p<0.001). Conclusion: It seems that flavonoid compounds of aqueous extract of C. intybus reduce ischemia - reperfusion injuries, suggesting its protective effect on heart function after ischemia. PMID:26693414

  12. Effect of spinal cord injury on the heart and cardiovascular fitness.

    PubMed

    Phillips, W T; Kiratli, B J; Sarkarati, M; Weraarchakul, G; Myers, J; Franklin, B A; Parkash, I; Froelicher, V

    1998-11-01

    The use of various FES protocols to encourage increases in physical activity and to augment physical fitness and reduce heart disease risk is a relatively new, but growing field of investigation. The evidence so far supports its use in improving potential health benefits for patients with SCI. Such benefits may include more efficient and safer cardiac function; greater stimulus for metabolic, cardiovascular, and pulmonary training adaptations; and greater stimulus for skeletal muscle training adaptations. In addition, the availability of relatively inexpensive commercial FES units to elicit muscular contractions, the ease of use of gel-less, reusable electrodes, and the increasing popularity of home and commercial upper body exercise equipment mean that such benefits are likely to be more accessible to the SCI population through increased convenience and decreased cost. The US Department of Health and Human Services has identified those with SCI as a "special population" whose health problems are accentuated, and so need to be specifically addressed. FES presents "a clear opportunity.... For health promotion and disease prevention efforts to improve the health prospects and functional independence of people with disabilities." As a corollary to this, the Centers for Disease Control and Prevention have recommended the development of techniques to prevent or ameliorate secondary disabilities in persons with a SCI. Patients with SCI have an increased susceptibility to cardiac morbidity and mortality in the acute and early stages of their injury. Most of these patients make an excellent adaptation except when confronted with infection or hypoxia. SCI by itself does not promote atherosclerosis; however, in association with multiple secondary conditions related to SCI, along with advancing age, patients with SCI are predisposed to relatively greater risk of heart disease. The epidemiologic significance of this is reflected in demographic studies that indicate an

  13. Three dimensional electromechanical model of porcine heart with penetrating wound injury.

    PubMed

    Usyk, Taras; Kerckhoffs, Roy

    2005-01-01

    The aim of this study is development a prototype computational model of the pig heart that can be used to predict physiological responses to a penetrating wound injury. The pig has been chosen for this model studies because it shares many anatomical similarities with humans. Three-dimensional cubic Hermite finite element meshes based on detailed measurements of porcine anatomy combined into an integrated anatomic model. The pig ventricular model includes detailed left and right ventricular geometry and myofiber and laminar sheet orientations throughout the mesh. The cardiac mesh was refined and monodomain equations for action potential propagation solved using well-established collocation-Galerkin finite element methods. The membrane kinetic equations for the action potential model was based on detailed cellular models of transmembrane ionic fluxes and intracellular calcium fluxes in canine ventricular myocytes and human atrial myocytes. We modified the anisotropic myocardial conductivity tensor on the endocardial surface of the ventricles by making use of a surface model fitted to measured of Purkinje fiber network anatomy. The mechanical model compute regional three-dimensional stress and strain distributions using anisotropic constitutive laws referred to local material coordinate axes defined by local myofiber and laminar sheet orientations. Passive myocardial mechanics modeled using exponential orthotropic strain energy functions. Active systolic myocardial stresses computed from a multi-scale model that uses crossbridge theory to predict calcium-activated sarcomere length- and velocity-dependent tension filament tension. Since the electrical and mechanical models use a common finite element mesh as the parent parametric framework and both models are solved within our custom finite element package, it is straightforward to couple these models, as we have recently done for a model of coupled ventricular electromechanics. We apply the coupled electromechanical

  14. Gαi2-mediated protection from ischaemic injury is modulated by endogenous RGS proteins in the mouse heart

    PubMed Central

    Waterson, Rachael E.; Thompson, Corbin G.; Mabe, Nathaniel W.; Kaur, Kuljeet; Talbot, Jeffery N.; Neubig, Richard R.; Rorabaugh, Boyd R.

    2011-01-01

    Aims Regulator of G protein signalling (RGS) proteins act as molecular ‘off switches’ that terminate G protein signalling by catalyzing the hydrolysis of Gα-bound GTP to GDP. Many different Gαi-coupled receptors have been implicated in the cardioprotective effects of ischaemic preconditioning. However, the role of RGS proteins in modulating cardioprotection has not been previously investigated. We used mice that were homozygous (GS/GS) or heterozygous (GS/+) for a mutation in Gαi2 rendering it RGS-insensitive (G184S) to determine whether interactions between endogenous RGS proteins and Gαi2 modulate Gαi-mediated protection from ischaemic injury. Methods and results Langendorff-perfused mouse hearts were subjected to 30 min global ischaemia and 2 h reperfusion. Infarcts in GS/GS (14.5% of area at risk) and GS/+ (22.6% of AAR) hearts were significantly smaller than those of +/+ hearts (37.2% of AAR) and recovery of contractile function was significantly enhanced in GS/GS and GS/+ hearts compared with +/+ hearts. The cardioprotective phenotype was not reversed by wortmannin or U0126 but was reversed by 5-hydroxydecanoic acid and HMR 1098, indicating that RGS-insensitive Gαi2 protects the heart through a mechanism that requires functional ATP-dependent potassium channels but does not require acute activation of extracellular-regulated kinase or Akt signalling pathways. Conclusions This is the first study to demonstrate that Gαi2-mediated cardioprotection is suppressed by RGS proteins. These data suggest that RGS proteins may provide novel therapeutic targets to protect the heart from ischaemic injury. PMID:21349876

  15. Acquired deficiency of tafazzin in the adult heart: Impact on mitochondrial function and response to cardiac injury.

    PubMed

    Szczepanek, Karol; Allegood, Jeremy; Aluri, Hema; Hu, Ying; Chen, Qun; Lesnefsky, Edward J

    2016-04-01

    The content and composition of cardiolipin (CL) is critical for preservation of mitochondrial oxidative phosphorylation (OXPHOS) and inner membrane integrity. Tafazzin (Taz) is an enzyme responsible for remodeling of immature CL containing mixed acyl groups into the mature tetralinoleyl form (C18:2)4-CL. We hypothesized that acquired defects in Taz in the mature heart would impact remodeling of CL and augment cardiac injury. The role of acquired Taz deficiency was studied using the inducible Taz knockdown (TazKD) mouse. Taz-specific shRNA is induced by doxycycline (DOX). One day of DOX intake decreased Taz mRNA in the heart to 20% vs. DOX-treated WT. Knockdown was initiated at an adult age and was stable during long term feeding. CL phenotype was assessed by (C18:2)4-CL content and was reduced 40% vs. WT at two months of DOX. TazKD showed increased production of reactive oxygen species and increased susceptibility to permeability transition pore opening at baseline. However, OXPHOS measured using the rate of oxygen consumption was unchanged in the setting of acquired Taz deficiency. Infarct size, measured in isolated buffer-perfused Langendorff hearts following 25min. Stop flow ischemia and 60min. Reperfusion was not altered in TazKD hearts. Thus, impaired Taz-function with onset at adult age does not enhance susceptibility to ischemia-reperfusion injury. PMID:26692032

  16. Aged rat hearts are not more susceptible to ischemia-reperfusion injury in vivo: role of glutathione.

    PubMed

    Leichtweis, S; Leeuwenburgh, C; Bejma, J; Ji, L L

    2001-05-15

    The current study tested the hypothesis that ischemia-reperfusion (I-R) can cause more severe myocardial dysfunction and oxidative damage in senescent rats than young adult rats. Male Fischer 344 rats at the age of 6 (adult) and 24 (old) months were subjected to an open-chest heart surgery and randomly assigned to one of the following treatments: ischemia only (I), with the occlusion of the main descending branch of the left coronary artery (LCA) for 30 min; I-R, with the release of LCA occlusion for 20 min; or sham (S) operation. Heart mechanical performance was monitored using a fluid-filled catheter inserted in the right carotid artery and advanced to the left ventricle. Ischemia caused similar reductions of left ventricle systolic pressure (LVSP) and contractility (+/-dP/dt) in adult and aged hearts. After I-R, adult hearts regained 82% (P<0.05) of the pre-ischemic LVSP, whereas the aged hearts regained 91% (P>0.05) of LVSP. There was no significant difference in the reduction of +/-dP/dt with I-R between adult and aged hearts. Old rats had lower pre-ischemic heart rate than adult rats, however, I-R caused no reduction of heart rate, and a smaller reduction of pressure-rate double product in the aged rats (10%, P>0.05) than the adult rats (23%, P<0.01). Aged rats demonstrated greater myocardial and plasma glutathione (GSH) concentrations prior to surgery, and maintained higher GSH levels and GSH:glutathione disulfide (GSSG) ratio with I-R. Aged hearts also had higher GSH peroxidase, GSH reductase and GSH sulfur-transferase activities than adult hearts, while I-R induced lipid peroxidation was similar. It is concluded that senescent hearts with intact circulatory and neural inputs are not more susceptible to I-R injury than adult hearts during myocardial I-R, partly because they have a greater GSH antioxidant protection. PMID:11295168

  17. The effect of acute stress exposure on ischemia and reperfusion injury in rat heart: role of oxytocin.

    PubMed

    Moghimian, Maryam; Faghihi, Mahdieh; Karimian, Seyed Morteza; Imani, Alireza

    2012-07-01

    Previous studies showed the protective effects of oxytocin (OT) on myocardial injury in ischemic and reperfused rat heart. Moreover, exposure to various stressors not only evokes sudden cardiovascular effects but also triggers the release of OT in the rat. The present study was aimed to evaluate the possible cardioprotective effects of endogenous OT released in response to stress (St), and effects of administration of exogenous OT on the ischemic-reperfused isolated heart of rats previously exposed to St. Wistar rats were divided into six groups: ischemia/reperfusion (IR); St: rats exposed to swim St for 10 min before anesthesia; St+atosiban (ATO): an OT receptor antagonist, was administered (1.5 mg/kg i.p.) prior to St; St+OT: OT was administered (0.03 mg/kg i.p.) prior to St; OT: OT was administrated prior to anesthesia; ATO was given prior to anesthesia. Isolated hearts were perfused with Krebs buffer solution by the Langendorff method and subjected to 30 min of regional ischemia followed by 60 min of reperfusion. The infarct size (IS) and creatine kinase MB isoenzyme (CK-MB) and lactate dehydrogenase (LDH) in coronary effluent were measured. Hemodynamic parameters were recorded throughout the experiment. The plasma concentrations of OT and corticosterone were significantly increased by St. Unexpectedly St decreased IR injury compared with the IR alone group. OT administration significantly inhibited myocardial injury, and administration of ATO with St abolished recovery of the rate pressure product, and increased IS and levels of CK-MB and LDH. These findings indicate that activation of cardiac OT receptors by OT released in response to St may participate in cardioprotection and inhibition of myocardial IR injury. PMID:22044052

  18. Histone Deacetylases Exert Class-Specific Roles in Conditioning the Brain and Heart Against Acute Ischemic Injury

    PubMed Central

    Aune, Sverre E.; Herr, Daniel J.; Kutz, Craig J.; Menick, Donald R.

    2015-01-01

    Ischemia-reperfusion (IR) injury comprises a significant portion of morbidity and mortality from heart and brain diseases worldwide. This enduring clinical problem has inspired myriad reports in the scientific literature of experimental interventions seeking to elucidate the pathology of IR injury. Elective cardiac surgery presents perhaps the most viable scenario for protecting the heart and brain from IR injury due to the opportunity to condition the organs prior to insult. The physiological parameters for the preconditioning of vital organs prior to insult through mechanical and pharmacological maneuvers have been heavily examined. These investigations have revealed new insights into how preconditioning alters cellular responses to IR injury. However, the promise of preconditioning remains unfulfilled at the clinical level, and research seeking to implicate cell signals essential to this protection continues. Recent discoveries in molecular biology have revealed that gene expression can be controlled through posttranslational modifications, without altering the chemical structure of the genetic code. In this scenario, gene expression is repressed by enzymes that cause chromatin compaction through catalytic removal of acetyl moieties from lysine residues on histones. These enzymes, called histone deacetylases (HDACs), can be inhibited pharmacologically, leading to the de-repression of protective genes. The discovery that HDACs can also alter the function of non-histone proteins through posttranslational deacetylation has expanded the potential impact of HDAC inhibitors for the treatment of human disease. HDAC inhibitors have been applied in a very small number of experimental models of IR. However, the scientific literature contains an increasing number of reports demonstrating that HDACs converge on preconditioning signals in the cell. This review will describe the influence of HDACs on major preconditioning signaling pathways in the heart and brain. PMID

  19. Prostaglandin E Receptor Subtype 4 Signaling in the Heart: Role in Ischemia/Reperfusion Injury and Cardiac Hypertrophy

    PubMed Central

    Cai, Yin; Tang, Eva Hoi Ching; Ma, Haichun

    2016-01-01

    Prostaglandin E2 (PGE2) is an endogenous lipid mediator, produced from the metabolism of arachidonic acids, upon the sequential actions of phospholipase A2, cyclooxygenases, and prostaglandin E synthases. The various biological functions governed by PGE2 are mediated through its four distinct prostaglandin E receptors (EPs), designated as EP1, EP2, EP3, and EP4, among which the EP4 receptor is the one most widely distributed in the heart. The availability of global or cardiac-specific EP4 knockout mice and the development of selective EP4 agonists/antagonists have provided substantial evidence to support the role of EP4 receptor in the heart. However, like any good drama, activation of PGE2-EP4 signaling exerts both protective and detrimental effects in the ischemic heart disease. Thus, the primary object of this review is to provide a comprehensive overview of the current progress of the PGE2-EP4 signaling in ischemic heart diseases, including cardiac hypertrophy and myocardial ischemia/reperfusion injury. A better understanding of PGE2-EP4 signaling should promote the development of more effective therapeutic approaches to treat the ischemic heart diseases without triggering unwanted side effects. PMID:27190998

  20. Role of platelet-activating factor in the reperfusion injury of rabbit ischemic heart

    SciTech Connect

    Montrucchio, G.; Alloatti, G.; Mariano, F.; de Paulis, R.; Comino, A.; Emanuelli, G.; Camussi, G. )

    1990-07-01

    This study shows that the administration of the PAF receptor antagonist SDZ 63.675 (5 mg/kg body weight) before reperfusion significantly reduced the hematologic and hemodynamic alterations, as well as the size of necrotic area in rabbits subjected to 40 minutes of coronary occlusion and reperfusion. Pretreatment with SDZ 63.675 prevented the reduction of platelet counts in the blood obtained from the right ventricle (86.6 +/- 2.8% of the control preischemia value) and the transient bradycardia (85.0 +/- 2.8%), the systemic hypotension (58.0 +/- 2.8%), and the increase in right ventricular pressure (125.0 +/- 3.6%) that were evident in the first minutes of reperfusion in untreated control rabbits. Two as well as 24 hours after reperfusion, the infarct size, judged by staining with tetrazolium, was significantly reduced in rabbits treated with SDZ 63.675 (infarct size in control animals, 66.0 +/- 2.9% and 63.46 +/- 2.09% of the risk region at 2 or 24 hours, respectively, compared with 38.9 +/- 5.2% and 37.11 +/- 2.44% of the risk region at 2 and 24 hours in rabbits treated with SDZ 63.675). This result was confirmed by histologic examination of cardiac tissue 24 hours after reperfusion. In addition, SDZ 63.675 markedly reduced the accumulation of 111In-oxine-labeled platelets that occurs 15 minutes after reperfusion in the central ischemic area of the heart and in the lungs. These results suggest that PAF plays a role in the evolution of myocardial injury observed during reperfusion.

  1. Comparison of Cystatin C and NGAL in Early Diagnosis of Acute Kidney Injury After Heart Transplantation.

    PubMed

    Hošková, Lenka; Franekova, Janka; Málek, Ivan; Kautzner, Josef; Szárszoi, Ondřej; Jabor, Antonín; Pinďák, Marian; Viklický, Ondřej; Melenovský, Vojtěch

    2016-01-01

    BACKGROUND Acute kidney injury (AKI) is a risk factor for adverse hospital outcomes in recipients of a heart transplantation (HTx). Timely recognition of AKI is crucial for the initiation of proper treatment. We hypothesized that serum or urine biomarkers can predict AKI. MATERIAL AND METHODS In this prospective study we evaluated 117 consecutive patients after HTx. AKI was defined as an increase of the serum creatinine level by ≥50% or a worsening of the renal function requiring renal replacement therapy during the first post-HTx week. We serially sampled serum cystatin C (S-cystatin C) as a marker of glomerular filtration and urinary neutrophil gelatinase-associated lipocalin (U-NGAL) as a marker of tubular damage. RESULTS A cohort of 30 patients (25.6%) fulfilled the criteria of AKI. S-cystatin C allowed the earliest separation between the AKI and non-AKI groups, with a significant difference present as soon as 3 h after surgery and it persisted on days 7, 10, and 30. The increase in S-cystatin C preceded the serum creatinine elevation by 4 days. In a multivariate analysis, S-cystatin C >1.6 mg/L at 3 h after HTx predicted AKI with OR 4.3 (95% CI: 1.6-11.5). U-NGAL was significantly higher at day 3 in the AKI group (p=0.003) and elevated S-cystatin C (≥2.54 mg/L on day 7) could predict 1-year mortality in these HTx recipients. CONCLUSIONS Our study showed that the measurement of S-cystatin C at 3 h after surgery may help to identify patients with high risk for renal complications. A persistent elevation of S-cystatin C also predicts 1-year mortality. PMID:27226081

  2. Heart rate-based training intensity and its impact on injury incidence among elite-level professional soccer players.

    PubMed

    Owen, Adam L; Forsyth, Jacky J; Wong, Del P; Dellal, Alexandre; Connelly, Sean P; Chamari, Karim

    2015-06-01

    Elite-level professional soccer players are suggested to have increased physical, technical, tactical, and psychological capabilities when compared with their subelite counterparts. Ensuring these players remain at the elite level generally involves training many different bodily systems to a high intensity or level within a short duration. This study aimed to examine whether an increase in training volume at high-intensity levels was related to injury incidence, or increased the odds of sustaining an injury. Training intensity was monitored through time spent in high-intensity (T-HI) and very high-intensity (T-VHI) zones of 85-<90% and ≥90% of maximal heart rate (HRmax), and all injuries were recorded over 2 consecutive seasons. Twenty-three, elite professional male soccer players (mean ± SD age, 25.6 ± 4.6 years; stature, 181.8 ± 6.8 cm; and body mass, 79.3 ± 8.1 kg) were studied throughout the 2-years span of the investigation. The results showed a mean total injury incidence of 18.8 (95% confidence interval [CI], 14.7-22.9) injuries per 1,000 hours of exposure. Significant correlations were found between training volume at T-HI and injury incidence (r = 0.57, p = 0.005). Further analysis revealed how players achieving more time in the T-VHI zone during training increased the odds of sustaining a match injury (odds ratio = 1.87; 95% CI, 1.12-3.12, p = 0.02) but did not increase the odds of sustaining a training injury. Reducing the number of competitive match injuries among elite-level professional players may be possible if greater focus is placed on the training intensity and volume over a period of time ensuring the potential reduction of fatigue or overuse injuries. In addition, it is important to understand the optimal training load at which adaptation occurs without raising the risk of injury. PMID:26010801

  3. Incidence of fetal bradycardia and effect of placental injury on fetal heart rate during second-trimester genetic amniocentesis.

    PubMed

    Hanprasertpong, T; Petpichetchian, C; Ponglopisit, S; Suksai, M; Kor-Anantakul, O; Geater, A; Pruksanusak, N; Hanprasertpong, J

    2016-05-01

    A prospective study was conducted for comparing the incidence of fetal bradycardia and level of fetal heart rate change following a second-trimester genetic amniocentesis with and without placental injury. A total of 257 and 495 participants in injured and non-injured groups were analysed. The incidence of fetal bradycardia following amniocentesis was not statistically different between the two groups (1.17%, [95% CI 0.24, 3.37] and 0.20%, [95% CI 0.005, 1.12]) in injured and non-injured placenta groups, respectively; p = 0.118). The mean change in baseline fetal heart rate before and after amniocentesis was also not significantly different between the two groups (p = 0.844). No fetal death or pregnancy loss occurred within 4 weeks after the procedure. All 4 bradycardia participants were normal and healthy and had an appropriate weight for their gestational age. We conclude that placental injury during a second-trimester genetic amniocentesis due to advanced maternal age poses only a low risk of fetal bradycardia, and there is no evidence of differences between subjects with injured and non-injured placenta in the changes in fetal heart rate. PMID:26512899

  4. Targeting hexokinase II to mitochondria to modulate energy metabolism and reduce ischaemia-reperfusion injury in heart.

    PubMed

    Nederlof, Rianne; Eerbeek, Otto; Hollmann, Markus W; Southworth, Richard; Zuurbier, Coert J

    2014-04-01

    Mitochondrially bound hexokinase II (mtHKII) has long been known to confer cancer cells with their resilience against cell death. More recently, mtHKII has emerged as a powerful protector against cardiac cell death. mtHKII protects against ischaemia-reperfusion (IR) injury in skeletal muscle and heart, attenuates cardiac hypertrophy and remodelling, and is one of the major end-effectors through which ischaemic preconditioning protects against myocardial IR injury. Mechanisms of mtHKII cardioprotection against reperfusion injury entail the maintenance of regulated outer mitochondrial membrane (OMM) permeability during ischaemia and reperfusion resulting in stabilization of mitochondrial membrane potential, the prevention of OMM breakage and cytochrome C release, and reduced reactive oxygen species production. Increasing mtHK may also have important metabolic consequences, such as improvement of glucose-induced insulin release, prevention of acidosis through enhanced coupling of glycolysis and glucose oxidation, and inhibition of fatty acid oxidation. Deficiencies in expression and distorted cellular signalling of HKII may contribute to the altered sensitivity of diabetes to cardiac ischaemic diseases. The interaction of HKII with the mitochondrion constitutes a powerful endogenous molecular mechanism to protect against cell death in almost all cell types examined (neurons, tumours, kidney, lung, skeletal muscle, heart). The challenge now is to harness mtHKII in the treatment of infarction, stroke, elective surgery and transplantation. Remote ischaemic preconditioning, metformin administration and miR-155/miR-144 manipulations are potential means of doing just that. PMID:24032601

  5. Cordyceps sinensis protects against liver and heart injuries in a rat model of chronic kidney disease: a metabolomic analysis

    PubMed Central

    Liu, Xia; Zhong, Fang; Tang, Xu-long; Lian, Fu-lin; Zhou, Qiao; Guo, Shan-mai; Liu, Jia-fu; Sun, Peng; Hao, Xu; Lu, Ying; Wang, Wei-ming; Chen, Nan; Zhang, Nai-xia

    2014-01-01

    Aim: To test the hypothesis that the traditional Chinese medicine Cordyceps sinensis could improve the metabolic function of extrarenal organs to achieve its anti-chronic kidney disease (CKD) effects. Methods: Male SD rats were divided into CKD rats (with 5/6-nephrectomy), CKD rats treated with Cordyceps sinensis (4 mg•kg-1•d-1, po), and sham-operated rats. After an 8-week treatment, metabolites were extracted from the hearts and livers of the rats, and then subjected to 1H-NMR-based metabolomic analysis. Results: Oxidative stress, energy metabolism, amino acid and protein metabolism and choline metabolism were considered as links between CKD and extrarenal organ dysfunction. Within the experimental period of 8 weeks, the metabolic disorders in the liver were more pronounced than in the heart, suggesting that CKD-related extrarenal organ dysfunctions occurred sequentially rather than simultaneously. Oral administration of Cordyceps sinensis exerted statistically significant rescue effects on the liver and heart by reversely regulating levels of those metabolites that are typically perturbed in CKD. Conclusion: Oral administration of Cordyceps sinensis significantly attenuates the liver and heart injuries in CKD rats. The 1H NMR-based metabolomic approach has provided a systematic view for understanding of CKD and the drug treatment, which can also be used to elucidate the mechanisms of action of other traditional Chinese medicines. PMID:24632844

  6. Targeting hexokinase II to mitochondria to modulate energy metabolism and reduce ischaemia-reperfusion injury in heart

    PubMed Central

    Nederlof, Rianne; Eerbeek, Otto; Hollmann, Markus W; Southworth, Richard; Zuurbier, Coert J

    2014-01-01

    Mitochondrially bound hexokinase II (mtHKII) has long been known to confer cancer cells with their resilience against cell death. More recently, mtHKII has emerged as a powerful protector against cardiac cell death. mtHKII protects against ischaemia-reperfusion (IR) injury in skeletal muscle and heart, attenuates cardiac hypertrophy and remodelling, and is one of the major end-effectors through which ischaemic preconditioning protects against myocardial IR injury. Mechanisms of mtHKII cardioprotection against reperfusion injury entail the maintenance of regulated outer mitochondrial membrane (OMM) permeability during ischaemia and reperfusion resulting in stabilization of mitochondrial membrane potential, the prevention of OMM breakage and cytochrome C release, and reduced reactive oxygen species production. Increasing mtHK may also have important metabolic consequences, such as improvement of glucose-induced insulin release, prevention of acidosis through enhanced coupling of glycolysis and glucose oxidation, and inhibition of fatty acid oxidation. Deficiencies in expression and distorted cellular signalling of HKII may contribute to the altered sensitivity of diabetes to cardiac ischaemic diseases. The interaction of HKII with the mitochondrion constitutes a powerful endogenous molecular mechanism to protect against cell death in almost all cell types examined (neurons, tumours, kidney, lung, skeletal muscle, heart). The challenge now is to harness mtHKII in the treatment of infarction, stroke, elective surgery and transplantation. Remote ischaemic preconditioning, metformin administration and miR-155/miR-144 manipulations are potential means of doing just that. LINKED ARTICLES This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue-8 PMID:24032601

  7. Peri-operative heart-type fatty acid binding protein is associated with acute kidney injury after cardiac surgery

    PubMed Central

    Schaub, Jennifer A.; Garg, Amit X.; Coca, Steven G.; Testani, Jeffrey M.; Shlipak, Michael G.; Eikelboom, John; Kavsak, Peter; McArthur, Eric; Shortt, Colleen; Whitlock, Richard; Parikh, Chirag R.

    2015-01-01

    Acute Kidney Injury (AKI) is a common complication after cardiac surgery and is associated with worse outcomes. Since heart fatty acid binding protein (H-FABP) is a myocardial protein that detects cardiac injury, we sought to determine if plasma H-FABP was associated with AKI in the TRIBE-AKI cohort; a multi-center cohort of 1219 patients at high risk for AKI who underwent cardiac surgery. The primary outcomes of interest were any AKI (Acute Kidney Injury Network (AKIN) stage 1 or higher) and severe AKI (AKIN stage 2 or higher). The secondary outcome was long-term mortality after discharge. Patients who developed AKI had higher levels of H-FABP pre- and post-operatively than patients who did not have AKI. In analyses adjusted for known AKI risk factors, first post-operative log(H-FABP) was associated with severe AKI (adjusted OR 5.39 [95% CI, 2.87-10.11] per unit increase), while pre-operative log(H-FABP) was associated with any AKI (2.07 [1.48-2.89]) and mortality (1.67 [1.17-2.37]). These relationships persisted after adjustment for change in serum creatinine (for first postoperative log(H-FABP)) and biomarkers of cardiac and kidney injury, including brain natriuretic peptide, cardiac troponin-I, interleukin-18, liver fatty acid binding protein, kidney injury molecule-1, and neutrophil gelatinase associated lipocalin. Thus, peri-operative plasma H-FABP levels may be used for risk-stratification of AKI and mortality following cardiac surgery. PMID:25830762

  8. Quantitative and qualitative analysis of heart mitochondria for evaluating the degree of myocardial injury utilizing atomic force microscopy.

    PubMed

    Lee, Gi-Ja; Jeong, Jae Hoon; Lee, Sora; Choi, Samjin; Pak, Youngmi Kim; Kim, Weon; Park, Hun-Kuk

    2013-01-01

    Mitochondrial dysfunction plays a central role in mediating both the necrotic and apoptotic components of reperfusion injury. Because mitochondrial swelling is one of the most important indicators of the beginning of mitochondrial permeability transition, quantification of morphological changes in mitochondria would be useful in evaluating the degree of IR injury, as well as the protective effects of various therapies. In this study, we characterized the morphological changes in heart mitochondria caused by the duration and severity of ischemia utilizing particle shape analysis on atomic force microscopy (AFM) topographic images. We also simultaneously investigated the nano-mechanical changes in rat heart mitochondria by injury using force-distance curve measurements. Rats were randomly divided into 3 groups: control group (n=3), myocardial ischemia without reperfusion (PI group, n=3), and myocardial ischemia with reperfusion (IR group, n=4). Normal mitochondria appeared ellipsoidal with a mean area of 3551±1559 nm(2) and mean perimeter of 217.54±52.09 nm (n=60). The mean area and perimeter of mitochondria in the IR groups increased to 28,181±21,248 nm(2) and 595.74±234.29 nm (n=40, p<0.0001 vs. control group, respectively), maintaining oval in shape. But, in the PI group, all parameters showed significant differences compared to parameters of the control group (n=35, p<0.0001). In particular, the mean axial ratio and roundness were significantly different from those in the IR group. Mitochondria in the PI group looked more spherical than those of control and IR groups. Adhesion force is the force before the last event on the retraction half of force-distance curve measurements, corresponding to the point where the tip and the surface loose contact. The adhesion forces of heart mitochondria in the IR and PI groups significantly decreased to 19.56±1.08 nN (n=30, p<0.0001) and 18.65±3.18 nN (n=30, p<0.0001), compared to normal mitochondria which had an adhesion

  9. The association of resting state heart rate variability and 24-hour blood pressure variability in spinal cord injury.

    PubMed

    Thayer, Julian F; Sollers, John J; Clamor, Annika; Koenig, Julian; Hagglund, Kristofer J

    2016-02-15

    Patients with high cervical complete spinal cord injuries (tetraplegia) sustain damage to the autonomic neural pathways that influence cardiovascular functioning and produce variability in the heart rate (HR) and blood pressure (BP). In non-injured individuals, an inverse relationship exists between resting autonomic control of the heart (as evidenced by HR variability (HRV)) and BP variability (BPV). This study examined the relationship between HRV, BP and BPV in individuals with tetraplegic (n=10) and paraplegic (n=10) spinal cord injuries, and a group of healthy controls (n=14). Resting HRV at baseline and 24-hour ambulatory BP measurements were collected from electrocardiogram measures of each participant. HRV was quantified using time- and frequency-domain measures. The standard deviation of the BP measurements was used as an index of BPV. Multivariate analyses of variance were performed to examine group differences for laboratory-based and 24-h dependent variables. The MANOVAs for HRV parameters (λ(14,50)=.352, p=.010, η(2)=.407) and for BP indices and HR (λ(16,48)=.318, p=.013, η(2)=.436) were significant. Furthermore, in line with existing evidence, we found that vagally mediated HRV was inversely related to BPV in healthy controls. However, this relationship did not hold for the tetraplegia group (ρ<|.42|), and mixed results were found for the paraplegia group (e.g., ρ<|.29| for time domain HRV, ρ>|.65| for low-frequency power). These results support the conclusion that the damage to the spinal sympathetic pathways to the heart found in people with tetraplegia causes a significant disruption in baroreflex control of BP. PMID:26810517

  10. Increased Heme Levels in the Heart Lead to Exacerbated Ischemic Injury

    PubMed Central

    Sawicki, Konrad Teodor; Shang, Meng; Wu, Rongxue; Chang, Hsiang-Chun; Khechaduri, Arineh; Sato, Tatsuya; Kamide, Christine; Liu, Ting; Naga Prasad, Sathyamangla V; Ardehali, Hossein

    2015-01-01

    Background Heme is an essential iron-containing molecule for cardiovascular physiology, but in excess it may increase oxidative stress. Failing human hearts have increased heme levels, with upregulation of the rate-limiting enzyme in heme synthesis, δ-aminolevulinic acid synthase 2 (ALAS2), which is normally not expressed in cardiomyocytes. We hypothesized that increased heme accumulation (through cardiac overexpression of ALAS2) leads to increased oxidative stress and cell death in the heart. Methods and Results We first showed that ALAS2 and heme levels are increased in the hearts of mice subjected to coronary ligation. To determine the causative role of increased heme in the development of heart failure, we generated transgenic mice with cardiac-specific overexpression of ALAS2. While ALAS2 transgenic mice have normal cardiac function at baseline, their hearts display increased heme content, higher oxidative stress, exacerbated cell death, and worsened cardiac function after coronary ligation compared to nontransgenic littermates. We confirmed in cultured cardiomyoblasts that the increased oxidative stress and cell death observed with ALAS2 overexpression is mediated by increased heme accumulation. Furthermore, knockdown of ALAS2 in cultured cardiomyoblasts exposed to hypoxia reversed the increases in heme content and cell death. Administration of the mitochondrial antioxidant MitoTempo to ALAS2-overexpressing cardiomyoblasts normalized the elevated oxidative stress and cell death levels to baseline, indicating that the effects of increased ALAS2 and heme are through elevated mitochondrial oxidative stress. The clinical relevance of these findings was supported by the finding of increased ALAS2 induction and heme accumulation in failing human hearts from patients with ischemic cardiomyopathy compared to nonischemic cardiomyopathy. Conclusions Heme accumulation is detrimental to cardiac function under ischemic conditions, and reducing heme in the heart may be a

  11. Ratiometric imaging of calcium during ischemia-reperfusion injury in isolated mouse hearts using Fura-2

    PubMed Central

    2012-01-01

    Background We present an easily implementable method for measuring Fura-2 fluorescence from isolated mouse hearts using a commercially available switching light source and CCD camera. After calibration, it provides a good estimate of intracellular [Ca2+] with both high spatial and temporal resolutions, permitting study of changes in dispersion of diastolic [Ca2+], Ca2+ transient dynamics, and conduction velocities in mouse hearts. In a proof-of-principle study, we imaged isolated Langendorff-perfused mouse hearts with reversible regional myocardial infarctions. Methods Isolated mouse hearts were perfused in the Landendorff-mode and loaded with Fura-2. Hearts were then paced rapidly and subjected to 15 minutes of regional ischemia by ligation of the left anterior descending coronary artery, following which the ligation was removed to allow reperfusion for 15 minutes. Fura-2 fluorescence was recorded at regular intervals using a high-speed CCD camera. The two wavelengths of excitation light were interleaved at a rate of 1 KHz with a computer controlled switching light source to illuminate the heart. Results Fura-2 produced consistent Ca2+ transients from different hearts. Ligating the coronary artery rapidly generated a well defined region with a dramatic rise in diastolic Ca2+ without a significant change in transient amplitude; Ca2+ handling normalized during reperfusion. Conduction velocity was reduced by around 50% during ischemia, and did not recover significantly when monitored for 15 minutes following reperfusion. Conclusions Our method of imaging Fura-2 from isolated whole hearts is capable of detecting pathological changes in intracellular Ca2+ levels in cardiac tissue. The persistent change in the conduction velocities indicates that changes to tissue connectivity rather than altered intracellular Ca2+ handling may be underlying the electrical instabilities commonly seen in patients following a myocardial infarction. PMID:22812644

  12. Role of Opioid Receptors Signaling in Remote Electrostimulation - Induced Protection against Ischemia/Reperfusion Injury in Rat Hearts

    PubMed Central

    Tsai, Hsin-Ju; Huang, Shiang-Suo; Tsou, Meng-Ting; Wang, Hsiao-Ting; Chiu, Jen-Hwey

    2015-01-01

    Aims Our previous studies demonstrated that remote electro-stimulation (RES) increased myocardial GSK3 phosphorylation and attenuated ischemia/ reperfusion (I/R) injury in rat hearts. However, the role of various opioid receptors (OR) subtypes in preconditioned RES-induced myocardial protection remains unknown. We investigated the role of OR subtype signaling in RES-induced cardioprotection against I/R injury of the rat heart. Methods & Results Male Spraque-Dawley rats were used. RES was performed on median nerves area with/without pretreatment with various receptors antagonists such as opioid receptor (OR) subtype receptors (KOR, DOR, and MOR). The expressions of Akt, GSK3, and PKCε expression were analyzed by Western blotting. When RES was preconditioned before the I/R model, the rat's hemodynamic index, infarction size, mortality and serum CK-MB were evaluated. Our results showed that Akt, GSK3 and PKCε expression levels were significantly increased in the RES group compared to the sham group, which were blocked by pretreatment with specific antagonists targeting KOR and DOR, but not MOR subtype. Using the I/R model, the duration of arrhythmia and infarct size were both significantly attenuated in RES group. The mortality rates of the sham RES group, the RES group, RES group + KOR antagonist, RES group + DOR/MOR antagonists (KOR left), RES group + DOR antagonist, and RES group + KOR/MOR antagonists (DOR left) were 50%, 20%, 67%, 13%, 50% and 55%, respectively. Conclusion The mechanism of RES-induced myocardial protection against I/R injury seems to involve multiple target pathways such as Akt, KOR and/or DOR signaling. PMID:26430750

  13. Exogenous Hydrogen Sulfide Postconditioning Protects Isolated Rat Hearts From Ischemia/Reperfusion Injury Through Sirt1/PGC-1α Signaling Pathway.

    PubMed

    Hu, Ming-Zhu; Zhou, Bo; Mao, Hong-Ya; Sheng, Qiong; Du, Bin; Chen, Jun-Liang; Pang, Qing-Feng; Ji, Yong

    2016-07-27

    Sirt1 is a highly conserved nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase which plays an important role in heart diseases. Studies performed with Sirt1 activators indicated that it protects cells from ischemia/ reperfusion (I/R) injury. The protective effects of H2S against I/R injury also have been recognized. Hence, the present study was designed to explore whether Sirt1/PGC-1α participates in the protection of exogenous H2S postconditioning against I/R injury in isolated rat hearts. Isolated rat hearts were subjected to 30 minutes of global ischemia followed by 60 minutes of reperfusion after 20 minutes of equilibrium. During this procedure, the hearts were exposed to NaHS (10 μmol/L) treatment in the absence or presence of the selective Sirt1 inhibitor EX-527 (10 μmol/L). NaHS exerted a protective effect on isolated rat hearts subjected to I/R, as shown by the improved expression of Sirt1/PGC-1α associated with restoration of Sirt1 nuclear localization, cardiac function, decreased myocardial infarct size, decreased myocardial enzyme release, and several biochemical parameters, including up-regulation of the ATP and SOD levels, and down-regulation of the MDA level. However, treatment with EX-527 could partially prevent the above effects of NaHS postconditioning. These results indicate that H2S confers protective effects against I/R injury through the activation of Sirt1/PGC1α. PMID:27357440

  14. Continuous inhibition of poly(ADP-ribose) polymerase does not reduce reperfusion injury in isolated rat heart.

    PubMed

    Nishizawa, Kenya; Yanagida, Shigeki; Yamagishi, Tadashi; Takayama, Eiichi; Bessho, Motoaki; Kusuhara, Masatoshi; Adachi, Takeshi; Ohsuzu, Fumitaka

    2013-07-01

    Poly(ADP-ribose) polymerase (PARP), an enzyme that is important to the regulation of nuclear function, is activated by DNA strand breakage. In massive DNA damage, PARP is overactivated, exhausting nicotinamide adenine dinucleotide and leading to cell death. Recent studies have succeeded in reducing cellular damage in ischemia/reperfusion by inhibiting PARP. However, PARP plays an important part in the DNA repair system, and its inhibition may be hazardous in certain situations. We compared the short-time inhibition of PARP against continuous inhibition during ischemia/reperfusion using isolated rat hearts. The hearts were reperfused after 21 minutes of ischemia with a bolus injection of 3-aminobenzamide (3-AB) (10 mg/kg) followed by continuous 3-AB infusion (50 μM) for the whole reperfusion period or for the first 6 minutes or without 3-AB. At the end of reperfusion, contractile function, high-energy phosphate content, nicotinamide adenine dinucleotide content, and infarcted area were significantly preserved in the 3-AB 6-minute group. In the 3-AB continuous group, these advantages were not apparent. At the end of reperfusion, PARP cleavage had significantly proceeded in the 3-AB continuous group, indicating initiation of the apoptotic cascade. Thus, continuous PARP inhibition by 3-AB does not reduce reperfusion injury in the isolated rat heart, which may be because of acceleration of apoptosis. PMID:23846805

  15. Pitx2 promotes heart repair by activating the antioxidant response after cardiac injury.

    PubMed

    Tao, Ge; Kahr, Peter C; Morikawa, Yuka; Zhang, Min; Rahmani, Mahdis; Heallen, Todd R; Li, Lele; Sun, Zhao; Olson, Eric N; Amendt, Brad A; Martin, James F

    2016-06-01

    Myocardial infarction results in compromised myocardial function and heart failure owing to insufficient cardiomyocyte self-renewal. Unlike many vertebrates, mammalian hearts have only a transient neonatal renewal capacity. Reactivating primitive reparative ability in the mature mammalian heart requires knowledge of the mechanisms that promote early heart repair. By testing an established Hippo-deficient heart regeneration mouse model for factors that promote renewal, here we show that the expression of Pitx2 is induced in injured, Hippo-deficient ventricles. Pitx2-deficient neonatal mouse hearts failed to repair after apex resection, whereas adult mouse cardiomyocytes with Pitx2 gain-of-function efficiently regenerated after myocardial infarction. Genomic analyses indicated that Pitx2 activated genes encoding electron transport chain components and reactive oxygen species scavengers. A subset of Pitx2 target genes was cooperatively regulated with the Hippo pathway effector Yap. Furthermore, Nrf2, a regulator of the antioxidant response, directly regulated the expression and subcellular localization of Pitx2. Pitx2 mutant myocardium had increased levels of reactive oxygen species, while antioxidant supplementation suppressed the Pitx2 loss-of-function phenotype. These findings reveal a genetic pathway activated by tissue damage that is essential for cardiac repair. PMID:27251288

  16. Mitochondrial ATP-sensitive K+ channels mediate the antioxidative influence of diosgenin on myocardial reperfusion injury in rat hearts.

    PubMed

    Badalzadeh, Reza; Yavari, Raana; Chalabiani, Dorna

    2015-07-01

    The contribution of reactive oxygen species and oxidative stress in the pathogenesis of ischemia-reperfusion (I/R) injury has been supported by many studies. The effect of diosgenin on oxidative stress induced by I/R injury was evaluated in this study. Rat hearts were subjected to 30 minutes of global ischemia followed by 90 minutes of reperfusion. 5-hydroxydecanoate (5-HD) was used before administration of diosgenin and before ischemia. The activities of myocardial creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured. Administration of diosgenin before ischemia significantly lowered CK and MDA levels as compared with control group (p < 0.05) and increased GPX (p < 0.05) and SOD (p < 0.01) activities in comparison with control group. Pre-administration of 5-HD significantly attenuated the protective effects of diosgenin. In conclusion, opening of mitochondrial ATP-sensitive K(+) channels and attenuating of oxidative stress can be suggested as underlying mechanisms for cardioprotective effect of diosgenin in I/R injury. PMID:26001291

  17. Pulmonary Instillation of Multi-Walled Carbon Nanotubes Promotes Coronary Vasoconstriction and Exacerbates Injury in Isolated Hearts

    PubMed Central

    Thompson, Leslie C.; Frasier, Chad R.; Sloan, Ruben C.; Mann, Erin E.; Harrison, Benjamin S.; Brown, Jared M.; Brown, David A.; Wingard, Christopher J.

    2014-01-01

    The growing use of multi-walled carbon nanotubes (MWCNTs) across industry has increased human exposures. We tested the hypothesis that pulmonary instillation of MWCNT would exacerbate cardiac ischemia/reperfusion (I/R) injury. One day following intratracheal instillation of 1, 10, or 100 μg MWCNT in Sprague-Dawley rats, we used a Langendorff isolated heart model to examine cardiac I/R injury. In the 100 μg MWCNT group we report increased premature ventricular contractions at baseline and increased myocardial infarction. This was associated with increased endothelin-1 (ET-1) release and depression of coronary flow during early reperfusion. We also tested if isolated coronary vascular responses were affected by MWCNT instillation and found trends for enhanced coronary tone, which were dependent on ET-1, cyclooxygenase, thromboxane, and Rho-kinase. We conclude that instillation of MWCNT promoted cardiac injury by depressing coronary flow, invoking vasoconstrictive mechanisms involving ET-1, cyclooxygenase, thromboxane, and Rho-kinase. PMID:23102262

  18. Cardioprotective Effect of Licochalcone D against Myocardial Ischemia/Reperfusion Injury in Langendorff-Perfused Rat Hearts

    PubMed Central

    Wang, Peng-long; Lu, Jie; Zhao, Hong; Liu, Shi-han; Zheng, Qiu-sheng; Li, Chang-gui

    2015-01-01

    Flavonoids are important components of ‘functional foods’, with beneficial effects on cardiovascular function. The present study was designed to investigate whether licochalcone D (LD) could be a cardioprotective agent in ischemia/reperfusion (I/R) injury and to shed light on its possible mechanism. Compared with the I/R group, LD treatment enhanced myocardial function (increased LVDP, dp/dtmax, dp/dtmin, HR and CR) and suppressed cardiac injury (decreased LDH, CK and myocardial infarct size). Moreover, LD treatment reversed the I/R-induced cleavage of caspase-3 and PARP, resulting in a significant decrease in proinflammatory factors and an increase in antioxidant capacity in I/R myocardial tissue. The mechanisms underlying the antiapoptosis, antiinflammation and antioxidant effects were related to the activation of the AKT pathway and to the blockage of the NF-κB/p65 and p38 MAPK pathways in the I/R-injured heart. Additionally, LD treatment markedly activated endothelial nitric oxide synthase (eNOS) and reduced nitric oxide (NO) production. The findings indicated that LD had real cardioprotective potential and provided support for the use of LD in myocardial I/R injury. PMID:26058040

  19. Cardioprotective Effect of Licochalcone D against Myocardial Ischemia/Reperfusion Injury in Langendorff-Perfused Rat Hearts.

    PubMed

    Yuan, Xuan; Niu, Hai-tao; Wang, Peng-long; Lu, Jie; Zhao, Hong; Liu, Shi-han; Zheng, Qiu-sheng; Li, Chang-gui

    2015-01-01

    Flavonoids are important components of 'functional foods', with beneficial effects on cardiovascular function. The present study was designed to investigate whether licochalcone D (LD) could be a cardioprotective agent in ischemia/reperfusion (I/R) injury and to shed light on its possible mechanism. Compared with the I/R group, LD treatment enhanced myocardial function (increased LVDP, dp/dtmax, dp/dtmin, HR and CR) and suppressed cardiac injury (decreased LDH, CK and myocardial infarct size). Moreover, LD treatment reversed the I/R-induced cleavage of caspase-3 and PARP, resulting in a significant decrease in proinflammatory factors and an increase in antioxidant capacity in I/R myocardial tissue. The mechanisms underlying the antiapoptosis, antiinflammation and antioxidant effects were related to the activation of the AKT pathway and to the blockage of the NF-κB/p65 and p38 MAPK pathways in the I/R-injured heart. Additionally, LD treatment markedly activated endothelial nitric oxide synthase (eNOS) and reduced nitric oxide (NO) production. The findings indicated that LD had real cardioprotective potential and provided support for the use of LD in myocardial I/R injury. PMID:26058040

  20. Gender differences in cardioprotection against ischemia/reperfusion injury in adult rat hearts: focus on Akt and protein kinase C signaling.

    PubMed

    Bae, Soochan; Zhang, Lubo

    2005-12-01

    Previous studies have reported the sex differences in heart susceptibility to ischemia/reperfusion (I/R) injury, but the mechanisms are not understood. The present study tested the hypothesis that Akt and protein kinase C (PKC)epsilon play an important role in the sexual dimorphism of heart susceptibility to I/R injury. Isolated hearts from 2-month-old male and female rats were subjected to I/R in the Langendorff preparation. The postischemic recovery of left ventricular function was significantly better, and infarct size was significantly smaller in female (37.1 +/- 1.9%) than in male (48.3 +/- 2.3%) hearts after 25-min ischemia followed by 2-h reperfusion. Inhibition of phosphatidylinositol 3-kinase/Akt pathway by wortmannin or PKC by chelerythrine chloride before ischemia significantly reduced postischemic recovery and increased infarct size in female but not male hearts. There were no differences in myocardial protein levels of heat shock protein 70, Akt, and PKCepsilon, respectively, between male and female rats. However, the ratio of phosphorylated (p)-Akt/Akt (0.58 +/- 0.05 versus 0.22 +/- 0.04; P < 0.05) and p-PKCepsilon/PKCepsilon (0.35 +/- 0.03 versus 0.22 +/- 0.02; P < 0.05) was significantly higher in female than in male hearts. In addition, there were significant increases in p-Akt and p-PKCepsilon levels during reperfusion in female but not in male hearts. The results suggest that increased p-Akt and p-PKCepsilon levels in female hearts contribute to the gender-related differences in heart susceptibility to I/R and play an important role in cardioprotection against I/R injury in females. PMID:16099927

  1. Framingham Risk Scores for coronary heart disease in a cohort of Saudi Arabian men and women with spinal cord injury.

    PubMed

    Hussain, Amjad; Qureshi, Ahmed Zaheer; Ayaz, Saeed Bin; Rathore, Farooq Azam

    2016-06-01

    People with spinal cord injury (SCI) are at increased risk of developing coronary heart disease (CHD). This study aimed at predicting CHD risk in a cohort of Saudi patients with SCI in comparison with patients without SCI and to correlate different demographic and clinical factors with Framingham Risk Score (FRS) in SCI patients. The study was conducted at the rehabilitation and the main hospitals of King Fahad Medical City, Riyadh, Saudi Arabia; on sixty patients with SCI and sixty controls of age ≥20 years. FRS was calculated on a web-based calculator. For the SCI group, sub-groups were made for statistical analysis based on gender, cigarette smoking, neurological level and completeness of injury. The mean FRS for the SCI group (2 ± 7.9) was significantly higher (P < 0.001) than the control group (-2.24 ± 3.4). The 10-year risk of developing CHD was low in 90 % of the SCI group and 100 % of the controls. The age, systolic blood pressure (SBP) and serum total cholesterol had a positive correlation to FRS in SCI patients and females had a significantly higher mean FRS than males (P = 0.03). There was no significant relation of resultant FRS with time since SCI, smoking history and neurological level or completeness of injury. Our sample of Saudi patients with SCI had a higher FRS as compared to controls, however, majority had a low risk of developing CHD in next 10 years. The age, SBP and total cholesterol surfaced as positive predictors of CHD in SCI patients. Time since SCI, smoking, and neurological level or completeness of injury did not influence the resultant FRS and thus the development of CHD. PMID:26292928

  2. The mitochondria-targeted anti-oxidant MitoQ decreases ischemia-reperfusion injury in a murine syngeneic heart transplant model

    PubMed Central

    Dare, Anna J.; Logan, Angela; Prime, Tracy A.; Rogatti, Sebastian; Goddard, Martin; Bolton, Eleanor M.; Bradley, J. Andrew; Pettigrew, Gavin J.; Murphy, Michael P.; Saeb-Parsy, Kourosh

    2015-01-01

    Background Free radical production and mitochondrial dysfunction during cardiac graft reperfusion is a major factor in post-transplant ischemia-reperfusion (IR) injury, an important underlying cause of primary graft dysfunction. We therefore assessed the efficacy of the mitochondria-targeted anti-oxidant MitoQ in reducing IR injury in a murine heterotopic cardiac transplant model. Methods Hearts from C57BL/6 donor mice were flushed with storage solution alone, solution containing the anti-oxidant MitoQ, or solution containing the non–anti-oxidant decyltriphenylphosphonium control and exposed to short (30 minutes) or prolonged (4 hour) cold preservation before transplantation. Grafts were transplanted into C57BL/6 recipients and analyzed for mitochondrial reactive oxygen species production, oxidative damage, serum troponin, beating score, and inflammatory markers 120 minutes or 24 hours post-transplant. Results MitoQ was taken up by the heart during cold storage. Prolonged cold preservation of donor hearts before IR increased IR injury (troponin I, beating score) and mitochondrial reactive oxygen species, mitochondrial DNA damage, protein carbonyls, and pro-inflammatory cytokine release 24 hours after transplant. Administration of MitoQ to the donor heart in the storage solution protected against this IR injury by blocking graft oxidative damage and dampening the early pro-inflammatory response in the recipient. Conclusions IR after heart transplantation results in mitochondrial oxidative damage that is potentiated by cold ischemia. Supplementing donor graft perfusion with the anti-oxidant MitoQ before transplantation should be studied further to reduce IR-related free radical production, the innate immune response to IR injury, and subsequent donor cardiac injury. PMID:26140808

  3. Resistance to Reperfusion Injury Following Short Term Postischemic Administration of Natural Honey in Globally Ischemic Isolated Rat Heart

    PubMed Central

    Vaez, Haleh; Samadzadeh, Mehrban; Zahednezhad, Fahimeh; Najafi, Moslem

    2012-01-01

    Purpose: Results of our previous study revealed that preischemic perfusion of honey before zero flow global ischemia had cardioprotective effects in rat. The present study investigated potential resistance to reperfusion injury following short term postischemic administration of natural honey in globally ischemic isolated rat heart. Methods: Male Wistar rats were divided into five groups (n=10-13). The rat hearts were isolated, mounted on a Langendorff apparatus, allowed to equilibrate for 30 min then subjected to 30 min global ischemia. In the control group, the hearts were reperfused with drug free normal Krebs-Henseleit (K/H) solution before ischemia and during 120 min reperfusion. In the treatment groups, reperfusion was initiated with K/H solution containing different concentration of honey (0.25, 0.5, 1 and 2%) for 15 min and was resumed until the end of 120 min with normal K/H solution. Results: In the control group, VEBs number was 784±199, while in honey concentration of 0.25, 0.5, 1 and 2%, it decreased to 83±23 (P<0.001), 138±48 (P<0.01), 142±37 (P<0.001) and 157±40 (P<0.01), respectively. Number and duration of VT and time spent in reversible VF were also reduced by honey. In the control group, the infarct size was 54.1±7.8%, however; honey (0.25, 0.5, 1 and 2%) markedly lowered the value to 12.4±2.4, 12.7±3.3, 11.3±2.6 and 7.9±1.7 (P<0.001), respectively. Conclusion: Postischemic administration of natural honey in global ischemia showed protective effects against ischemia/reperfusion (I/R) injuries in isolated rat heart. Antioxidant and radical scavenging activity, lipoperoxidation inhibition, reduction of necrotized tissue, presence of rich energy sources, various type of vitamins, minerals and enzymes and formation of NO-contain metabolites may probably involve in those cardioprotective effects. PMID:24312792

  4. Binding of elastin peptides to S-Gal protects the heart against ischemia/reperfusion injury by triggering the RISK pathway.

    PubMed

    Robinet, Arnaud; Millart, Hervé; Oszust, Floriane; Hornebeck, William; Bellon, Georges

    2007-07-01

    Elastin peptides (EPs) generated by hydrolysis of elastic fibers by elastinolytic enzymes display a wide spectrum of biological activities. Here, we investigated their influence on rat heart ischemia-mediated injury using the Langendorff ex vivo model. EPs, i.e., kappa elastin, at 1.32- and 660-nM concentrations, when administered before the ischemia period, elicited a beneficial influence against ischemia by accelerating the recovery rate of heart contractile parameters and by decreasing significantly creatine kinase release and heart necrosis area when measured at the onset of the reperfusion. All effects were S-Gal-dependent, as being reproduced by (VGVAPG)3 and as being inhibited by receptor antagonists, such as lactose and V14 peptide (VVGSPSAQDEASPL). EPs interaction with S-Gal triggered NO release and activation of PI3-kinase/Akt and ERK1/2 in human coronary endothelial cells (HCAECs) and rat neonatal cardiomyocytes (RCs). This signaling pathway, as designated as RISK, for reperfusion injury salvage kinase pathway, was shown to be responsible for the beneficial influence of EPs on ischemia/reperfusion injury on the basis of its inhibition by specific pharmacological inhibitors. EPs survival activity was attained at a concentration averaging that present into the blood circulation, supporting the contention that these matrikines might offer a natural protection against cardiac injury in young and adult individuals. Such protective effect might be lost with aging, since we found that hearts from 24-month-old rats did not respond to EPs. PMID:17341689

  5. Comparison of Heart Rate Response to Tennis Activity between Persons with and without Spinal Cord Injuries: Implications for a Training Threshold

    ERIC Educational Resources Information Center

    Barfield, J. P.; Malone, Laurie A.; Coleman, Tristica A.

    2009-01-01

    The purpose of this study was to evaluate the ability of individuals with spinal cord injury (SCI) to reach a training threshold during on-court sport activity. Monitors collected heart rate (HR) data every 5 s for 11 wheelchair tennis players (WCT) with low paraplegia and 11 able-bodied controls matched on experience and skill level (ABT).…

  6. Computer model analysis of the relationship of ST-segment and ST-segment/heart rate slope response to the constituents of the ischemic injury source.

    PubMed

    Hyttinen, J; Viik, J; Lehtinen, R; Plonsey, R; Malmivuo, J

    1997-07-01

    The objective of the study was to investigate a proposed linear relationship between the extent of myocardial ischemic injury and the ST-segment/heart rate (ST/HR) slope by computer simulation of the injury sources arising in exercise electrocardiographic (ECG) tests. The extent and location of the ischemic injury were simulated for both single- and multivessel coronary artery disease by use of an accurate source-volume conductor model which assumes a linear relationship between heart rate and extent of ischemia. The results indicated that in some cases the ST/HR slope in leads II, aVF, and especially V5 may be related to the extent of ischemia. However, the simulations demonstrated that neither the ST-segment deviation nor the ST/HR slope was directly proportional to either the area of the ischemic boundary or the number of vessels occluded. Furthermore, in multivessel coronary artery disease, the temporal and spatial diversity of the generated multiple injury sources distorted the presumed linearity between ST-segment deviation and heart rate. It was concluded that the ST/HR slope and ST-segment deviation of the 12-lead ECG are not able to indicate extent of ischemic injury or number of vessels occluded. PMID:9261724

  7. Inhibition of inflammation and oxidative stress by an imidazopyridine derivative X22 prevents heart injury from obesity.

    PubMed

    Qian, Yuanyuan; Zhang, Yali; Zhong, Peng; Peng, Kesong; Xu, Zheng; Chen, Xuemei; Lu, Kongqin; Chen, Gaozhi; Li, Xiaokun; Liang, Guang

    2016-08-01

    Inflammation and oxidative stress plays an important role in the development of obesity-related complications and cardiovascular disease. Benzimidazole and imidazopyridine compounds are a class of compounds with a variety of activities, including anti-inflammatory, antioxidant and anti-cancer. X22 is an imidazopyridine derivative we synthesized and evaluated previously for anti-inflammatory activity in lipopolysaccharide-stimulated macrophages. However, its ability to alleviate obesity-induced heart injury via its anti-inflammatory actions was unclear. This study was designed to evaluate the cardioprotective effects of X22 using cell culture studies and a high-fat diet rat model. We observed that palmitic acid treatment in cardiac-derived H9c2 cells induced a significant increase in reactive oxygen species, inflammation, apoptosis, fibrosis and hypertrophy. All of these changes were inhibited by treatment with X22. Furthermore, oral administration of X22 suppressed high-fat diet-induced oxidative stress, inflammation, apoptosis, hypertrophy and fibrosis in rat heart tissues and decreased serum lipid concentration. We also found that the anti-inflammatory and anti-oxidative actions of X22 were associated with Nrf2 activation and nuclear factor-kappaB (NF-κB) inhibition, respectively, both in vitro and in vivo. The results of this study indicate that X22 may be a promising cardioprotective agent and that Nrf2 and NF-κB may be important therapeutic targets for obesity-related complications. PMID:27019072

  8. Pulmonary ischemia/reperfusion injury: a quantitative study of structure and function in isolated heart-lungs of the rat.

    PubMed

    Fehrenbach, H; Schepelmann, D; Albes, J M; Bando, T; Fischer, F; Fehrenbach, A; Stolte, N; Wahlers, T; Richter, J

    1999-05-01

    Early graft dysfunction after lung transplantation is a significant and unpredictable problem. Our study aimed at a detailed investigation of structure-function correlations in a rat isolated heart-lung model ofischemia/ reperfusion injury. Variable degrees of injury were induced by preservation with potassium-modified Euro-Collins solutions, 2 hr of cold ischemia, and 40 min of reperfusion. Pulmonary artery pressure (Ppa), pulmonary vascular resistance (PVR), peak inspiratory pressure (PIP), and perfusate gases (deltaPO2, deltaPCO2) were recorded during reperfusion. Right lungs were used to calculate W/D-weight ratios. Nineteen experimental and six control left lungs were fixed for light and electron microscopy by vascular perfusion. Systematic random samples were analyzed by stereology to determine absolute and relative volumes of lung structures, the amount of interstitial and intraalveolar edema, and the extent of epithelial injury. Lectin- and immunohistochemistry using established epithelial cell markers were performed in three animals per group to reveal sites of severe focal damage. Experimental lungs showed a wide range in severity of ischemia/ reperfusion injury. Intraalveolar edema fluid amounted to 77-909 mm3 with a mean of 448+/-250 mm3 as compared with 22+/-22 mm3 in control lungs (P<0.001). Perfusate oxygenation (deltaPO2) decreased from 30.5+/-15.2 to 21.7+/-15.2 mm Hg (P=0.05) recorded after 5 and 40 minutes of reperfusion. In experimental lungs, a surface fraction of 1% to 58% of total type I pneumocyte surface was damaged. Intraalveolar edema per gas exchange region (Vv ape,P) and deltaPO2 were related according to deltaPO2 = 96 - 60 x log10(Vv ape,P) [mm Hg]. The extent of epithelial injury did not correlate with deltaPO2 nor with intraalveolar edema, but increased significantly with PVR. Lectin- and immunohistochemistry revealed focal severe damage to the alveolar epithelium at the border of perivascular cuffs. PMID:10321996

  9. Participation of heart mitochondria in myocardial protection against ischemia/reperfusion injury: benefit effects of short-term adaptation processes.

    PubMed

    Ferko, M; Kancirová, I; Jašová, M; Waczulíková, I; Čarnická, S; Kucharská, J; Uličná, O; Vančová, O; Muráriková, M; Ravingerová, T; Ziegelhöffer, A

    2015-01-01

    Acute streptozotocin diabetes mellitus (DM) as well as remote ischemic preconditioning (RPC) has shown a favorable effect on the postischemic-reperfusion function of the myocardium. Cardioprotective mechanisms offered by these experimental models involve the mitochondria with the changes in functional properties of membrane as the end-effector. The aim was to find out whether separate effects of RPC and DM would stimulate the mechanisms of cardioprotection to a maximal level or whether RPC and DM conditions would cooperate in stimulation of cardioprotection. Experiments were performed on male Wistar rats divided into groups: control, DM, RPC and DM treated by RPC (RPC+DM). RPC protocol of 3 cycles of 5-min hind limb ischemia followed by 5-min reperfusion was used. Ischemic-reperfusion injury was induced by 30-min ischemia followed by 40-min reperfusion of the hearts in Langendorff mode. Mitochondria were isolated by differential centrifugation, infarct size assessed by staining with 1 % 2,3,5-triphenyltetrazolium chloride, mitochondrial membrane fluidity with a fluorescent probe DPH, CoQ(9) and CoQ(10) with HPLC. Results revealed that RPC as well as DM decreased the infarct size and preserved mitochondrial function by increasing the mitochondrial membrane fluidity. Both used models separately offered a sufficient protection against ischemic-reperfusion injury without an additive effect of their combination. PMID:26674282

  10. Prevention and Treatment of Functional and Structural Radiation Injury in the Rat Heart by Pentoxifylline and Alpha-Tocopherol

    SciTech Connect

    Boerma, Marjan Roberto, Kerrey A.; Hauer-Jensen, Martin

    2008-09-01

    Purpose: Radiation-induced heart disease (RIHD) is a severe side effect of thoracic radiotherapy. This study examined the effects of pentoxifylline (PTX) and {alpha}-tocopherol on cardiac injury in a rat model of RIHD. Methods and Materials: Male Sprague-Dawley rats received fractionated local heart irradiation with a daily dose of 9 Gy for 5 days and were observed for 6 months after irradiation. Rats were treated with a combination of PTX, 100 mg/kg/day, and {alpha}-tocopherol (20 IU/kg/day) and received these compounds either from 1 week before until 6 months after irradiation or starting 3 months after irradiation, a time point at which histopathologic changes become apparent in our model of RIHD. Results: Radiation-induced increases in left ventricular diastolic pressure (in mm Hg: 35 {+-} 6 after sham-irradiation, 82 {+-} 11 after irradiation) were significantly reduced by PTX and {alpha}-tocopherol (early treatment: 48 {+-} 7; late treatment: 53 {+-} 6). PTX and {alpha}-tocopherol significantly reduced deposition of collagen types I (radiation only: 3.5 {+-} 0.2 {mu}m{sup 2} per 100 {mu}m{sup 2}; early treatment: 2.7 {+-} 0.8; late treatment: 2.2 {+-} 0.2) and III (radiation only: 13.9 {+-} 0.8; early treatment: 11.0 {+-} 1.2; late treatment: 10.6 {+-} 0.8). On the other hand, radiation-induced alterations in heart/body weight ratios, myocardial degeneration, left ventricular mast cell densities, and most echocardiographic parameters were not significantly altered by PTX and {alpha}-tocopherol. Conclusions: Treatment with PTX and {alpha}-tocopherol may have beneficial effects on radiation-induced myocardial fibrosis and left ventricular function, both when started before irradiation and when started later during the process of RIHD.

  11. CD38 Deficiency Protects the Heart from Ischemia/Reperfusion Injury through Activating SIRT1/FOXOs-Mediated Antioxidative Stress Pathway

    PubMed Central

    Guan, Xiao-Hui; Liu, Xiao-Hong; Hong, Xuan; Zhao, Ning; Xiao, Yun-Fei; Wang, Ling-Fang; Qian, Yi-Song; Deng, Ke-Yu; Ji, Guangju; Fu, Mingui

    2016-01-01

    Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac muscle. We previously observed that CD38 deficiency remarkably protects mouse embryonic fibroblasts (MEFs) from oxidative stress-induced injury. However, whether CD38 deficiency protects from I/R injury in the heart is not explored. Here, we showed that the hearts of CD38 deficient mice or wild type mice supplied with exogenous NAD were significantly protected from ischemia/reperfusion injury, seen as reduction of the myocardial infarct sizes when the mice were subjected to 30 min ischemia followed by 24 hours of reperfusion. Consistently, the protection of CD38 deficiency on hypoxia/reoxygenation (H/R) injury was confirmed with a CD38 knockdown H9c2 stable cell line. Furthermore, we observed that knockdown of CD38 remarkably inhibited ROS generation and intracellular Ca2+ overloading induced by H/R in H9c2 cells. The FOXO1 and FOXO3 expressions were significantly elevated by H/R injury in CD38 knockdown cells compared with normal H9c2 cells. The cell immunofluorescence assay showed that FOXO1 nuclear translocation was significantly increased in CD38 knockdown H9c2 cells. In addition, we demonstrated that the increase of FOXO1 nuclear translocation was associated with the increased expressions of antioxidant catalase and SOD2 and the attenuated expression of the ROS generation enzyme NOX4. In conclusion, our results provide new evidence that CD38 deficiency protects the heart from I/R injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway. PMID:27547294

  12. Effect of plant polyphenols on ischemia-reperfusion injury of the isolated rat heart and vessels.

    PubMed

    Brosková, Z; Drábiková, K; Sotníková, R; Fialová, S; Knezl, V

    2013-07-01

    In the present study, we investigated the potential protective effect of selected natural substances in a rat model of heart and mesenteric ischemia-reperfusion (I/R). Experiments were performed on isolated Langendorff-perfused rat hearts, subjected to 30-min global ischemia, followed by 30-min reperfusion. Arbutin, curcumin, rosmarinic acid and extract of Mentha x villosa were applied in the concentration of 1 × 10⁻⁵ mol/l 10 min before the onset of ischemia and during reperfusion, through the perfusion medium. Mesenteric ischemia was induced by clamping the superior mesenteric artery (SMA) for 60 min, subsequent reperfusion lasted 30 min. Production of reactive oxygen species (ROS) by SMA ex vivo was determined by luminol-enhanced chemiluminiscence (CL). The effect of the substances was tested after their incubation with tissue. Curcumin and extract of Mentha x villosa were found to be the most effective in reducing reperfusion-induced dysrhythmias--ventricular tachycardia and fibrillation. This effect was accompanied by bradycardic effect. The mesenteric I/R induced an increase in CL in vascular tissue which was dampened by substances tested. All substances tested were found to have antioxidant properties, as demonstrated by a reduction in ROS production in mesenteric vessels. This effect was confirmed in curcumin and extract of Mentha x villosa which reduced reperfusion dyshythmias. PMID:22933407

  13. Mesenchymal stem cells preconditioned with trimetazidine promote neovascularization of hearts under hypoxia/reoxygenation injury

    PubMed Central

    Hu, Xiaowu; Yang, Junjie; Wang, Ying; Zhang, You; Ii, Masaaki; Shen, Zhenya; Hui, Jie

    2015-01-01

    Background: Cell-based angiogenesis is a promising treatment for ischemic diseases; however, survival of implanted cells is impaired by the ischemic microenvironment. In this study, mesenchymal stem cells (MSCs) for cell transplantation were preconditioned with trimetazidine (TMZ). We hypothesized that TMZ enhances the survival rate of MSCs under hypoxic stimuli through up-regulation of HIF1-α. Methods and results: Bone marrow-derived rat mesenchymal stem cells were preconditioned with 10 μM TMZ for 6 h. TMZ preconditioning of MSCs remarkably increased cell viability and the expression of HIF1-α and Bcl-2, when cells were under hypoxia/reoxygenation (H/R) stimuli. But the protective effects of TMZ were abolished after knocking down of HIF-1α. Three days after implantation of the cells into the peri-ischemic zone of rat myocardial ischemia-reperfusion (I/R) injury model, survival of the TMZ-preconditioned MSCs was high. Furthermore, capillary density and cardiac function were significantly better in the rats implanted with TMZ-preconditioned MSCs 28 days after cell injection. Conclusions: TMZ preconditioning increased the survival rate of MSCs, through up-regulation of HIF1-α, thus contributing to neovascularization and improved cardiac function of rats subjected to myocardial I/R injury. PMID:26629255

  14. CD8+ T-Cells Expressing Interferon Gamma or Perforin Play Antagonistic Roles in Heart Injury in Experimental Trypanosoma Cruzi-Elicited Cardiomyopathy

    PubMed Central

    Cipitelli, Márcio da Costa; Vinagre, Nathália Ferreira; Rodrigues, Maurício Martins; Gazzinelli, Ricardo Tostes; Lannes-Vieira, Joseli

    2012-01-01

    In Chagas disease, CD8+ T-cells are critical for the control of Trypanosoma cruzi during acute infection. Conversely, CD8+ T-cell accumulation in the myocardium during chronic infection may cause tissue injury leading to chronic chagasic cardiomyopathy (CCC). Here we explored the role of CD8+ T-cells in T. cruzi-elicited heart injury in C57BL/6 mice infected with the Colombian strain. Cardiomyocyte lesion evaluated by creatine kinase-MB isoenzyme activity levels in the serum and electrical abnormalities revealed by electrocardiogram were not associated with the intensity of heart parasitism and myocarditis in the chronic infection. Further, there was no association between heart injury and systemic anti-T. cruzi CD8+ T-cell capacity to produce interferon-gamma (IFNγ) and to perform specific cytotoxicity. Heart injury, however, paralleled accumulation of anti-T. cruzi cells in the cardiac tissue. In T. cruzi infection, most of the CD8+ T-cells segregated into IFNγ+ perforin (Pfn)neg or IFNγnegPfn+ cell populations. Colonization of the cardiac tissue by anti-T. cruzi CD8+Pfn+ cells paralleled the worsening of CCC. The adoptive cell transfer to T. cruzi-infected cd8−/− recipients showed that the CD8+ cells from infected ifnγ−/−pfn+/+ donors migrate towards the cardiac tissue to a greater extent and caused a more severe cardiomyocyte lesion than CD8+ cells from ifnγ+/+pfn−/− donors. Moreover, the reconstitution of naïve cd8−/− mice with CD8+ cells from naïve ifnγ+/+pfn−/− donors ameliorated T. cruzi-elicited heart injury paralleled IFNγ+ cells accumulation, whereas reconstitution with CD8+ cells from naïve ifnγ−/−pfn+/+ donors led to an aggravation of the cardiomyocyte lesion, which was associated with the accumulation of Pfn+ cells in the cardiac tissue. Our data support a possible antagonist effect of CD8+Pfn+ and CD8+IFNγ+ cells during CCC. CD8+IFNγ+ cells may exert a beneficial role, whereas CD8+Pfn+ may play a detrimental role

  15. Preoperative heart rate and myocardial injury after non-cardiac surgery: results of a predefined secondary analysis of the VISION study

    PubMed Central

    Abbott, T. E. F.; Ackland, G. L.; Archbold, R. A.; Wragg, A.; Kam, E.; Ahmad, T.; Khan, A. W.; Niebrzegowska, E.; Rodseth, R. N.; Devereaux, P. J.; Pearse, R. M.

    2016-01-01

    Background Increased baseline heart rate is associated with cardiovascular risk and all-cause mortality in the general population. We hypothesized that elevated preoperative heart rate increases the risk of myocardial injury after non-cardiac surgery (MINS). Methods We performed a secondary analysis of a prospective international cohort study of patients aged ≥45 yr undergoing non-cardiac surgery. Preoperative heart rate was defined as the last measurement before induction of anaesthesia. The sample was divided into deciles by heart rate. Multivariable logistic regression models were used to determine relationships between preoperative heart rate and MINS (determined by serum troponin concentration), myocardial infarction (MI), and death within 30 days of surgery. Separate models were used to test the relationship between these outcomes and predefined binary heart rate thresholds. Results Patients with missing outcomes or heart rate data were excluded from respective analyses. Of 15 087 patients, 1197 (7.9%) sustained MINS, 454 of 16 007 patients (2.8%) sustained MI, and 315 of 16 037 patients (2.0%) died. The highest heart rate decile (>96 beats min−1) was independently associated with MINS {odds ratio (OR) 1.48 [1.23–1.77]; P<0.01}, MI (OR 1.71 [1.34–2.18]; P<0.01), and mortality (OR 3.16 [2.45–4.07]; P<0.01). The lowest decile (<60 beats min−1) was independently associated with reduced mortality (OR 0.50 [0.29–0.88]; P=0.02), but not MINS or MI. The predefined binary thresholds were also associated with MINS, but more weakly than the highest heart rate decile. Conclusions Preoperative heart rate >96 beats min−1 is associated with MINS, MI, and mortality after non-cardiac surgery. This association persists after accounting for potential confounding factors. Clinical trial registration NCT00512109. PMID:27440628

  16. Nonylphenol disrupts the cardio-protective effects of 17β-estradiol on ischemia/reperfusion injury in isolated hearts of guinea pig.

    PubMed

    Wang, Yan; Hu, Huiyuan; Zhao, Meimi; Zhao, Jinsheng; Yin, Dandan; Sun, Xuefei; Liu, Shuyuan; Gao, Qinghua; Yu, Lifeng; Hao, Liying

    2013-01-01

    Nonylphenol (NP), a widely distributed, toxic, endocrine-disrupting chemical, has estrogenic properties. However, its cardiac effects remain unclear. In this study, the effects of NP on isolated guinea pig hearts were studied in three separate experiments. First, hearts were perfused with 10⁻⁷ M NP or 10⁻⁵ M NP to determine whether NP was toxic to isolated healthy hearts. Next, hearts were subjected to 50 min of ischemia and 60 min of reperfusion (I50R60) with 10⁻⁷ M NP or 10⁻⁵ M NP to determine whether NP could aggravate ischemia/reperfusion (I/R) injury. Finally, the interaction of the cardio-protective agent 17β-estradiol (E₂) with NP was studied using 10⁻⁷ M E₂, 10⁻⁷ M E₂ plus 10⁻⁷ M NP, and 10⁻⁷ M E₂ plus 10⁻⁵ M NP. Heart rate (HR) and coronary flow (CF) were significantly decreased and the leakage of lactate dehydrogenase (LDH) in effluent was increased in the 10⁻⁵ M NP group. However, there were no obvious changes in HR, CF, the leakage of LDH or creatine kinase (CK), or the activity of superoxide dismutase in either of the NP treatments in the I50R60 model. Treatment with 10⁻⁷ M E₂ attenuated I/R injury by increasing HR, decreasing the leakage of LDH and CK, and decreasing infarct size. However, these effects were reversed by both concentrations of NP. These data demonstrate that NP had direct toxic effects on normal hearts and NP might disrupt the cardio-protective effects of E₂ on I/R injury. PMID:24067721

  17. Cardioprotective Effects of Total Flavonoids Extracted from Xinjiang Sprig Rosa rugosa against Acute Ischemia/Reperfusion-Induced Myocardial Injury in Isolated Rat Heart.

    PubMed

    Hou, Xuejiao; Han, Jichun; Yuan, Changsheng; Ren, Huanhuan; Zhang, Ya; Zhang, Tao; Xu, Lixia; Zheng, Qiusheng; Chen, Wen

    2016-01-01

    This study evaluated the antioxidative and cardioprotective effects of total flavonoids extracted from Xinjiang sprig Rosa rugosa on ischemia/reperfusion (I/R) injury using an isolated Langendorff rat heart model. The possible mechanism of Xinjiang sprig rose total flavonoid (XSRTF) against I/R injury was also studied. XSRTF (5, 10, and 20 µg/mL) dissolved in Krebs-Henseleit buffer was administered to isolated rat heart. The XSRTF showed remarkable scavenging effects against 1,1-diphenyl-2-picrylhydrazyl, hydroxyl, and superoxide anion radicals in vitro. XSRTF pretreatment improved the heart rate, increased LVDP, and decreased CK and LDH levels in coronary flow. This pretreatment also increased SOD activity and GSH/GSSG ratio but decreased MDA, TNF-α, and CRP levels and IL-8 and IL-6 activities. The infarct size and cell apoptosis in the hearts from the XSRTF-treated group were lower than those in the hearts from the I/R group. Therefore, the cardioprotective effects of XSRTF may be attributed to its antioxidant, antiapoptotic, and anti-inflammatory activities. PMID:25617974

  18. Reduced mitochondrial Ca2+ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts

    PubMed Central

    Camara, Amadou K. S.; Heisner, James S.; Riess, Matthias L.; Aldakkak, Mohammed; Stowe, David F.

    2012-01-01

    Oxidative damage and impaired cytosolic Ca2+ concentration ([Ca2+]cyto) handling are associated with mitochondrial [Ca2+] ([Ca2+]mito) overload and depressed functional recovery after cardiac ischemia-reperfusion (I/R) injury. We hypothesized that hearts from old guinea pigs would demonstrate impaired [Ca2+]mito handling, poor functional recovery, and a more oxidized state after I/R injury compared with hearts from young guinea pigs. Hearts from young (∼4 wk) and old (>52 wk) guinea pigs were isolated and perfused with Krebs-Ringer solution (2.1 mM Ca2+ concentration at 37°C). Left ventricular pressure (LVP, mmHg) was measured with a balloon, and NADH, [Ca2+]mito (nM), and [Ca2+]cyto (nM) were measured by fluorescence with a fiber optic probe placed against the left ventricular free wall. After baseline (BL) measurements, hearts were subjected to 30 min global ischemia and 120 min reperfusion (REP). In old vs. young hearts we found: 1) percent infarct size was lower (27 ± 9 vs. 57 ± 2); 2) developed LVP (systolic-diastolic) was higher at 10 min (57 ± 11 vs. 29 ± 2) and 60 min (55 ± 10 vs. 32 ± 2) REP; 3) diastolic LVP was lower at 10 and 60 min REP (6 ± 3 vs. 29 ± 4 and 3 ± 3 vs. 21 ± 4 mmHg); 4) mean [Ca2+]cyto was higher during ischemia (837 ± 39 vs. 541 ± 39), but [Ca2+]mito was lower (545 ± 62 vs. 975 ± 38); 5) [Ca2+]mito was lower at 10 and 60 min REP (129 ± 2 vs. 293 ± 23 and 122 ± 2 vs. 234 ± 15); 6) reduced inotropic responses to dopamine and digoxin; and 7) NADH was elevated during ischemia in both groups and lower than BL during REP. Contrary to our stated hypotheses, old hearts showed reduced [Ca2+]mito, decreased infarction, and improved basal mechanical function after I/R injury compared with young hearts; no differences were noted in redox state due to age. In this model, aging-associated protection may be linked to limited [Ca2+]mito loading after I/R injury despite higher [Ca2+]cyto load during ischemia in old vs. young hearts

  19. Early dysautonomia detected by heart rate variability predicts late depression in female patients following mild traumatic brain injury.

    PubMed

    Sung, Chih-Wei; Lee, Hsin-Chien; Chiang, Yung-Hsiao; Chiu, Wen-Ta; Chu, Shu-Fen; Ou, Ju-Chi; Tsai, Shin-Han; Liao, Kuo-Hsing; Lin, Chien-Min; Lin, Jia-Wei; Chen, Gunng-Shinng; Li, Wei-Jiun; Wang, Jia-Yi

    2016-04-01

    Depression is one of the frequent complications following a mild traumatic brain injury (mTBI). Recent research indicated that abnormalities in the autonomic nervous system (ANS) can be evaluated by a noninvasive power spectral analysis of the heart rate variability (HRV). In this study, we investigated whether a frequency-domain analysis of HRV was correlated with late depression in mTBI patients. In total, 181 patients diagnosed with mTBI and 83 volunteers as healthy controls were recruited in 2010-2014. Beck Depression Inventory (BDI) scores were used to evaluate depression in the 1st week of assessment and at 1.5-, 3-, 6-, 12-, and 18-month follow-ups. Correlation and logistic regression analyses of the 1st week HRV parameters with BDI scores at 18 months were performed in individual female mTBI patients. Female mTBI patients were more vulnerable to depression accompanied by reduced HRV compared to healthy controls. Over time, depression was aggravated in female mTBI patients but was alleviated in male mTBI patients. A significantly lower parasympathetic proportion of the ANS was noted at 18 months with respect to the 1st week in female mTBI patients. In addition, depression in female mTBI patients at 18 months after injury was significantly correlated with a decrease in the parasympathetic proportion of the ANS in the 1st week (ρ = -0.411; p < .05). Dysautonomia resulted in higher risks of depression in female mTBI patients. We concluded that early dysautonomia following an mTBI contributes to late depression in female mTBI patients. PMID:26560198

  20. Gypenosides alleviate myocardial ischemia-reperfusion injury via attenuation of oxidative stress and preservation of mitochondrial function in rat heart.

    PubMed

    Yu, Haijie; Guan, Qigang; Guo, Liang; Zhang, Haishan; Pang, Xuefeng; Cheng, Ying; Zhang, Xingang; Sun, Yingxian

    2016-05-01

    Gypenosides (GP) are the predominant components of Gynostemma pentaphyllum, a Chinese herb medicine that has been widely used for the treatment of chronic inflammation, hyperlipidemia, and cardiovascular disease. GP has been demonstrated to exert protective effects on the liver and brain against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the heart during myocardial I/R is unclear. In this study, we demonstrate that pre-treatment with GP dose-dependently limits infarct size, alleviates I/R-induced pathological changes in the myocardium, and preserves left ventricular function in a rat model of cardiac I/R injury. In addition, GP pre-treatment reduces oxidative stress and protects the intracellular antioxidant machinery in the myocardium. Further, we show that the cardioprotective effect of GP is associated with the preservation of mitochondrial function in the cardiomyocytes, as indicated by ATP level, enzymatic activities of complex I, II, and IV on the mitochondrial respiration chain, and the activity of citrate synthase in the citric acid cycle for energy generation. Moreover, GP maintains mitochondrial membrane integrity and inhibits the release of cytochrome c from the mitochondria to the cytosol. The cytoprotective effect of GP is further confirmed in vitro in H9c2 cardiomyoblast cell line with oxygen-glucose deprivation and reperfusion (OGD/R), and the results indicate that GP protects cell viability, reduces oxidative stress, and preserves mitochondrial function. In conclusion, our study suggests that GP may be of clinical value in cytoprotection during acute myocardial infarction and reperfusion. PMID:26800973

  1. Nitric oxide synthase protects the heart against ischemia-reperfusion injury in rabbits.

    PubMed

    Hoshida, S; Yamashita, N; Igarashi, J; Nishida, M; Hori, M; Kamada, T; Kuzuya, T; Tada, M

    1995-07-01

    The role of nitric oxide (NO) in myocardial ischemia-reperfusion injury is still controversial. To determine the role of NO in the propagation of myocardial injury in a coronary artery occlusion-reperfusion model, we examined the effect of a competitive NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), with and without L-arginine, on the size of the infarct resulting from coronary artery occlusion (30 min) followed by reperfusion (48 hr) in rabbits. L-NAME (300 micrograms/kg, as a bolus, and 100 micrograms/kg/min, i.v.) with and without L-arginine (30 mg/kg, as a bolus, and 10 mg/kg/min, i.v.) was administered immediately before coronary occlusion to 60 min after reperfusion. The infarct size in the L-NAME-treated rabbits (75.1% +/- 5.0%, n = 7), assessed as a percentage of infarcted region/ischemic region, was significantly larger than that of control rabbits (51.2% +/- 7.4%, n = 7; P < .05). The increase in infarct size was significantly attenuated by the treatment with L-NAME and L-arginine (62.0% +/- 4.0%, n = 7). However, the infarct size for the treatment with L-NAME and D-arginine (76.7% +/- 5.7%, n = 6) did not differ from that in the L-NAME-treated rabbits. There was no significant difference in the infarct size between L-arginine-treated (60.1% +/- 7.3%, n = 6) and control rabbits. Rate-pressure products, as an index of myocardial oxygen consumption, were comparable in all the groups.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7542338

  2. Perioperative Myocardial Injury after Adult Heart Transplant: Determinants and Prognostic Value

    PubMed Central

    Romano, Gianpaolo; Maiello, Ciro; Buonocore, Marianna; Bancone, Ciro; Della Corte, Alessandro; Galdieri, Nicola; Nappi, Gianantonio; Amarelli, Cristiano

    2015-01-01

    Background and Aim of the Study Implications of Cardiac troponin (cTnI) release after cardiac transplantation are still unclear. This study disclosed risk factors and prognostic implication of cTnI early levels in a single centre cohort operated on between January 1999 and December 2010. Methods Data on 362 consecutive recipients (mean age: 47.8±13.7, 20.2% female, 18.2% diabetics, 22.1% with previous cardiac operations, 27.6% hospitalized, 84.9±29.4 ml/min preoperative glomerular filtration rate) were analyzed using multivariable logistic regression modeling. Target outcomes were determinants of troponin release, early graft failure (EGF), acute kidney injury (AKI) and operative death. Results Mean cTnI release measured 24 hours after transplant was 10.9±11.6 μg/L. Overall hospital mortality was 10.8%, EGF 10.5%, and AKI was 12.2%. cTnI release>10 μg/L proved an independent predictor of EGF (OR 2.2; 95% CI, 1.06–4.6) and AKI (OR 1.031; 95% CI, 1.001-1.064). EGF, in turn, proved a determinant of hospital mortality. Risk factors for cTnI>10 μg/L release were: status 2B (OR 0.35; 95% CI, 0.18-0.69, protective), duration of the ischemic period (OR 1.006; 95% CI, 1.001-1.011), previous cardiac operation (OR 2.9; 95% CI, 1.67-5.0), and left ventricular hypertrophy (OR 3.3; 95% CI, 1.9-5.6). Conclusions Myocardial enzyme leakage clearly emerged as an epiphenomenon of more complicated clinical course. The complex interplay between surgical procedure features, graft characteristics and recipient end-organ function highlights cTnI release as a risk marker of graft failure and acute kidney injury. The search for optimal myocardial preservation is still an issue. PMID:25942400

  3. ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury

    PubMed Central

    Minutoli, Letteria; Puzzolo, Domenico; Rinaldi, Mariagrazia; Irrera, Natasha; Marini, Herbert; Arcoraci, Vincenzo; Bitto, Alessandra; Crea, Giovanni; Pisani, Antonina; Squadrito, Francesco; Trichilo, Vincenzo; Bruschetta, Daniele; Micali, Antonio; Altavilla, Domenica

    2016-01-01

    Ischemia and reperfusion (I/R) causes a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to the ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, and inflammatory responses to cell death. In normal conditions, ROS mediate important beneficial responses. When their production is prolonged or elevated, harmful events are observed with peculiar cellular changes. In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. The mechanisms underlying the activation of NLRP3 are several and not completely elucidated. It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation. Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated. PMID:27127546

  4. A dynamic epicardial injury response supports progenitor cell activity during zebrafish heart regeneration.

    PubMed

    Lepilina, Alexandra; Coon, Ashley N; Kikuchi, Kazu; Holdway, Jennifer E; Roberts, Richard W; Burns, C Geoffrey; Poss, Kenneth D

    2006-11-01

    Zebrafish possess a unique yet poorly understood capacity for cardiac regeneration. Here, we show that regeneration proceeds through two coordinated stages following resection of the ventricular apex. First a blastema is formed, comprised of progenitor cells that express precardiac markers, undergo differentiation, and proliferate. Second, epicardial tissue surrounding both cardiac chambers induces developmental markers and rapidly expands, creating a new epithelial cover for the exposed myocardium. A subpopulation of these epicardial cells undergoes epithelial-to-mesenchymal transition (EMT), invades the wound, and provides new vasculature to regenerating muscle. During regeneration, the ligand fgf17b is induced in myocardium, while receptors fgfr2 and fgfr4 are induced in adjacent epicardial-derived cells. When fibroblast growth factors (Fgf) signaling is experimentally blocked by expression of a dominant-negative Fgf receptor, epicardial EMT and coronary neovascularization fail, prematurely arresting regeneration. Our findings reveal injury responses by myocardial and epicardial tissues that collaborate in an Fgf-dependent manner to achieve cardiac regeneration. PMID:17081981

  5. Loss of ATP-Sensitive Potassium Channel Surface Expression in Heart Failure Underlies Dysregulation of Action Potential Duration and Myocardial Vulnerability to Injury.

    PubMed

    Gao, Zhan; Sierra, Ana; Zhu, Zhiyong; Koganti, Siva Rama Krishna; Subbotina, Ekaterina; Maheshwari, Ankit; Anderson, Mark E; Zingman, Leonid V; Hodgson-Zingman, Denice M

    2016-01-01

    The search for new approaches to treatment and prevention of heart failure is a major challenge in medicine. The adenosine triphosphate-sensitive potassium (KATP) channel has been long associated with the ability to preserve myocardial function and viability under stress. High surface expression of membrane KATP channels ensures a rapid energy-sparing reduction in action potential duration (APD) in response to metabolic challenges, while cellular signaling that reduces surface KATP channel expression blunts APD shortening, thus sacrificing energetic efficiency in exchange for greater cellular calcium entry and increased contractile force. In healthy hearts, calcium/calmodulin-dependent protein kinase II (CaMKII) phosphorylates the Kir6.2 KATP channel subunit initiating a cascade responsible for KATP channel endocytosis. Here, activation of CaMKII in a transaortic banding (TAB) model of heart failure is coupled with a 35-40% reduction in surface expression of KATP channels compared to hearts from sham-operated mice. Linkage between KATP channel expression and CaMKII is verified in isolated cardiomyocytes in which activation of CaMKII results in downregulation of KATP channel current. Accordingly, shortening of monophasic APD is slowed in response to hypoxia or heart rate acceleration in failing compared to non-failing hearts, a phenomenon previously shown to result in significant increases in oxygen consumption. Even in the absence of coronary artery disease, failing myocardium can be further injured by ischemia due to a mismatch between metabolic supply and demand. Ischemia-reperfusion injury, following ischemic preconditioning, is diminished in hearts with CaMKII inhibition compared to wild-type hearts and this advantage is largely eliminated when myocardial KATP channel expression is absent, supporting that the myocardial protective benefit of CaMKII inhibition in heart failure may be substantially mediated by KATP channels. Recognition of Ca

  6. Loss of ATP-Sensitive Potassium Channel Surface Expression in Heart Failure Underlies Dysregulation of Action Potential Duration and Myocardial Vulnerability to Injury

    PubMed Central

    Gao, Zhan; Sierra, Ana; Zhu, Zhiyong; Koganti, Siva Rama Krishna; Subbotina, Ekaterina; Maheshwari, Ankit; Anderson, Mark E.; Zingman, Leonid V.; Hodgson-Zingman, Denice M.

    2016-01-01

    The search for new approaches to treatment and prevention of heart failure is a major challenge in medicine. The adenosine triphosphate-sensitive potassium (KATP) channel has been long associated with the ability to preserve myocardial function and viability under stress. High surface expression of membrane KATP channels ensures a rapid energy-sparing reduction in action potential duration (APD) in response to metabolic challenges, while cellular signaling that reduces surface KATP channel expression blunts APD shortening, thus sacrificing energetic efficiency in exchange for greater cellular calcium entry and increased contractile force. In healthy hearts, calcium/calmodulin-dependent protein kinase II (CaMKII) phosphorylates the Kir6.2 KATP channel subunit initiating a cascade responsible for KATP channel endocytosis. Here, activation of CaMKII in a transaortic banding (TAB) model of heart failure is coupled with a 35–40% reduction in surface expression of KATP channels compared to hearts from sham-operated mice. Linkage between KATP channel expression and CaMKII is verified in isolated cardiomyocytes in which activation of CaMKII results in downregulation of KATP channel current. Accordingly, shortening of monophasic APD is slowed in response to hypoxia or heart rate acceleration in failing compared to non-failing hearts, a phenomenon previously shown to result in significant increases in oxygen consumption. Even in the absence of coronary artery disease, failing myocardium can be further injured by ischemia due to a mismatch between metabolic supply and demand. Ischemia-reperfusion injury, following ischemic preconditioning, is diminished in hearts with CaMKII inhibition compared to wild-type hearts and this advantage is largely eliminated when myocardial KATP channel expression is absent, supporting that the myocardial protective benefit of CaMKII inhibition in heart failure may be substantially mediated by KATP channels. Recognition of Ca

  7. Is oxidative stress primarily involved in reperfusion injury of the ischemic heart

    SciTech Connect

    Nohl, H.; Stolze, K.; Napetschnig, S.; Ishikawa, T. )

    1991-01-01

    Reperfusion injury of ischemic organs is suggested to result from metabolic derangements initiating an imbalanced formation of free oxygen radicals. Most investigators in this field have used the spin-trap 5,5'-dimethyl-N-pyrroline-N-oxide (DMPO) to stabilize these short-lived radicals and make them visible by means of the electron spin resonance (ESR) technique. ESR signals obtained from intravascular DMPO were reported to indicate the formation of free OH. radicals and, in some cases, also carbon-centered radicals. We were unable to confirm these findings. Carbon-centered radicals were not obtained irrespectively of conditions studied, while oxygen-centered DMPO-adducts could only be detected in minor amounts. Instead, we observed an ascorbyl-related ESR signal. The addition of ethylenediaminetetraacetic acid (EDTA), which was used by many investigators in this field, was found to greatly influence ESR-spectra of the reperfusion fluid. The ascorbyl radical concentration was clearly reduced and the DMPO-OH. adduct became more prominent. The addition of iron further stimulated this change eliciting a Fenton-type reaction responsible for DMPO-OH.-related ESR spectra in the perfusate after ischemia. Accordingly, we observed the release of iron and ascorbic acid into the perfusate as a consequence of ischemia. We could demonstrate that iron in the presence of ascorbate and EDTA causes both types of radicals detected in the perfusate. DMPO-OH. generation in the presence of EDTA was found to result from free OH. radicals that were not generated in the absence of EDTA.

  8. Simvastatin alleviates myocardial contractile dysfunction and lethal ischemic injury in rat heart independent of cholesterol-lowering effects.

    PubMed

    ADAMEOVA, A; HARCAROVA, A; MATEJIKOVA, J; PANCZA, D; KUZELOVA, M; CARNICKA, S; SVEC, P; BARTEKOVA, M; STYK, J; Ravingerová, T

    2009-01-01

    Statins, the inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are most frequently used drugs in the prevention of coronary artery disease due to their cholesterol-lowering activity. However, it is not exactly known whether these effects of statins or those independent of cholesterol decrease account for the protection against myocardial ischemia-reperfusion (I/R) injury. In this study, we investigated the effect of 5-day treatment with simvastatin (10 mg/kg) in Langendorff-perfused hearts of healthy control (C) and diabetic-hypercholesterolemic (D-H; streptozotocin + high fat-cholesterol diet, 5 days) rats subjected to 30-min global ischemia followed by 40-min reperfusion for the examination of postischemic contractile dysfunction and reperfusion-induced ventricular arrhythmias or to 30-min (left anterior descending) coronary artery occlusion and 2-h reperfusion for the infarct size determination (IS; tetrazolium staining). Postischemic recovery of left ventricular developed pressure (LVDP) in animals with D-H was improved by simvastatin therapy (62.7+/-18.2 % of preischemic values vs. 30.3+/-5.7 % in the untreated D-H; P<0.05), similar to the values in the simvastatin-treated C group, which were 2.5-fold higher than those in the untreated C group. No ventricular fibrillation occurred in the simvastatin-treated C and D-H animals during reperfusion. Likewise, simvastatin shortened the duration of ventricular tachycardia (10.2+/-8.1 s and 57.8+/-29.3 s in C and D-H vs. 143.6+/-28.6 s and 159.3+/-44.3 s in untreated C and D-H, respectively, both P<0.05). The decreased arrhythmogenesis in the simvastatin-treated groups correlated with the limitation of IS (in % of risk area) by 66 % and 62 % in C and D-H groups, respectively. However, simvastatin treatment decreased plasma cholesterol levels neither in the D-H animals nor in C. The results indicate that other effects of statins (independent of cholesterol lowering) are involved in the

  9. Electrical injury

    MedlinePlus

    ... damage, especially to the heart, muscles, or brain. Electric current can cause injury in three ways: Cardiac arrest ... How long you were in contact with the electricity How the electricity moved through your body Your ...

  10. Sports Injuries

    MedlinePlus

    ... heart, to help decrease swelling. The Body’s Healing Process From the moment a bone breaks or a ... what happens at each stage of the healing process: At the moment of injury: Chemicals are released ...

  11. Ischemic postconditioning protects the heart against ischemia-reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria.

    PubMed

    Hu, L; Wang, J; Zhu, H; Wu, X; Zhou, L; Song, Y; Zhu, S; Hao, M; Liu, C; Fan, Y; Wang, Y; Li, Q

    2016-01-01

    As a result of its spatial confinement in cardiomyocytes, neuronal nitric oxide synthase (nNOS) is thought to regulate mitochondrial and sarcoplasmic reticulum (SR) function by maintaining nitroso-redox balance and Ca(2+) cycling. Thus, we hypothesize that ischemic postconditioning (IPostC) protects hearts against ischemic/reperfusion (I/R) injury through an nNOS-mediated pathway. Isolated mouse hearts were subjected to I/R injury in a Langendorff apparatus, H9C2 cells and primary neonatal rat cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) in vitro. IPostC, compared with I/R, decreased infarct size and improved cardiac function, and the selective nNOS inhibitors abolished these effects. IPostC recovered nNOS activity and arginase expression. IPostC also increased AMP kinase (AMPK) phosphorylation and alleviated oxidative stress, and nNOS and AMPK inhibition abolished these effects. IPostC increased nitrotyrosine production in the cytosol but decreased it in mitochondria. Enhanced phospholamban (PLB) phosphorylation, normalized SR function and decreased Ca(2+) overload were observed following the recovery of nNOS activity, and nNOS inhibition abolished these effects. Similar effects of IPostC were demonstrated in cardiomyocytes in vitro. IPostC decreased oxidative stress partially by regulating uncoupled nNOS and the nNOS/AMPK/peroxisome proliferator-activated receptor gamma coactivator 1 alpha/superoxide dismutase axis, and improved SR function through increasing SR Ca(2+) load. These results suggest that IPostC protected hearts against I/R injury via an nNOS-mediated pathway. PMID:27171264

  12. Ischemic postconditioning protects the heart against ischemia–reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria

    PubMed Central

    Hu, L; Wang, J; Zhu, H; Wu, X; Zhou, L; Song, Y; Zhu, S; Hao, M; Liu, C; Fan, Y; Wang, Y; Li, Q

    2016-01-01

    As a result of its spatial confinement in cardiomyocytes, neuronal nitric oxide synthase (nNOS) is thought to regulate mitochondrial and sarcoplasmic reticulum (SR) function by maintaining nitroso-redox balance and Ca2+ cycling. Thus, we hypothesize that ischemic postconditioning (IPostC) protects hearts against ischemic/reperfusion (I/R) injury through an nNOS-mediated pathway. Isolated mouse hearts were subjected to I/R injury in a Langendorff apparatus, H9C2 cells and primary neonatal rat cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) in vitro. IPostC, compared with I/R, decreased infarct size and improved cardiac function, and the selective nNOS inhibitors abolished these effects. IPostC recovered nNOS activity and arginase expression. IPostC also increased AMP kinase (AMPK) phosphorylation and alleviated oxidative stress, and nNOS and AMPK inhibition abolished these effects. IPostC increased nitrotyrosine production in the cytosol but decreased it in mitochondria. Enhanced phospholamban (PLB) phosphorylation, normalized SR function and decreased Ca2+ overload were observed following the recovery of nNOS activity, and nNOS inhibition abolished these effects. Similar effects of IPostC were demonstrated in cardiomyocytes in vitro. IPostC decreased oxidative stress partially by regulating uncoupled nNOS and the nNOS/AMPK/peroxisome proliferator-activated receptor gamma coactivator 1 alpha/superoxide dismutase axis, and improved SR function through increasing SR Ca2+ load. These results suggest that IPostC protected hearts against I/R injury via an nNOS-mediated pathway. PMID:27171264

  13. On the pivotal role of PPARα in adaptation of the heart to hypoxia and why fat in the diet increases hypoxic injury.

    PubMed

    Cole, Mark A; Abd Jamil, Amira H; Heather, Lisa C; Murray, Andrew J; Sutton, Elizabeth R; Slingo, Mary; Sebag-Montefiore, Liam; Tan, Suat Cheng; Aksentijević, Dunja; Gildea, Ottilie S; Stuckey, Daniel J; Yeoh, Kar Kheng; Carr, Carolyn A; Evans, Rhys D; Aasum, Ellen; Schofield, Christopher J; Ratcliffe, Peter J; Neubauer, Stefan; Robbins, Peter A; Clarke, Kieran

    2016-08-01

    The role of peroxisome proliferator-activated receptor α (PPARα)-mediated metabolic remodeling in cardiac adaptation to hypoxia has yet to be defined. Here, mice were housed in hypoxia for 3 wk before in vivo contractile function was measured using cine MRI. In isolated, perfused hearts, energetics were measured using (31)P magnetic resonance spectroscopy (MRS), and glycolysis and fatty acid oxidation were measured using [(3)H] labeling. Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions. A high-fat diet increased cardiac PPARα expression, fatty acid oxidation, and UCP3 levels with decreased glycolysis. Hypoxia was unable to alter the high PPARα expression or reverse the metabolic changes caused by the high-fat diet, with the result that [ATP] and contractile function decreased significantly. The adaptive metabolic changes caused by hypoxia in control mouse hearts were found to have occurred already in PPARα-deficient (PPARα(-/-)) mouse hearts and sustained function in hypoxia despite an inability for further metabolic remodeling. We conclude that decreased cardiac PPARα expression is essential for adaptive metabolic remodeling in hypoxia, but is prevented by dietary fat.-Cole, M. A., Abd Jamil, A. H., Heather, L. C., Murray, A. J., Sutton, E. R., Slingo, M., Sebag-Montefiore, L., Tan, S. C., Aksentijević, D., Gildea, O. S., Stuckey, D. J., Yeoh, K. K., Carr, C. A., Evans, R. D., Aasum, E., Schofield, C. J., Ratcliffe, P. J., Neubauer, S., Robbins, P. A., Clarke, K. On the pivotal role of PPARα in adaptation of the heart to hypoxia and why fat in the diet increases hypoxic injury. PMID:27103577

  14. Evaluation of General Toxicity, Anti-Oxidant Activity and Effects of Ficus Carica Leaves Extract on Ischemia/Reperfusion Injuries in Isolated Heart of Rat

    PubMed Central

    Allahyari, Saeideh; Delazar, Abbas; Najafi, Moslem

    2014-01-01

    Purpose: This study was aimed to evaluate general toxicity, anti-oxidant activity and effects of Ficus carica leaves extract on ischemia/reperfusion injuries. Methods: Antioxidant activity, total phenolic and flavonoid compounds of 70% methanolic extract of Ficus carica leaves were measured. The general toxicity test was carried out by brine shrimp lethality assay. Isolated hearts of male rats were mounted on a Langendorff apparatus and perfused with modified Krebs-Henseleit solution. In control group, the hearts were perfused with normal Krebs solution, however, treatment groups received enriched solution with the extract (0.04, 0.2 and 1 mg/ml) during stabilization and reperfusion (after 30 min global ischemia), respectively. Cardiac arrhythmias were analyzed and TTC method was used for infarct size determination. Results: The extract displayed antioxidant activity in the DPPH assay (RC50=0.06666 mg/ml). Total phenolic content was 12.29 mg GAE/100 g dry sample and the amount of flavonoids was calculated 40.729 mg/g. LD50 value by brine shrimp test was 0.158 mg/ml. The extract decreased number of VEBs, incidence and duration of Rev VF with clear reduction in infarct size and infarct volume (P<0.001). Conclusion: Ficus carica decreased ischemia/reperfusion-induced injuries. These protections are probably due to antioxidant capacity and the existence of flavonoid and phenolic compounds in the extract. PMID:25671192

  15. Discrepancy in calcium release from the sarcoplasmic reticulum and intracellular acidic stores for the protection of the heart against ischemia/reperfusion injury.

    PubMed

    Khalaf, Aseel; Babiker, Fawzi

    2016-09-01

    We and others have demonstrated a protective effect of pacing postconditioning (PPC) against ischemia/reperfusion (I/R) injury. However, the mechanisms underlying this protection are not completely clear. In the present study, we evaluated the effects of calcium release from the sarcoplasmic reticulum (SR) and the novel intracellular acidic stores (AS). Isolated rat hearts (n = 6 per group) were subjected to coronary occlusion followed by reperfusion using a modified Langendorff system. Cardiac hemodynamics and contractility were assessed using a data acquisition program, and cardiac injury was evaluated by creatine kinase (CK) and lactate dehydrogenase (LDH) levels. Hearts were subjected to 30 min of regional ischemia, produced by ligation of the left anterior descending (LAD) coronary artery, followed by 30 min of reperfusion. The hearts were also subjected to PPC (3 cycles of 30 s of left ventricle (LV) pacing alternated with 30 s of right atrium (RA) pacing) and/or were treated during reperfusion with agonists or antagonists of release of calcium from SR or AS. PPC significantly (P < 0.05) normalized LV, contractility, and coronary vascular dynamics and significantly (P < 0.001) decreased heart enzyme levels compared to the control treatments. The blockade of SR calcium release resulted in a significant (P < 0.01) recovery in LV function and contractility and a significant reduction in CK and LDH levels (P < 0.01) when applied alone or in combination with PPC. Interestingly, the release of calcium from AS alone or in combination with PPC significantly improved LV function and contractility (P < 0.05) and significantly decreased the CK and LDH levels (P < 0.01) compared to the control treatments. An additive effect was produced when agonism of calcium release from AS or blockade of calcium release from the SR was combined with PPC. Calcium release from AS and blockade of calcium release from the SR protect the heart against I

  16. FTY720 prevents ischemia/reperfusion injury-associated arrhythmias in an ex vivo rat heart model via activation of Pak1/Akt signaling.

    PubMed

    Egom, E Eroume A; Ke, Yunbo; Musa, Hanny; Mohamed, Tamer M A; Wang, Tao; Cartwright, Elizabeth; Solaro, R John; Lei, Ming

    2010-02-01

    Recent studies demonstrated a role of sphingosine-1-phosphate (S1P) in the protection against the stress of ischemia/reperfusion (I/R) injury. In experiments reported here, we have investigated the signaling through the S1P cascade by FTY720, a sphingolipid drug candidate displaying structural similarity to S1P, underlying the S1P cardioprotective effect. In ex vivo rat heart and isolated sinoatrial node models, FTY720 significantly prevented arrhythmic events associated with I/R injury including premature ventricular beats, VT, and sinus bradycardia as well as A-V conduction block. Real-time PCR and Western blot analysis demonstrated the expression of the S1P receptor transcript pools and corresponding proteins including S1P1, S1P2, and S1P3 in tissues dissected from sinoatrial node, atrium and ventricle. FTY720 (25 nM) significantly blunted the depression of the levels of phospho-Pak1 and phospho-Akt with ischemia and with reperfusion. There was a significant increase in phospho-Pak1 levels by 35%, 199%, and 205% after 5, 10, and 15 min of treatment with 25 nM FTY720 compared with control nontreated myocytes. However, there was no significant difference in the levels of total Pak1 expression between nontreated and FTY720 treated. Phospho-Akt levels were increased by 44%, 63%, and 61% after 5, 10, and 15 min of treatment with 25 nM FTY720, respectively. Our data provide the first evidence that FTY720 prevents I/R injury-associated arrhythmias and indicate its potential significance as an important and new agent protecting against I/R injury. Our data also indicate, for the first time, that the cardioprotective effect of FTY720 is likely to involve activation of signaling through the Pak1. PMID:19852968

  17. A novel highly selective adenosine A1 receptor agonist VCP28 reduces ischemia injury in a cardiac cell line and ischemia-reperfusion injury in isolated rat hearts at concentrations that do not affect heart rate.

    PubMed

    Urmaliya, Vijay B; Pouton, Colin W; Devine, Shane M; Haynes, John M; Warfe, Lyndon; Scammells, Peter J; White, Paul J

    2010-09-01

    The cardioprotective effects of a novel adenosine A1 receptor agonist N6-(2,2,5,5-tetramethylpyrrolidin-1-yloxyl-3-ylmethyl) adenosine (VCP28) were compared with the selective adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) in a H9c2(2-1) cardiac cell line-simulated ischemia (SI) model (12 hours) and a global ischemia (30 minutes) and reperfusion (60 minutes) model in isolated rat heart model. H9c2(2-1) cells were treated with CPA and VCP28 at the start of ischemia for entire ischemic duration, whereas isolated rat hearts were treated at the onset of reperfusion for 15 minutes. In the H9c2(2-1) cells SI model, CPA and VCP28 (100 nM) significantly (P < 0.05, n = 5-6) reduced the proportion of nonviable cells (30.88% +/- 2.49% and 16.17% +/- 3.77% of SI group, respectively) and lactate dehydrogenase efflux. In isolated rat hearts, CPA and VCP28 significantly (n = 6-8, P < 0.05) improved post-ischemic contractility (dP/dt(max), 81.69% +/- 10.96%, 91.07% +/- 19.87% of baseline, respectively), left ventricular developed pressure, and end diastolic pressure and reduced infarct size. The adenosine A1 receptor antagonist abolished the cardioprotective effects of CPA and VCP28 in SI model and isolated rat hearts. In conclusion, the adenosine A1 receptor agonist VCP28 has equal cardioprotective effects to the prototype A1 agonist CPA at concentrations that have no effect on heart rate. PMID:20571427

  18. Assessing Cardiac Injury in Mice With Dual Energy-MicroCT, 4D-MicroCT, and MicroSPECT Imaging After Partial Heart Irradiation

    SciTech Connect

    Lee, Chang-Lung; Min, Hooney; Befera, Nicholas; Clark, Darin; Qi, Yi; Das, Shiva; Johnson, G. Allan; Badea, Cristian T.; Kirsch, David G.

    2014-03-01

    Purpose: To develop a mouse model of cardiac injury after partial heart irradiation (PHI) and to test whether dual energy (DE)-microCT and 4-dimensional (4D)-microCT can be used to assess cardiac injury after PHI to complement myocardial perfusion imaging using micro-single photon emission computed tomography (SPECT). Methods and Materials: To study cardiac injury from tangent field irradiation in mice, we used a small-field biological irradiator to deliver a single dose of 12 Gy x-rays to approximately one-third of the left ventricle (LV) of Tie2Cre; p53{sup FL/+} and Tie2Cre; p53{sup FL/−} mice, where 1 or both alleles of p53 are deleted in endothelial cells. Four and 8 weeks after irradiation, mice were injected with gold and iodinated nanoparticle-based contrast agents, and imaged with DE-microCT and 4D-microCT to evaluate myocardial vascular permeability and cardiac function, respectively. Additionally, the same mice were imaged with microSPECT to assess myocardial perfusion. Results: After PHI with tangent fields, DE-microCT scans showed a time-dependent increase in accumulation of gold nanoparticles (AuNp) in the myocardium of Tie2Cre; p53{sup FL/−} mice. In Tie2Cre; p53{sup FL/−} mice, extravasation of AuNp was observed within the irradiated LV, whereas in the myocardium of Tie2Cre; p53{sup FL/+} mice, AuNp were restricted to blood vessels. In addition, data from DE-microCT and microSPECT showed a linear correlation (R{sup 2} = 0.97) between the fraction of the LV that accumulated AuNp and the fraction of LV with a perfusion defect. Furthermore, 4D-microCT scans demonstrated that PHI caused a markedly decreased ejection fraction, and higher end-diastolic and end-systolic volumes, to develop in Tie2Cre; p53{sup FL/−} mice, which were associated with compensatory cardiac hypertrophy of the heart that was not irradiated. Conclusions: Our results show that DE-microCT and 4D-microCT with nanoparticle-based contrast agents are novel imaging approaches

  19. Absence of malonyl coenzyme A decarboxylase in mice increases cardiac glucose oxidation and protects the heart from ischemic injury

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Acute pharmacological inhibition of cardiac malonyl coenzyme A decarboxylase (MCD) protects the heart from ischemic damage by inhibiting fatty acid oxidation and stimulating glucose oxidation. However, it is unknown whether chronic inhibition of MCD results in altered cardiac function, energy metabo...

  20. CDK9 and its repressor LARP7 modulate cardiomyocyte proliferation and response to injury in the zebrafish heart

    PubMed Central

    Matrone, Gianfranco; Wilson, Kathryn S.; Maqsood, Sana; Mullins, John J.; Tucker, Carl S.; Denvir, Martin A.

    2015-01-01

    ABSTRACT Cyclin dependent kinase (Cdk)9 acts through the positive transcription elongation factor-b (P-TEFb) complex to activate and expand transcription through RNA polymerase II. It has also been shown to regulate cardiomyocyte hypertrophy, with recent evidence linking it to cardiomyocyte proliferation. We hypothesised that modification of CDK9 activity could both impair and enhance the cardiac response to injury by modifying cardiomyocyte proliferation. Cdk9 expression and activity were inhibited in the zebrafish (Danio rerio) embryo. We show that dephosphorylation of residue Ser2 on the C-terminal domain of RNA polymerase II is associated with impaired cardiac structure and function, and cardiomyocyte proliferation and also results in impaired functional recovery following cardiac laser injury. In contrast, de-repression of Cdk9 activity, through knockdown of La-related protein (Larp7) increases phosphorylation of Ser2 in RNA polymerase II and increases cardiomyocyte proliferation. Larp7 knockdown rescued the structural and functional phenotype associated with knockdown of Cdk9. The balance of Cdk9 and Larp7 plays a key role in cardiomyocyte proliferation and response to injury. Larp7 represents a potentially novel therapeutic target to promote cardiomyocyte proliferation and recovery from injury. PMID:26542022

  1. 5-HT2 receptor blocker sarpogrelate prevents downregulation of antiapoptotic protein Bcl-2 and protects the heart against ischemia-reperfusion injury.

    PubMed

    Rajesh, Katare Gopalrao; Suzuki, Ryoko; Maeda, Hironori; Murio, Yamamoto; Sasaguri, Shiro

    2006-09-27

    Even though reperfusion is the treatment of choice in patients admitted with acute myocardial infarction, reperfusion itself has been demonstrated to activate various pathological factors especially following procedures of cardiac revascularization. 5-hydroxytryptamine (5HT) is one such factor activated during reperfusion and is known to trigger the post ischemic contractile dysfunction and pathological apoptosis. Here we demonstrate the potential effects of the 5-HT(2)A antagonist sarpogrelate in protecting the myocardium against reperfusion injury of heart. Male Wistar rats weighing between 220 and 240 g were subjected to 30 min left coronary artery (LCA) occlusion and 120 min reperfusion. Sarpogrelate (4 mg/kg) was infused intravenously for 30 min either before LCA occlusion or at reperfusion. Following reperfusion the samples were collected for infarction area, immunohistochemistry, western blotting and myocardial metabolite analysis. Sarpogrelate infusion before ischemia resulted in (a) significant recovery of post ischemic cardiac functions (LVDP, EDP), (b) significant reduction in the infarct size among the risk area after triphenyl tetrazolium chloride staining (p<0.001), (c) decreased tissue water content (p<0.05), (d) well preserved myocardial ATP (p<0.05), (e) reduction in Bcl-2 downregulation and caspase 3 activation and (g) less prevalence of apoptotic cells (3.1+/-0.4% to 15.2+/-0.6%, drug versus control). Treating the rats with sarpogrelate during reperfusion also showed similar results. This study thus demonstrates the protective effects of sarpogrelate and supports the role for 5-HT2A inhibition in preventing the reperfusion injury of the heart. PMID:16876202

  2. Umbilical Neutrophil Gelatinase-Associated Lipocalin Level as an Early Predictor of Acute Kidney Injury in Neonates with Hypoplastic Left Heart Syndrome

    PubMed Central

    Walencka, Zofia; Więcek, Andrzej

    2015-01-01

    Acute kidney injury (AKI) is a primarily described complication after unbalanced systemic perfusion in neonates with congenital heart defects, including hypoplastic left heart syndrome (HLHS). The aim of the study was to compare the umbilical NGAL concentrations between neonates born with HLHS and healthy infants, as well as to analyze whether the determination of NGAL level could predict AKI in neonates with prenatally diagnosed HLHS. Twenty-one neonates with prenatally diagnosed HLHS were enrolled as study group and 30 healthy neonates served as controls. Perinatal characteristics and postnatal parameters were extracted from the hospital neonatal database. In umbilical cord blood, we determined plasma NGAL concentrations, acid base balance, and lactate and creatinine levels. In neonates with HLHS, complications (respiratory insufficiency, circulatory failure, NEC, IVH, and AKI) were recorded until the day of cardiosurgery. We observed in neonates with HLHS higher umbilical NGAL levels compared to controls. Among 8 neonates with HLHS and diagnosed AKI stage 1, we observed elevated NGAL levels in comparison to those newborns without AKI. Umbilical NGAL could predict, with high sensitivity and specificity, AKI development in study neonates. We suggest that the umbilical blood NGAL concentration may be an early marker to predict AKI in neonates with HLHS. PMID:25699275

  3. Umbilical neutrophil gelatinase-associated lipocalin level as an early predictor of acute kidney injury in neonates with hypoplastic left heart syndrome.

    PubMed

    Surmiak, Piotr; Baumert, Małgorzata; Fiala, Małgorzata; Walencka, Zofia; Więcek, Andrzej

    2015-01-01

    Acute kidney injury (AKI) is a primarily described complication after unbalanced systemic perfusion in neonates with congenital heart defects, including hypoplastic left heart syndrome (HLHS). The aim of the study was to compare the umbilical NGAL concentrations between neonates born with HLHS and healthy infants, as well as to analyze whether the determination of NGAL level could predict AKI in neonates with prenatally diagnosed HLHS. Twenty-one neonates with prenatally diagnosed HLHS were enrolled as study group and 30 healthy neonates served as controls. Perinatal characteristics and postnatal parameters were extracted from the hospital neonatal database. In umbilical cord blood, we determined plasma NGAL concentrations, acid base balance, and lactate and creatinine levels. In neonates with HLHS, complications (respiratory insufficiency, circulatory failure, NEC, IVH, and AKI) were recorded until the day of cardiosurgery. We observed in neonates with HLHS higher umbilical NGAL levels compared to controls. Among 8 neonates with HLHS and diagnosed AKI stage 1, we observed elevated NGAL levels in comparison to those newborns without AKI. Umbilical NGAL could predict, with high sensitivity and specificity, AKI development in study neonates. We suggest that the umbilical blood NGAL concentration may be an early marker to predict AKI in neonates with HLHS. PMID:25699275

  4. Prehospital heart rate and blood pressure increase the positive predictive value of the Glasgow Coma Scale for high-mortality traumatic brain injury.

    PubMed

    Reisner, Andrew; Chen, Xiaoxiao; Kumar, Kamal; Reifman, Jaques

    2014-05-15

    We hypothesized that vital signs could be used to improve the association between a trauma patient's prehospital Glasgow Coma Scale (GCS) score and his or her clinical condition. Previously, abnormally low and high blood pressures have both been associated with higher mortality for patients with traumatic brain injury (TBI). We undertook a retrospective analysis of 1384 adult prehospital trauma patients. Vital-sign data were electronically archived and analyzed. We examined the relative risk of severe head Abbreviated Injury Scale (AIS) 5-6 as a function of the GCS, systolic blood pressure (SBP), heart rate (HR), and respiratory rate (RR). We created multi-variate logistic regression models and, using DeLong's test, compared their area under receiver operating characteristic curves (ROC AUCs) for three outcomes: head AIS 5-6, all-cause mortality, and either head AIS 5-6 or neurosurgical procedure. We found significant bimodal relationships between head AIS 5-6 versus SBP and HR, but not RR. When the GCS was <15, ROC AUCs were significantly higher for a multi-variate regression model (GCS, SBP, and HR) versus GCS alone. In particular, patients with abnormalities in all parameters (GCS, SBP, and HR) were significantly more likely to have high-mortality TBI versus those with abnormalities in GCS alone. This could be useful for mobilizing resources (e.g., neurosurgeons and operating rooms at the receiving hospital) and might enable new prehospital management protocols where therapies are selected based on TBI mortality risk. PMID:24372334

  5. Reduced heart rate variability in chronic severe traumatic brain injury: Association with impaired emotional and social functioning, and potential for treatment using biofeedback.

    PubMed

    Francis, Heather M; Fisher, Alana; Rushby, Jacqueline A; McDonald, Skye

    2016-01-01

    Heart rate variability (HRV) may provide an index of capacity for social functioning and may be remediated by HRV biofeedback. Given reductions in HRV are found following traumatic brain injury (TBI), the present study aimed to determine whether lower HRV in TBI is associated with social function, and whether HRV biofeedback might be a useful remediation technique in this population. Resting state HRV and measures of social and emotional processing were collected in 30 individuals with severe TBI (3-34 years post-injury) and 30 controls. This was followed by a single session of HRV biofeedback. HRV was positively associated with social cognition and empathy, and negatively associated with alexithymia for the TBI group. Both TBI and control groups showed significantly increased HRV on both time-domain (i.e., SDNN, rMSSD) and frequency-domain measures (LF, HF, LF:HF ratio) during biofeedback compared to baseline. These results suggest that decreased HRV is linked to social and emotional function following severe TBI, and may be a novel target for therapy using HRV biofeedback techniques. PMID:25627984

  6. Curcumin protects hearts from FFA-induced injury by activating Nrf2 and inactivating NF-κB both in vitro and in vivo.

    PubMed

    Zeng, Chunlai; Zhong, Peng; Zhao, Yunjie; Kanchana, Karvannan; Zhang, Yali; Khan, Zia A; Chakrabarti, Subrata; Wu, Lianpin; Wang, Jingying; Liang, Guang

    2015-02-01

    Obesity and increased free fatty acid (FFA) level are tightly linked, leading to the development of cardiovascular disorders. Curcumin is a natural product from Curcuma longa with multiple bioactivities and is known to have cardioprotective effects in several cellular and animal models. The current study was designed to evaluate the cardioprotective effects of curcumin and demonstrate the underlying mechanism in FFA-induced cardiac injury. Using cell culture studies and high fat in vivo model, we explored the mechanistic basis of anti-inflammatory and antioxidant activities of curcumin. We observed that palmitate (PA) treatment in cardiac derived H9C2 cells induced a marked increase in reactive oxygen species, inflammation, apoptosis and hypertrophy. All of these changes were effectively suppressed by curcumin treatment. In addition, oral administration of curcumin at 50mg/kg completely suppressed high fat diet-induced oxidative stress, inflammation, apoptosis, fibrosis, hypertrophy and tissue remodeling in mice. The beneficial actions of curcumin are closely associated with its ability to increase Nrf2 expression and inhibit NF-κB activation. Thus, both in vitro and in vivo studies showed a promising role of curcumin as a cardioprotective agent against palmitate and high fat diet mediated cardiac dysfunction. We indicated the regulatory roles of Nrf2 and NF-κB in obesity-induced heart injury, and suggested that they may be important therapeutic targets in the treatment of obesity-related disorders. PMID:25444713

  7. Mild Type 2 Diabetes Mellitus Reduces the Susceptibility of the Heart to Ischemia/Reperfusion Injury: Identification of Underlying Gene Expression Changes

    PubMed Central

    Korkmaz-Icöz, Sevil; Lehner, Alice; Li, Shiliang; Vater, Adrian; Radovits, Tamás; Hegedűs, Péter; Ruppert, Mihály; Brlecic, Paige; Zorn, Markus; Karck, Matthias; Szabó, Gábor

    2015-01-01

    Despite clinical studies indicating that diabetic hearts are more sensitive to ischemia/reperfusion injury, experimental data is contradictory. Although mild diabetes prior to ischemia/reperfusion may induce a myocardial adaptation, further research is still needed. Nondiabetic Wistar (W) and type 2 diabetic Goto-Kakizaki (GK) rats (16-week-old) underwent 45 min occlusion of the left anterior descending coronary artery and 24 h reperfusion. The plasma glucose level was significantly higher in diabetic rats compared to the nondiabetics. Diabetes mellitus was associated with ventricular hypertrophy and increased interstitial fibrosis. Inducing myocardial infarction increased the glucose levels in diabetic compared to nondiabetic rats. Furthermore, the infarct size was smaller in GK rats than in the control group. Systolic and diastolic functions were impaired in W + MI and did not reach statistical significance in GK + MI animals compared to the corresponding controls. Among the 125 genes surveyed, 35 genes showed a significant change in expression in GK + MI compared to W + MI rats. Short-term diabetes promotes compensatory mechanisms that may provide cardioprotection against ischemia/reperfusion injury, at least in part, by increased antioxidants and the upregulation of the prosurvival PI3K/Akt pathway, by the downregulation of apoptotic genes, proinflammatory cytokine TNF-α, profibrogenic TGF-β, and hypertrophic marker α-actin-1. PMID:26229969

  8. Increased endogenous ascorbyl free radical formation with singlet oxygen scavengers in reperfusion injury: an EPR and functional recovery study in rat hearts.

    PubMed

    Lee, J W; Bobst, E V; Wang, Y G; Ashraf, M M; Bobst, A M

    2000-12-01

    The objective of this study was to investigate the effect of singlet oxygen ((1)O2) scavengers on functional recovery and ascorbyl free radical (AFR) formation in isolated ischemic rat hearts. Hearts were subjected to 40 min. of global ischemia followed by 30 min. of reperfusion. Hemodynamics were measured as heart rate (HR), coronary flow (CF), left ventricular developed pressure (LVDP) and contractility (dP/dt). Electron paramagnetic resonance (EPR) spectroscopy was used to measure AFR release in coronary perfusate during the first two min. of reperfusion as a function of ROS scavengers. Relative to ischemic controls the administration of the (1)O2 scavengers 2,2,6,6-tetramethyl-4-piperidone x HCl (4-oxo-TEMP), carnosine (beta-alanyl-L-histidine) or a combination of the two significantly improved functional recovery as measured by LVDP. While no AFR signal was detected in coronary perfusate collected during preischemic perfusion with and without (1)O2 scavengers, the AFR background signal due to ischemia was significantly increased with the (1)O2 and *O2- scavengers. No such increase was observed with the hydroxyl radical (*OH) scavenger mannitol. Besides the AFR increase with the (1)O2 and *O2- scavengers the functional recovery was only significantly improved with the (1)O2 scavengers. In contrast to previous AFR studies we found with endogenous AFR that an increased AFR formation is not necessarily only reflecting increased oxidative stress but can also report improved functional recovery. Combining the hemodynamic data with increased AFR formation in the presence of several different ROS scavengers gives supportive evidence for (1)O2 also being involved in reperfusion injury. PMID:11156483

  9. Protective effect of the extract of Yi-Qi-Fu-Mai preparation on hypoxia-induced heart injury in mice.

    PubMed

    Feng, Ya-Qian; Ju, Ai-Chun; Liu, Chun-Hua; Wang, Ting; Yu, Bo-Yang; Qi, Jin

    2016-06-01

    Yi-Qi-Fu-Mai (YQFM) is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation (EYQFM), the EYQFM (1.4, 2.8, and 5.5 g·kg(-1)·d(-1)) was assessed for its heart-protective effect in a chronic intermittent hypoxia (CIH) animal model (oxygen pressure 7%-8%, 20 min per day) for 28 days of treatment. Betaloc (0.151 6 g·kg(-1)·d(-1)) was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions (EF), stroke volume (SV), expression of creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model. PMID:27473956

  10. Berberine protects rat heart from ischemia/reperfusion injury via activating JAK2/STAT3 signaling and attenuating endoplasmic reticulum stress

    PubMed Central

    Zhao, Guo-long; Yu, Li-ming; Gao, Wen-li; Duan, Wei-xun; Jiang, Bo; Liu, Xu-dong; Zhang, Bin; Liu, Zhen-hua; Zhai, Meng-en; Jin, Zhen-xiao; Yu, Shi-qiang; Wang, Yun

    2016-01-01

    Aim: Berberine (BBR), an isoquinoline-derived alkaloid isolated from Rhizoma coptidis, exerts cardioprotective effects. Because endoplasmic reticulum (ER) stress plays a pivotal role in myocardial ischemia/reperfusion (MI/R)-induced apoptosis, it was interesting to examine whether the protective effects of BBR resulted from modulating ER stress levels during MI/R injury, and to define the signaling mechanisms in this process. Methods: Male rats were treated with BBR (200 mg·kg−1·d−1, ig) for 2 weeks, and then subjected to MI/R surgery. Cardiac dimensions and function were assessed using echocardiography. Myocardial infarct size and apoptosis was examined. Total serum LDH levels and CK activities, superoxide production, MDA levels and the antioxidant SOD activities in heart tissue were determined. An in vitro study was performed on cultured rat embryonic myocardium-derived cells H9C2 exposed to simulated ischemia/reperfusion (SIR). The expression of apoptotic, ER stress-related and signaling proteins were assessed using Western blot analyses. Results: Pretreatment with BBR significantly reduced MI/R-induced myocardial infarct size, improved cardiac function, and suppressed myocardial apoptosis and oxidative damage. Furthermore, pretreatment with BBR suppressed MI/R-induced ER stress, evidenced by down-regulating the phosphorylation levels of myocardial PERK and eIF2α and the expression of ATF4 and CHOP in heart tissues. Pretreatment with BBR also activated the JAK2/STAT3 signaling pathway in heart tissues, and co-treatment with AG490, a specific JAK2/STAT3 inhibitor, blocked not only the protective effects of BBR, but also the inhibition of BBR on MI/R-induced ER stress. In H9C2 cells, treatment with BBR (50 μmol/L) markedly reduced SIR-induced cell apoptosis, oxidative stress and ER stress, which were abolished by transfection with JAK2 siRNA. Conclusion: BBR ameliorates MI/R injury in rats by activating the AK2/STAT3 signaling pathway and attenuating ER

  11. The Effect of Lipopolysaccharide on Ischemic-Reperfusion Injury of Heart: A Double Hit Model of Myocardial Ischemia and Endotoxemia

    PubMed Central

    Nader, Nader D.; Asgeri, Mehrdad; Davari-Farid, Sina; Pourafkari, Leili; Ahmadpour, Faraz; Porhomayon, Jahan; Javadzadeghan, Hassan; Negargar, Sohrab; Knight, Paul R.

    2015-01-01

    Introduction: Myocardial ischemia may coincide and interact with sepsis and inflammation. Our objective was to examine the effects of bacterial endotoxin on myocardial functions and cell injury during acute ischemia. Methods: Rabbits were pretreated with incremental doses of E. Coli lipopolysaccharide (LPS) or normal saline. Myocardial ischemia was induced by 50-minute occlusion of left anterior descending artery. S-TNFaR was additionally used to block the effects LPS. Results: Ventricular contractility as it was measured by dp/dt during systole decreased from 2445± 1298 to 1422 ± 944 mm Hg/s, P = .019. Isovolumetric relaxation time as an index of diastolic function was prolonged from 50±18 ms to 102± 64 ms following ischemia. Pretreatment with low concentrations of LPS (<1 μg) had no effect on dp/dt, while at higher concentrations it suppressed both contractility and prolonged IVRT. Cell injury as measured by cardiac troponin I level increased to 15.1± 3.2 ng/dL following ischemia and continued to rise with higher doses of LPS. While blocking TNFa did not improve the myocardial contractility after ischemia, it eliminated additional deleterious effects of LPS. Conclusion: Lower doses of LPS had no deleterious effect on myocardial function, whereas higher doses of this endotoxin cause cardiac dysfunction and increased extent of injury. PMID:26430494

  12. Pericarditis - after heart attack

    MedlinePlus

    Dressler syndrome; Post-MI pericarditis; Post-cardiac injury syndrome; Postcardiotomy pericarditis ... Two types of pericarditis can occur after a heart attack . Early pericarditis: This form most occurs within ...

  13. The Long-Term Consumption of Ginseng Extract Reduces the Susceptibility of Intermediate-Aged Hearts to Acute Ischemia Reperfusion Injury

    PubMed Central

    Luo, Pei; Dong, Gengting; Liu, Liang; Zhou, Hua

    2015-01-01

    susceptibility of intermediate-aged hearts to acute ischemia reperfusion injury in rats. These effects might be mediated through the activation of Akt/eNOS, suppression of Erk/caspase 7 and upregulation of Sirt1 and Sirt3 in intermediate-aged rats. PMID:26650753

  14. Heart Health

    MedlinePlus

    ... Connected Home » Heart Health Heath and Aging Heart Health Your Heart Changes to Your Heart With ... are both taking steps toward heart health. Your Heart Your heart is a strong muscle about the ...

  15. Neurogenic stunned myocardium - do we consider this diagnosis in patients with acute central nervous system injury and acute heart failure?

    PubMed

    Mierzewska-Schmidt, Magdalena; Gawecka, Agnieszka

    2015-01-01

    Neurogenic stunned myocardium (NSM) is defined as myocardial injury and dysfunction of a sudden onset, occurring after various types of acute brain injury as a result of an imbalance in the autonomic nervous system. The typical spectrum of clinically observed abnormalities includes acute left ventricular failure, not uncommonly progressing to cardiogenic shock with hypotension that requires inotropic agents, pulmonary oedema and various arrhythmias. Commonly-seen electrocardiographic changes include: prolonged QT interval, ST segment changes, T-wave inversion, a new Q-wave or U-wave. Echocardiography shows both an impaired both systolic and diastolic function of the left ventricle. Biochemical markers of NSM comprise metabolic acidosis and increased cardiac enzymes and markers: creatine kinase (CK), and CK-MB, troponin I and B-type natriuretic peptide. The main cause of NSM is myocardial injury induced by local catecholamine release from nerve endings within the myocardium. Recently, a theory has been proposed to classify NSM as one of the stress-related cardiomyopathies, together with Takotsubo cardiomyopathy, acute left ventricular failure in the critically ill, cardiomyopathy associated with pheochromacytoma and exogenous catecholamine administration. The occurrence of NSM increases the risk of life-threatening complications, death, and worsens neurologic outcome. As far as we know, treatment should generally focus on the underlying neurologic process in order to maximize neurologic recovery. Improvement in neurologic pathology leads to rapid improvement in cardiac function and its full recovery, as NSM is a fully reversible condition if the patient survives. Awareness of the existence of NSM and a deeper knowledge of its etiopathology may reduce diagnostic errors, optimise its treatment. PMID:25940334

  16. Anthocyanins protected hearts against ischemic injury by reducing MMP-2 activity via Akt/P38 pathways

    PubMed Central

    Hao, Jie; Du, Hong; Li, Weiwei; Liu, Fan; Lu, Jingchao; Yang, Xiuchun; Cui, Wei

    2016-01-01

    Growing evidences suggest that there are close associations between anthocyanins and cardiac protection. However, little is known about the detailed roles of anthocyanins in regulating extracellular matrix (ECM) remodeling. Incubation of primary cultured fibroblasts with anthocyanins reduced both intracellular collagen expression and extracellular collagen secretion. Down-regulation of collagen production was also shown in infarcted cardiac tissues after permanent coronary artery ligation in mice treated with anthocyanins. The phosphorylation levels of Akt and/or P-38 were significantly increased by anthocyanins supplementation in primary cultured fibroblasts. Gelatin zymography analysis of matrix metalloproteinase-2 (MMP-2) activity in conditioned medium collected from fibroblasts demonstrated that anthocyanins treatment significantly reduced MMP-2 activity. These results demonstrated that anthocyanins play a role in mediating myocardial ECM remodeling and that the Akt/P-38 pathways mediate these protective effects on hearts. PMID:27158396

  17. Heart Health - Brave Heart

    MedlinePlus

    ... Bar Home Current Issue Past Issues Cover Story Heart Health Brave Heart Past Issues / Winter 2009 Table of Contents For ... you can have a good life after a heart attack." Lifestyle Changes Surviving—and thriving—after such ...

  18. Baseline Prevalence of Heart Diseases, Hypertension, Diabetes, and Obesity in Persons with Acute Traumatic Spinal Cord Injury: Potential Threats in the Recovery Trajectory

    PubMed Central

    2013-01-01

    Background: Chronic diseases impede the recovery trajectory of acutely injured persons with traumatic spinal cord injury (TSCI). This study compares the odds of prevalent heart disease, hypertension, diabetes mellitus, and obesity between persons with TSCI and persons with lower extremity fractures (LEF) who were discharged from acute care facilities. Methods: 1,776 patients with acute TSCI (cases) and 1,780 randomly selected patients with LEF (controls) discharged from January 1, 1998, through December 31, 2009, from all nonfederal hospitals were identified. Data extracted from uniform billing files were compared between cases and controls in a multivariable logistic regression model controlling for sociodemographic and clinical covariables. Results: Thirty percent of patients with acute TSCI had at least 1 of 4 conditions compared with 18% of patients with LEF (P < .0001). Persons with acute TSCI were 4 times more likely (odds ratio [OR], 4.05; 95% CI, 1.65–9.97) to have obesity, 2.7 times more likely to have heart disease (P < .001), 2 times more likely to have hypertension (P < .001), and 1.7 times more likely to have diabetes (P = .044) at the onset of TSCI. Disproportionately more Blacks than Whites have TSCI and chronic diseases. Conclusion: This study suggests that there is an increased burden of cardiovascular and cardiometabolic diseases among persons with acute TSCI compared with LEF trauma controls. Unattended comorbid conditions will affect quality of life and the recovery process. This warrants continuous monitoring and management of chronic diseases during the rehabilitation process. PMID:23960701

  19. Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase–derived PGD2 biosynthesis

    PubMed Central

    Tokudome, Satori; Sano, Motoaki; Shinmura, Ken; Matsuhashi, Tomohiro; Morizane, Shintaro; Moriyama, Hidenori; Tamaki, Kayoko; Hayashida, Kentaro; Nakanishi, Hiroki; Yoshikawa, Noritada; Shimizu, Noriaki; Endo, Jin; Katayama, Takaharu; Murata, Mitsushige; Yuasa, Shinsuke; Kaneda, Ruri; Tomita, Kengo; Eguchi, Naomi; Urade, Yoshihiro; Asano, Koichiro; Utsunomiya, Yasunori; Suzuki, Takeshi; Taguchi, Ryo; Tanaka, Hirotoshi; Fukuda, Keiichi

    2009-01-01

    Lipocalin-type prostaglandin D synthase (L-PGDS), which was originally identified as an enzyme responsible for PGD2 biosynthesis in the brain, is highly expressed in the myocardium, including in cardiomyocytes. However, the factors that control expression of the gene encoding L-PGDS and the pathophysiologic role of L-PGDS in cardiomyocytes are poorly understood. In the present study, we demonstrate that glucocorticoids, which act as repressors of prostaglandin biosynthesis in most cell types, upregulated the expression of L-PGDS together with cytosolic calcium-dependent phospholipase A2 and COX2 via the glucocorticoid receptor (GR) in rat cardiomyocytes. Accordingly, PGD2 was the most prominently induced prostaglandin in vivo in mouse hearts and in vitro in cultured rat cardiomyocytes after exposure to GR-selective agonists. In isolated Langendorff-perfused mouse hearts, dexamethasone alleviated ischemia/reperfusion injury. This cardioprotective effect was completely abrogated by either pharmacologic inhibition of COX2 or disruption of the gene encoding L-PGDS. In in vivo ischemia/reperfusion experiments, dexamethasone reduced infarct size in wild-type mice. This cardioprotective effect of dexamethasone was markedly reduced in L-PGDS–deficient mice. In cultured rat cardiomyocytes, PGD2 protected against cell death induced by anoxia/reoxygenation via the D-type prostanoid receptor and the ERK1/2-mediated pathway. Taken together, these results suggest what we believe to be a novel interaction between glucocorticoid-GR signaling and the cardiomyocyte survival pathway mediated by the arachidonic acid cascade. PMID:19451694

  20. Angiotensin II type 2 receptor ligand PD123319 attenuates hyperoxia-induced lung and heart injury at a low dose in newborn rats

    PubMed Central

    Sengers, Rozemarijn M. A.; Laghmani, El Houari; Chen, Xueyu; Lindeboom, Melissa P. H. A.; Roks, Anton J. M.; Folkerts, Gert; Walther, Frans J.

    2014-01-01

    Intervening in angiotensin (Ang)-II type 2 receptor (AT2) signaling may have therapeutic potential for bronchopulmonary dysplasia (BPD) by attenuating lung inflammation and preventing arterial hypertension (PAH)-induced right ventricular hypertrophy (RVH). We first investigated the role of AT2 inhibition with PD123319 (0.5 and 2 mg·kg−1·day−1) on the beneficial effect of AT2 agonist LP2–3 (5 μg/kg twice a day) on RVH in newborn rats with hyperoxia-induced BPD. Next we determined the cardiopulmonary effects of PD123319 (0.1 mg·kg−1·day−1) in two models: early treatment during continuous exposure to hyperoxia for 10 days and late treatment starting on day 6 in rat pups exposed postnatally to hyperoxia for 9 days, followed by a 9-day recovery period in room air. Parameters investigated included lung and heart histopathology, fibrin deposition, vascular leakage, and differential mRNA expression. Ten days of coadministration of LP2–3 and PD123319 abolished the beneficial effects of LP2–3 on RVH in experimental BPD. In the early treatment model PD123319 attenuated cardiopulmonary injury by reducing alveolar septal thickness, pulmonary influx of inflammatory cells, including macrophages and neutrophils, medial wall thickness of small arterioles, and extravascular collagen III deposition, and by preventing RVH. In the late treatment model PD123319 diminished PAH and RVH, demonstrating that PAH is reversible in the neonatal period. At high concentrations PD123319 blocks the beneficial effects of the AT2-agonist LP2–3 on RVH. At low concentrations PD123319 attenuates cardiopulmonary injury by reducing pulmonary inflammation and fibrosis and preventing PAH-induced RVH but does not affect alveolar and vascular development in newborn rats with experimental BPD. PMID:24951776

  1. The transplantation of Akt-overexpressing amniotic fluid-derived mesenchymal stem cells protects the heart against ischemia-reperfusion injury in rabbits.

    PubMed

    Wang, Yan; Li, Yigang; Song, Lei; Li, Yanyan; Jiang, Shan; Zhang, Song

    2016-07-01

    Amniotic fluid-derived mesenchymal stem cells (AFMSCs) are an attractive cell source for applications in regenerative medicine, due to characteristics such as proliferative capacity and multipotency. In addition, Akt, a serine‑threonine kinase, maintains stem cells by promoting viability and proliferation. Whether the transplantation of Akt-overexpressing AFMSCs protects the heart against ischemia‑reperfusion (I/R) injury has yet to be elucidated. Accordingly, the Akt gene was overexpressed in AFMSCs using lentiviral transduction, and Akt‑AFMSCs were transplanted into the ischemic myocardium of rabbits prior to reperfusion. Any protective effects resulting from this procedure were subsequently sought after three weeks later. A histological examination revealed that there was a decrease in intramyocardial inflammation and ultrastructural damage, and an increase in capillary density and in the levels of GATA binding protein 4, connexin 43 and cardiac troponin T in the Akt‑AFMSC group compared with the control group. A significant decrease in cardiomyocyte apoptosis, accompanying an increase in phosphorylated Akt and B‑cell lymphoma 2 (Bcl-2) and a decrease in caspase‑3, was also observed. Furthermore, the left ventricular function was markedly augmented in the Akt‑AFMSC group compared with the control group. These observations suggested that the protective effect of AFMSCs may be due to the delivery of secreted cytokines, promotion of neoangiogenesis, prevention of cardiomyocyte apoptosis, transdifferentiation into cardiomyocytes and promotion of the viability of AFMSCs, which are assisted by Akt gene modification. Taken together, the results of the present study have indicated that transplantation of Akt-AFMSCs is able to alleviate myocardial I/R injury and improve cardiac function. PMID:27151366

  2. The transplantation of Akt-overexpressing amniotic fluid-derived mesenchymal stem cells protects the heart against ischemia-reperfusion injury in rabbits

    PubMed Central

    WANG, YAN; LI, YIGANG; SONG, LEI; LI, YANYAN; JIANG, SHAN; ZHANG, SONG

    2016-01-01

    Amniotic fluid-derived mesenchymal stem cells (AFMSCs) are an attractive cell source for applications in regenerative medicine, due to characteristics such as proliferative capacity and multipotency. In addition, Akt, a serine-threonine kinase, maintains stem cells by promoting viability and proliferation. Whether the transplantation of Akt-overexpressing AFMSCs protects the heart against ischemia-reperfusion (I/R) injury has yet to be elucidated. Accordingly, the Akt gene was overexpressed in AFMSCs using lentiviral transduction, and Akt-AFMSCs were transplanted into the ischemic myocardium of rabbits prior to reperfusion. Any protective effects resulting from this procedure were subsequently sought after three weeks later. A histological examination revealed that there was a decrease in intramyocardial inflammation and ultrastructural damage, and an increase in capillary density and in the levels of GATA binding protein 4, connexin 43 and cardiac troponin T in the Akt-AFMSC group compared with the control group. A significant decrease in cardiomyocyte apoptosis, accompanying an increase in phosphorylated Akt and B-cell lymphoma 2 (Bcl-2) and a decrease in caspase-3, was also observed. Furthermore, the left ventricular function was markedly augmented in the Akt-AFMSC group compared with the control group. These observations suggested that the protective effect of AFMSCs may be due to the delivery of secreted cytokines, promotion of neoangiogenesis, prevention of cardiomyocyte apoptosis, transdifferentiation into cardiomyocytes and promotion of the viability of AFMSCs, which are assisted by Akt gene modification. Taken together, the results of the present study have indicated that transplantation of Akt-AFMSCs is able to alleviate myocardial I/R injury and improve cardiac function. PMID:27151366

  3. Heart transplant

    MedlinePlus

    ... 10 years. Alternative Names Cardiac transplant; Transplant - heart; Transplantation - heart Images Heart, section through the middle Heart, ... 28. Bernstein D. Pediatric heart and heart-lung transplantation. In: Kliegman RM, Behrman RE, Jenson HB, Stanton ...

  4. Heart Failure

    MedlinePlus

    ... version of this page please turn Javascript on. Heart Failure What is Heart Failure? In heart failure, the heart cannot pump enough ... failure often experience tiredness and shortness of breath. Heart Failure is Serious Heart failure is a serious and ...

  5. Hemodynamic effects of left atrial or left ventricular cannulation for acute circulatory support in a bovine model of left heart injury.

    PubMed

    Kapur, Navin K; Paruchuri, Vikram; Pham, Duc Thinh; Reyelt, Lara; Murphy, Barbara; Beale, Corinna; Bogins, Courtney; Wiener, Daniel; Nilson, James; Esposito, Michele; Perkins, Scott; Perides, George; Karas, Richard H

    2015-01-01

    Our objective was to examine the hemodynamic effects of a trans-aortic axial flow catheter (Impella CP) in the left ventricle (LV) versus left atrial (LA) to femoral artery bypass using a centrifugal pump (TandemHeart: TH) in a bovine model of acute LV injury. In three male calves, we performed sequential activation of a CP then TH device in each animal. After 60 minutes of left anterior descending artery ligation, a CP was activated at maximal power. The CP was then removed and the TH activated at 5,500 then a maximum of 7,500 rotations per minute (RPM). The CP generated a maximum 3.1 ± 0.2 L/minute (LPM) of flow, whereas the TH at 5,500 and 7,500 RPM generated 3.1 ± 0.4 and 4.4 ± 0.3 LPM. At 3.1 LPM, the CP and TH reduced LV stroke work (LVSW) similarly. The TH reduced stroke volume, whereas the CP did not. The CP reduced end-systolic pressure, whereas the TH did not. At a maximum flow of 4.4 LPM, the TH provided a greater reduction in LVSW than maximal CP activation. This is the first report to compare the hemodynamic effects of trans-aortic LV unloading versus LA-to-femoral artery (FA) bypass. PMID:25485565

  6. Drp1 loss-of-function reduces cardiomyocyte oxygen dependence protecting the heart from ischemia-reperfusion injury.

    PubMed

    Zepeda, Ramiro; Kuzmicic, Jovan; Parra, Valentina; Troncoso, Rodrigo; Pennanen, Christian; Riquelme, Jaime A; Pedrozo, Zully; Chiong, Mario; Sánchez, Gina; Lavandero, Sergio

    2014-06-01

    Mitochondria are key organelles for ATP production in cardiomyocytes, which is regulated by processes of fission and fusion. We hypothesized that the mitochondria fusion protein dynamin-related protein 1 (Drp1) inhibition, attenuates ischemia-reperfusion (I/R) injury through modifications in mitochondrial metabolism. Rats were subjected to I/R through coronary artery ligation, and isolated cardiomyocytes were treated with an ischemia-mimicking solution. In vivo, cardiac function, myocardial infarction area, and mitochondrial morphology were determined, whereas in vitro, viability, mitochondrial membrane potential, intracellular ATP levels, and oxygen consumption rate (OCR) were assessed. In both models, an adenovirus expressing Drp1 dominant-negative K38A (Drp1K38A) was used to induce Drp1 loss-of-function. Our results showed that I/R stimulated mitochondrial fission. Myocardial infarction size and cell death induced by I/R were significantly reduced, whereas cardiac function after I/R was improved in Drp1K38A-treated rats compared with controls. Drp1K38A-transduced cardiomyocytes showed lower OCR with no decrease in intracellular ATP levels, and on I/R, a larger decrease in OCR with a smaller reduction in intracellular ATP level was observed. However, proton leak-associated oxygen consumption was comparatively higher in Drp1K38A-treated cardiomyocytes, suggesting a protective mitochondrial uncoupling effect against I/R. Collectively, our results show that Drp1 inhibition triggers cardioprotection by reducing mitochondrial metabolism during I/R. PMID:24477044

  7. Cordycepin, 3'-deoxyadenosine, prevents rat hearts from ischemia/reperfusion injury via activation of Akt/GSK-3β/p70S6K signaling pathway and HO-1 expression.

    PubMed

    Park, Eun-Seok; Kang, Do-Hyun; Yang, Min-Kyu; Kang, Jun Chul; Jang, Yong Chang; Park, Jong Seok; Kim, Si-Kwan; Shin, Hwa-Sup

    2014-03-01

    Cordycepin (3'-deoxyadenosine) isolated from Cordyceps militaris, a species of the fungal genus Cordyceps, has been shown to exhibit many pharmacological functions, such as anticancer, anti-inflammatory, and antioxidant activities. In this study, we investigated the preventive role of cordycepin in ischemic/reperfusion (I/R) injury of isolated rat hearts and anesthetized rats. After Sprague-Dawley rats received cordycepin (3, 10, and 30 mg/kg) or control (0.5 % carboxyl methylcellulose) orally once a day for a week, hearts were isolated and mounted on Langendorff heart perfusion system. Isolated hearts were perfused with Krebs-Henseleit buffer for 15-min pre-ischemic stabilization period and subjected to 30-min global ischemia and 30-min reperfusion. Cordycepin administration (10 mg/kg, p.o.) significantly increased left ventricular developed pressure during the reperfusion period compared to that in the control group, but without any effect on coronary flow. Cordycepin (10 mg/kg, p.o.) significantly increased the phosphorylation of Akt/GSK-3β/p70S6K pathways, which are known to modulate multiple survival pathways. In addition, cordycepin decreased Bax and cleaved caspase-3 expression while increasing Bcl-2 expression, Bcl-2/Bax ratio, and heme oxygenase (HO-1) expression in isolated rat hearts. In anesthetized rats subjected to 30 min occlusion of left anterior descending coronary artery/2.5-h reperfusion, cordycepin (1, 3, and 10 mg/kg, i.v.) administered 15 min before the onset of ischemia dose-dependently decreased the infarct size in left ventricle. In conclusion, cordycepin could be an attractive therapeutic candidate with oral activity against I/R-associated heart diseases such as myocardial infarction. PMID:24178833

  8. Mechanism of sphingosine-1-phosphate induced cardioprotection against I/R injury in diabetic rat heart: Possible involvement of glycogen synthase kinase 3β and mitochondrial permeability transition pore.

    PubMed

    Rana, Ajay; Sharma, Saurabh

    2016-02-01

    There is growing evidence that diabetes mellitus causes attenuation of the bioactive metabolite of membrane sphingolipids, sphingosine-1-phosphate, and this may be a key mechanism in the decreased cardioprotective effect of ischaemic preconditioning (IPC) in the diabetic heart. Thus, this study has been designed to investigate the role and pharmacological potential of sphingosine-1-phosphate in diabetic rat heart. Diabetes was produced in Wistar rats by administration of a low dose of streptozotocin (STZ) (35 mg/kg, i.p., once) and feeding a high fat diet (HFD) for 6 weeks. Isolated rat heart was subjected to 30 min ischaemia followed by 120 min of reperfusion (I/R). The heart was subjected to pre-ischaemic treatment (before ischaemia for 20 min) and pharmacological preconditioning with the S1P agonist FTY720 (0.6 μmol/L) with and without atractyloside (an mPTP opener; in the last episode of reperfusion before I/R). Myocardial infarction was assessed in terms of increase in lactate dehydrogenase (LDH), creatinine kinase-MB (CK-MB), myeloperoxidase (MPO) level and infarct size (triphenyltetrazolium chloride staining). Immunohistochemistry analysis was done for assessment of tumour necrosis factor (TNF)-α and glycogen synthase kinase (GSK)-3β level in cardiac tissue. Pre-ischaemic treatment and pharmacological preconditioning with FTY720 significantly decreased I/R-induced myocardial infarction, TNF-alpha, GSK-3β level and release of LDH and CK-MB as compared to control group. The cardioprotective effect of S1P agonist was significantly attenuated by atractyloside. It may be concluded that S1P agonist FTY720 prevents the diabetic heart from ischaemic reperfusion injury, possibly through inhibition of GSK-3β and regulation of opening of mitochondrial permeability transition pore. PMID:26582369

  9. Urotensin-ⅡReceptor Antagonist SB-710411 Protects Rat Heart against Ischemia-Reperfusion Injury via RhoA/ROCK Pathway

    PubMed Central

    Luo, Sheng-Yong; Chen, Shuo; Qin, Yi-De; Chen, Zhi-Wu

    2016-01-01

    Aim SB-710411 is a rat selective urotensin-II (U-II) receptor antagonist, which can block U-II-induced contraction of the aorta and inhibit U-II-induced myocardial fibrosis in rats. However, the effect of SB-710411 on myocardial ischemia-reperfusion (I/R) injury is unclear. The present study was designed to investigate whether SB-710411 has a protective effect on myocardial I/R injury in rats and the possible mechanisms. Methods and Results Myocardial I/R injury was induced by occluding the left anterior descending coronary artery in adult male Sprague-Dawley rats. Hemodynamic parameters, electrocardiogram (ECG), infarct size, histological alteration, lactate dehydrogenase (LDH), creatine phosphokinase-MB (CK-MB), cardiac troponin I (cTnI), RhoA, and the protein expressions of U-II receptor (UTR), ROCK1 and ROCK2 were evaluated. Cardiac I/R injury significantly up-regulated the expressions of UTR, ROCK1 and ROCK2 proteins in rat myocardium. SB-710411 1.0 and 2.0 μg/kg significantly reduced cardiac I/R-induced the infarct size and histological damage in rat myocardium, markedly inhibited the changes of hemodynamic parameters and the increases of ST-segment in ECG, the serum LDH and CK-MB activities and cTnI level in rats subjected to myocardial I/R injury. Furthermore, SB-710411 obviously prevented myocardial I/R-increased RhoA activity and UTR, ROCK1 and ROCK2 protein expressions. Conclusions Our results indicate that cardiac I/R injury increases myocardial UTR expression, and SB-710411 has a potent protective effect on myocardial I/R injury in rats. The cardioprotection may be associated with the inhibition of UTR-RhoA/ROCK pathway. PMID:26771557

  10. Open heart surgery

    MedlinePlus

    ... Heart bypass surgery (coronary artery bypass graft - CABG) Heart transplant Heart valve surgery Hypoplastic left heart repair Minimally ... Heart bypass surgery Heart bypass surgery - minimally invasive Heart transplant Heart valve surgery Hypoplastic left heart syndrome Patent ...

  11. Heart Attack

    MedlinePlus

    ... attack treatment works best when it's given right after symptoms occur. Prompt treatment of a heart attack can help prevent or limit damage to the heart and prevent sudden death. Call 9-1-1 Right Away A heart ...

  12. Heart attack

    MedlinePlus

    ... infarction; Non-ST-elevation myocardial infarction; NSTEMI; CAD-heart attack; Coronary artery disease-heart attack ... made up of cholesterol and other cells. A heart attack may occur when: A tear in the ...

  13. Heart Block

    MedlinePlus

    ... Block Explore Heart Block What Is... Electrical System & EKG Results Types Causes Who Is at Risk Signs & ... heart block. Doctors use a test called an EKG (electrocardiogram) to help diagnose heart block. This test ...

  14. Heart Anatomy

    MedlinePlus

    ... Incredible Machine Bonus poster (PDF) The Human Heart Anatomy Blood The Conduction System The Coronary Arteries The ... of the Leg Vasculature of the Torso Heart anatomy illustrations and animations for grades K-6. Heart ...

  15. Heart attack

    MedlinePlus

    ... a heart attack take part in a cardiac rehabilitation program. ... al. eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine . 10th ed. Philadelphia, PA: Elsevier Saunders; 2014: ...

  16. Disturbance effects of PM₁₀ on iNOS and eNOS mRNA expression levels and antioxidant activity induced by ischemia-reperfusion injury in isolated rat heart: protective role of vanillic acid.

    PubMed

    Dianat, Mahin; Radmanesh, Esmat; Badavi, Mohammad; Mard, Seyed Ali; Goudarzi, Gholamraza

    2016-03-01

    Myocardial infarction is the acute condition of myocardial necrosis that occurs as a result of imbalance between coronary blood supply and myocardial demand. Air pollution increases the risk of death from cardiovascular diseases (CVDs). The aim of this study was to investigate the effects of particulate matter (PM) on oxidative stress, the expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) messenger RNA (mRNA) level induced by ischemia-reperfusion injury, and the protective effects of vanillic acid (VA) in the isolated rat heart. Male Wistar rats were randomly divided into eight groups (n = 10), namely control, VAc, sham, VA, PMa (0.5 mg/kg), PMb (2.5 mg/kg), PMc (5 mg/kg), and PMc + VA groups. Particles with an aerodynamic diameter <10 μm (PM10) was instilled into the trachea through a fine intubation tube. Two days following the PM10 instillation, the animal's hearts were isolated and transferred to a Langendorff apparatus. The hearts were subjected to 30 min of global ischemia followed by 60 min of reperfusion. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), xanthine oxidase (XOX), and lactate dehydrogenase (LDH) were measured using special kits. Reverse transcription polymerase chain reaction (RT-PCR) was used to determine levels of iNOS and eNOS mRNA. An increase in left ventricular end-diastolic pressure (LVEDP), S-T elevation, and oxidative stress in PM10 groups was observed. Ischemia-reperfusion (I/R) induction showed a significant augment in the expression of iNOS mRNA level and a significant decrease in the expression eNOS mRNA level. This effect was more pronounced in the PM groups than in the control and sham groups. Vanillic acid caused a significant decrease in LVEDP, S-T elevation, and also a significant difference in eNOS mRNA expression level, antioxidant enzymes, iNOS mRNA expression level, and oxidative stress occurred on myocardial dysfunction

  17. Heart Attack

    MedlinePlus

    ... have a heart attack. About half of them die. Many people have permanent heart damage or die because they don't get help immediately. It's ... few hours causes the affected heart muscle to die. NIH: National Heart, Lung, and Blood Institute

  18. Heart Transplantation

    MedlinePlus

    A heart transplant removes a damaged or diseased heart and replaces it with a healthy one. The healthy heart comes from a donor who has died. It is the last resort for people with heart failure when all other treatments have failed. The ...

  19. Heart Diseases

    MedlinePlus

    ... you're like most people, you think that heart disease is a problem for others. But heart disease is the number one killer in the ... of disability. There are many different forms of heart disease. The most common cause of heart disease ...

  20. Heart Diseases

    MedlinePlus

    ... re like most people, you think that heart disease is a problem for others. But heart disease is the number one killer in the U.S. ... disability. There are many different forms of heart disease. The most common cause of heart disease is ...

  1. Role of Neutrophil Gelatinase-Associated Lipocalin in the Diagnosis and Early Treatment of Acute Kidney Injury in a Case Series of Patients with Acute Decompensated Heart Failure: A Case Series

    PubMed Central

    Fogolari, Marta; Morolla, Davide; Capone, Federico; Costantino, Sebastiano; Spoto, Silvia; De Cesaris, Marina; Lo Presti, Alessandra; Ciccozzi, Massimo; Dicuonzo, Giordano

    2016-01-01

    Patients with acute decompensated heart failure (ADHF) frequently develop worsening in renal function until Acute Kidney Injury (AKI). The use of kidney injury biomarkers could be useful in the early diagnosis of AKI. In the present study, the role of the neutrophil gelatinase-associated lipocalin (NGAL), compared to the standard creatinine, in ADHF patients, was analyzed to evaluate if an early treatment could affect the outcome. A case series of 24 ADHF patients was enrolled and patients randomly divided in two groups (Group A and Group B). In Group A, NGAL, creatinine, and eGFR were measured, while in Group B, creatinine and eGFR alone were measured. NGAL was measured by turbidimetric immunoassay and creatinine using an enzymatic spectrophotometric method. In presence of AKI, creatinine increase and eGFR decrease were significantly lower in Group A than in Group B, whereas in absence of AKI the difference between the two groups was not significant. Hospitalization stay was significantly lower in Group A (receiving early treatment based on NGAL) than in Group B. In ADHF patients, plasma NGAL in combination with creatinine was superior to the standard creatinine in the diagnosis and early treatment of AKI with a better outcome and a decreased hospital stay. PMID:27022499

  2. Optimized Heart Sampling and Systematic Evaluation of Cardiac Therapies in Mouse Models of Ischemic Injury: Assessment of Cardiac Remodeling and Semi-Automated Quantification of Myocardial Infarct Size.

    PubMed

    Valente, Mariana; Araújo, Ana; Esteves, Tiago; Laundos, Tiago L; Freire, Ana G; Quelhas, Pedro; Pinto-do-Ó, Perpétua; Nascimento, Diana S

    2015-01-01

    Cardiac therapies are commonly tested preclinically in small-animal models of myocardial infarction. Following functional evaluation, post-mortem histological analysis is essential to assess morphological and molecular alterations underlying the effectiveness of treatment. However, non-methodical and inadequate sampling of the left ventricle often leads to misinterpretations and variability, making direct study comparisons unreliable. Protocols are provided for representative sampling of the ischemic mouse heart followed by morphometric analysis of the left ventricle. Extending the use of this sampling to other types of in situ analysis is also illustrated through the assessment of neovascularization and cellular engraftment in a cell-based therapy setting. This is of interest to the general cardiovascular research community as it details methods for standardization and simplification of histo-morphometric evaluation of emergent heart therapies. © 2015 by John Wiley & Sons, Inc. PMID:26629776

  3. INO-4885 [5,10,15,20-tetra[N-(benzyl-4'-carboxylate)-2-pyridinium]-21H,23H-porphine iron(III) chloride], a peroxynitrite decomposition catalyst, protects the heart against reperfusion injury in mice.

    PubMed

    Jiao, Xiang-Ying; Gao, Erhe; Yuan, Yuexin; Wang, Yajing; Lau, Wayne Bond; Koch, Walter; Ma, Xin-Liang; Tao, Ling

    2009-03-01

    Oxidative/nitrative stress caused by peroxynitrite, the reaction product of superoxide (O2(.-)) and nitric oxide (NO), is the primary cause of myocardial ischemia/reperfusion injury. The present study determined whether INO-4885 [5,10,15,20-tetra[N-(benzyl-4'-carboxylate)-2-pyridinium]-21H,23H-porphine iron(III) chloride], a new peroxynitrite decomposition catalyst, may provide cellular protection and protect heart from myocardial ischemia/reperfusion injury. Adult male mice were subjected to 30 min of ischemia and 3 or 24 h of reperfusion. Mice were randomized to receive vehicle, INO-4885 without catalytic moiety, or INO-4885 (3-300 microg/kg i.p.) 10 min before reperfusion. Infarct size, apoptosis, nitrotyrosine content, NO/O2(.-) production, and inducible nitric-oxide synthase (iNOS)/NADPH oxidase expression were determined. INO-4885 treatment reduced ischemia/reperfusion-induced protein nitration and caspase 3 activation in a dose-dependent fashion in the range of 3 to 100 microg/kg. However, doses exceeding 100 microg/kg produced nonspecific effects and attenuated its protective ability. At the optimal dose (30 microg/kg), INO-4885 significantly reduced infarct size (p < 0.01), decreased apoptosis (p < 0.01), and reduced tissue nitrotyrosine content (p < 0.01). As expected, INO-4885 had no effect on ischemia/reperfusion-induced iNOS expression and NO overproduction. To our surprise, this compound significantly reduced superoxide production and partially blocked NADPH oxidase overexpression in the ischemic/reperfused cardiac tissue. Additional experiments demonstrated that INO-4885 provided better cardioprotection than N-(3-(aminomethyl)benzyl)acetamidine (1400W, a selective iNOS inhibitor), apocynin (an NADPH oxidase inhibitor), or Tiron (a cell-permeable superoxide scavenger). Taken together, our data demonstrated that INO-4885 is a cardioprotective molecule that attenuates myocardial reperfusion injury by facilitating peroxynitrite decomposition and

  4. Urethral Injuries

    MedlinePlus

    ... Injuries Ureteral Injuries Urethral Injuries Injuries to the Penis and Scrotum Most urethral injuries occur in men. ... leakage of urine into the tissues of the penis, scrotum, abdominal wall, or perineum (the area between ...

  5. Nasal vaccination with troponin reduces troponin specific T-cell responses and improves heart function in myocardial ischemia–reperfusion injury

    PubMed Central

    Frenkel, Dan; Pachori, Alok S.; Zhang, Lunan; Dembinsky-Vaknin, Adi; Farfara, Dorit; Petrovic-Stojkovic, Sanja; Dzau, Victor J.

    2009-01-01

    Myocardial ischemia with subsequent reperfusion (MI/R) can lead to significant myocardial damage. Ischemia initiates inflammation at the blood–microvascular endothelial cell interface and contributes significantly to both acute injury and repair of the damaged tissue. We have found that MI/R injury in mice is associated with a cellular immune response to troponin. Myocardial cells exclusively synthesize troponin and release the troponin into the bloodstream following injury. Mucosally administered proteins induce T cells that secrete anti-inflammatory cytokines such as IL-10 and transforming growth factor β at the anatomical site where the protein localizes. We found that nasal administration of the three subunits of troponin (C, I and T isoforms), given prior to or 1 h following MI/R, decreased infarct size by 40% measured 24 h later. At 1.5 months following MI/R, there was a 50% reduction in infarct size and improvement in cardiac function as measured by echocardiography. Protection was associated with a reduction of cellular immunity to troponin. Immunohistochemistry demonstrated increased IL-10 and reduced IFN-γ in the area surrounding the ischemic infarct following nasal troponin. Adoptive transfer of CD4+ T cells to mice from nasally troponin-treated mice 1 h after the MI/R decreased infarct size by 72%, whereas CD4+ T cells from IL-10−/− mice or nasally BSA-treated mice had no effect. Our results demonstrate that IL-10-secreting CD4+ T cells induced by nasal troponin reduce injury following MI/R. Modulation of cardiac inflammation by nasal troponin provides a novel treatment to decrease myocardial damage and enhance recovery after myocardial ischemia. PMID:19515797

  6. Lipotoxicity in the Heart

    PubMed Central

    Wende, Adam R.; Abel, E. Dale

    2009-01-01

    Obesity and insulin resistance are associated with ectopic lipid deposition in multiple tissues, including the heart. Excess lipid may be stored as triglycerides, but are also shunted into non-oxidative pathways that disrupt normal cellular signaling leading to organ dysfunction and in some cases apoptosis, a process termed lipotoxicity. Various pathophysiological mechanisms have been proposed to lead to lipotoxic tissue injury, which might vary by cell type. Specific mechanisms by which lipotoxicity alters cardiac structure and function are incompletely understood, but are beginning to be elucidated. This review will focus on mechanisms that have been proposed to lead to lipotoxic injury in the heart and will review the state of knowledge regarding potential causes and correlates of increased myocardial lipid content in animal models and humans. We will seek to highlight those areas where additional research is warranted. PMID:19818871

  7. Biomarkers in acute heart failure.

    PubMed

    Mallick, Aditi; Januzzi, James L

    2015-06-01

    The care of patients with acutely decompensated heart failure is being reshaped by the availability and understanding of several novel and emerging heart failure biomarkers. The gold standard biomarkers in heart failure are B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide, which play an important role in the diagnosis, prognosis, and management of acute decompensated heart failure. Novel biomarkers that are increasingly involved in the processes of myocardial injury, neurohormonal activation, and ventricular remodeling are showing promise in improving diagnosis and prognosis among patients with acute decompensated heart failure. These include midregional proatrial natriuretic peptide, soluble ST2, galectin-3, highly-sensitive troponin, and midregional proadrenomedullin. There has also been an emergence of biomarkers for evaluation of acute decompensated heart failure that assist in the differential diagnosis of dyspnea, such as procalcitonin (for identification of acute pneumonia), as well as markers that predict complications of acute decompensated heart failure, such as renal injury markers. In this article, we will review the pathophysiology and usefulness of established and emerging biomarkers for the clinical diagnosis, prognosis, and management of acute decompensated heart failure. PMID:25911167

  8. Pathophysiology of Heart Failure.

    PubMed

    Tanai, Edit; Frantz, Stefan

    2015-01-01

    Heart failure is considered an epidemic disease in the modern world affecting approximately 1% to 2% of adult population. It presents a multifactorial, systemic disease, in which--after cardiac injury--structural, neurohumoral, cellular, and molecular mechanisms are activated and act as a network to maintain physiological functioning. These coordinated, complex processes lead to excessive volume overload, increased sympathetic activity, circulation redistribution, and result in different, parallel developing clinical signs and symptoms. These signs and symptoms sum up to an unspecific clinical picture; thus invasive and noninvasive diagnostic tools are used to get an accurate diagnosis and to specify the underlying cause. The most important, outcome determining factor in heart failure is its constant progression. Constant optimizing of pharmatherapeutical regimes, novel targets, and fine regulation of these processes try to keep these compensatory mechanisms in a physiological range. Beside pharmacological therapy, interventional and surgical therapy options give new chances in the management of heart failure. For the optimization and establishment of these and novel therapeutical approaches, complete and comprehensive understanding of the underlying mechanisms is essentially needed. Besides diagnosis and treatment, efforts should be made for better prevention in heart failure by treatment of risk factors, or identifying and following risk groups. This summary of the pathophysiology of heart failure tries to give a compact overview of basic mechanisms and of the novel unfolding, progressive theory of heart failure to contribute to a more comprehensive knowledge of the disease. PMID:26756631

  9. Multi-Strain Probiotics Inhibit Cardiac Myopathies and Autophagy to Prevent Heart Injury in High-Fat Diet-Fed Rats

    PubMed Central

    Lai, Chao-Hung; Tsai, Cheng-Chih; Kuo, Wei-Wen; Ho, Tsung-Jung; Day, Cecilia-Hsuan; Pai, Pei-ying; Chung, Li-Chin; Huang, Chun-Chih; Wang, Hsueh-Fang; Liao, Po-Hsiang; Huang, Chih-Yang

    2016-01-01

    High-fat diets induce obesity, leading to cardiomyocyte fibrosis and autophagy imbalance. In addition, no previous studies have indicated that probiotics have potential health effects associated with cardiac fibrosis and autophagy in obese rats. This study investigates the effects of probiotics on high-fat (HF) diet-induced obesity and cardiac fibrosis and autophagy in rat hearts. Eight-week-old male Wistar rats were separated randomly into five equally sized experimental groups: Normal diet (control) and high-fat (HF) diet groups and groups fed a high-fat diet supplemented with low (HL), medium (HM) or high (HH) doses of multi-strain probiotic powders. These experiments were designed for an 8-week trial period. The myocardial architecture of the left ventricle was evaluated using Masson's trichrome staining and immunohistochemistry staining. Key probiotics-related pathway molecules were analyzed using western blotting. Abnormal myocardial architecture and enlarged interstitial spaces were observed in HF hearts. These interstitial spaces were significantly decreased in groups provided with multi-strain probiotics compared with HF hearts. Western blot analysis demonstrated that key components of the TGF/MMP2/MMP9 fibrosis pathways and ERK5/uPA/ANP cardiac hypertrophy pathways were significantly suppressed in probiotic groups compared to the HF group. Autophagy balance is very important in cardiomyocytes. In this study, we observed that the beclin-1/LC3B/Atg7 autophagy pathway in HF was increased after probiotic supplementation was significantly decreased. Together, these results suggest that oral administration of probiotics may attenuate cardiomyocyte fibrosis and cardiac hypertrophy and the autophagy-signaling pathway in obese rats. PMID:27076784

  10. Multi-Strain Probiotics Inhibit Cardiac Myopathies and Autophagy to Prevent Heart Injury in High-Fat Diet-Fed Rats.

    PubMed

    Lai, Chao-Hung; Tsai, Cheng-Chih; Kuo, Wei-Wen; Ho, Tsung-Jung; Day, Cecilia-Hsuan; Pai, Pei-Ying; Chung, Li-Chin; Huang, Chun-Chih; Wang, Hsueh-Fang; Liao, Po-Hsiang; Huang, Chih-Yang

    2016-01-01

    High-fat diets induce obesity, leading to cardiomyocyte fibrosis and autophagy imbalance. In addition, no previous studies have indicated that probiotics have potential health effects associated with cardiac fibrosis and autophagy in obese rats. This study investigates the effects of probiotics on high-fat (HF) diet-induced obesity and cardiac fibrosis and autophagy in rat hearts. Eight-week-old male Wistar rats were separated randomly into five equally sized experimental groups: Normal diet (control) and high-fat (HF) diet groups and groups fed a high-fat diet supplemented with low (HL), medium (HM) or high (HH) doses of multi-strain probiotic powders. These experiments were designed for an 8-week trial period. The myocardial architecture of the left ventricle was evaluated using Masson's trichrome staining and immunohistochemistry staining. Key probiotics-related pathway molecules were analyzed using western blotting. Abnormal myocardial architecture and enlarged interstitial spaces were observed in HF hearts. These interstitial spaces were significantly decreased in groups provided with multi-strain probiotics compared with HF hearts. Western blot analysis demonstrated that key components of the TGF/MMP2/MMP9 fibrosis pathways and ERK5/uPA/ANP cardiac hypertrophy pathways were significantly suppressed in probiotic groups compared to the HF group. Autophagy balance is very important in cardiomyocytes. In this study, we observed that the beclin-1/LC3B/Atg7 autophagy pathway in HF was increased after probiotic supplementation was significantly decreased. Together, these results suggest that oral administration of probiotics may attenuate cardiomyocyte fibrosis and cardiac hypertrophy and the autophagy-signaling pathway in obese rats. PMID:27076784

  11. Apelin-13 protects the heart against ischemia-reperfusion injury through the RISK-GSK-3β-mPTP pathway

    PubMed Central

    Li, Hui; Tang, Lei; Ge, Guanghao; Ma, Jiangwei; Qiao, Zengyong; Liu, Huajin; Fang, Weiyi

    2015-01-01

    Introduction Apelin plays an important role in the protection against myocardial ischemia-reperfusion (I/R) injury, while the mechanism still remains unclear. In the current study, we aimed to evaluate the protective effect of apelin-13, and the main mechanism. Material and methods The in vivo I/R injury model (Sprague-Dawley rat) was established, then infarct size, expression levels of phospho-protein kinase B (p-Akt), phospho-extracellular signal-regulated kinase (p-ERK) and phospho-glycogen synthase kinase-3β (p-GSK-3β) were measured. The fluorescence intensity of tetramethylrhodamine ethyl ester perchlorate (TMRE) of the isolated myocardial cells was determined to evaluate the opening of the mitochondrial permeability transition pore (mPTP) caused by oxidant stress and hypoxia/reoxygenation. Results For the established I/R injury model, apelin-13 and SB216763 (GSK-3β inhibitor) significantly reduced the infarct size (p < 0.05), which could be abolished by LY294002 (PI3K inhibitor), PD98059 (MEK inhibitor) and atractyloside (mPTP accelerator). The enhanced expression levels of p-Akt, p-ERK and p-GSK-3β caused by apelin-13 (p < 0.05) could be counteracted by LY294002 and PD98059. The reduced fluorescence intensity of TMRE in the H2O2/apelin-13 and H2O2/SB216763 treated groups was significantly lower (p < 0.05), indicating that apelin-13 and SB216763 could reduce the decline in mitochondrial membrane potential caused by oxidant stress, and the fluorescence intensity in the hypoxia/reoxygenation + apelin-13 group was significantly lower (p < 0.05), which suggested that apelin-13 could inhibit the mitochondrial membrane potential changes induced by hypoxia/reoxygenation. Conclusions The protective mechanism of apelin-13 might be that inactivation of GSK-3β could inhibit the opening of mPTP by activating PI3K/Akt and ERK1/2 involved in the reperfusion injury salvage kinase (RISK) pathway. PMID:26528352

  12. Heart pacemaker

    MedlinePlus

    ... 1 ounce. Most pacemakers have 2 parts: The generator contains the battery and the information to control ... are wires that connect the heart to the generator and carry the electrical messages to the heart. ...

  13. Heart Health

    MedlinePlus

    ... nih.gov/Go4Life Heart Health Just like an engine makes a car go, your heart keeps your ... all at once —10-minute periods will do. Start by doing activities you enjoy—brisk walking, dancing, ...

  14. Heart Disease

    MedlinePlus

    ... with heart disease? What do my cholesterol and triglyceride numbers mean? How can I lower my cholesterol? ... weight Know your numbers (blood pressure, cholesterol, and triglycerides) You can reduce your chances of getting heart ...

  15. Heart Failure

    MedlinePlus

    ... arrhythmias) The use of toxic substances (such as alcohol or drug abuse) Congenital heart defect (a heart problem you were born with) Diabetes Thyroid problems Diagnosis & Tests How will my doctor know if I ...

  16. Heart palpitations

    MedlinePlus

    Heart palpitations can be due to: Anxiety, stress, panic attack, or fear Caffeine intake Nicotine intake Cocaine or other illegal drugs Diet pills Exercise Fever However, some palpitations are due to an abnormal heart rhythm, ...

  17. Heart Disease

    MedlinePlus

    ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke Prevention ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke Prevention ...

  18. Sevoflurane postconditioning reduces myocardial reperfusion injury in rat isolated hearts via activation of PI3K/Akt signaling and modulation of Bcl-2 family proteins*

    PubMed Central

    Yu, Li-na; Yu, Jing; Zhang, Feng-jiang; Yang, Mei-juan; Ding, Ting-ting; Wang, Jun-kuan; He, Wei; Fang, Tao; Chen, Gang; Yan, Min

    2010-01-01

    Sevoflurane postconditioning reduces myocardial infarct size. The objective of this study was to examine the role of the phosphatidylinositol-3-kinase (PI3K)/Akt pathway in anesthetic postconditioning and to determine whether PI3K/Akt signaling modulates the expression of pro- and antiapoptotic proteins in sevoflurane postconditioning. Isolated and perfused rat hearts were prepared first, and then randomly assigned to the following groups: Sham-operation (Sham), ischemia/reperfusion (Con), sevoflurane postconditioning (SPC), Sham plus 100 nmol/L wortmannin (Sham+Wort), Con+Wort, SPC+Wort, and Con+dimethylsulphoxide (DMSO). Sevoflurane postconditioning was induced by administration of sevoflurane (2.5%, v/v) for 10 min from the onset of reperfusion. Left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximum increase in rate of LVDP (+dP/dt), maximum decrease in rate of LVDP (−dP/dt), heart rate (HR), and coronary flow (CF) were measured at baseline, R30 min (30 min of reperfusion), R60 min, R90 min, and R120 min. Creatine kinase (CK) and lactate dehydrogenase (LDH) were measured after 5 min and 10 min reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining at the end of reperfusion. Total Akt and phosphorylated Akt (phospho-Akt), Bax, Bcl-2, Bad, and phospho-Bad were determined by Western blot analysis. Analysis of variance (ANOVA) and Student-Newman-Keuls’ test were used to investigate the significance of differences between groups. The LVDP, ±dP/dt, and CF were higher and LVEDP was lower in the SPC group than in the Con group at all points of reperfusion (P<0.05). The SPC group had significantly reduced CK and LDH release and decreased infarct size compared with the Con group [(22.9±8)% vs. (42.4±9.4)%, respectively; P<0.05]. The SPC group also had increased the expression of phosphor-Akt, Bcl-2, and phospho-Bad, and decreased the expression of Bax. Wortmannin abolished the

  19. Heart Attack

    MedlinePlus

    ... a million people in the U.S. have a heart attack. About half of them die. Many people have permanent heart damage or die because they don't get ... It's important to know the symptoms of a heart attack and call 9-1-1 if someone ...

  20. Cardiac Per2 Functions as Novel Link between Fatty Acid Metabolism and Myocardial Inflammation during Ischemia and Reperfusion Injury of the Heart

    PubMed Central

    Bonney, Stephanie; Kominsky, Doug; Brodsky, Kelley; Eltzschig, Holger; Walker, Lori; Eckle, Tobias

    2013-01-01

    Disruption of peripheral circadian rhyme pathways dominantly leads to metabolic disorders. Studies on circadian rhythm proteins in the heart indicated a role for Clock or Per2 in cardiac metabolism. In contrast to Clock−/−, Per2−/− mice have larger infarct sizes with deficient lactate production during myocardial ischemia. To test the hypothesis that cardiac Per2 represents an important regulator of cardiac metabolism during myocardial ischemia, we measured lactate during reperfusion in Per1−/−, Per2−/− or wildtype mice. As lactate measurements in whole blood indicated an exclusive role of Per2 in controlling lactate production during myocardial ischemia, we next performed gene array studies using various ischemia-reperfusion protocols comparing wildtype and Per2−/− mice. Surprisingly, high-throughput gene array analysis revealed dominantly lipid metabolism as the differentially regulated pathway in wildtype mice when compared to Per2−/−. In all ischemia-reperfusion protocols used, the enzyme enoyl-CoA hydratase, which is essential in fatty acid beta-oxidation, was regulated in wildtype animals only. Studies using nuclear magnet resonance imaging (NMRI) confirmed altered fatty acid populations with higher mono-unsaturated fatty acid levels in hearts from Per2−/− mice. Unexpectedly, studies on gene regulation during reperfusion revealed solely pro inflammatory genes as differentially regulated ‘Per2-genes’. Subsequent studies on inflammatory markers showed increasing IL-6 or TNFα levels during reperfusion in Per2−/− mice. In summary, these studies reveal an important role of cardiac Per2 for fatty acid metabolism and inflammation during myocardial ischemia and reperfusion, respectively. PMID:23977055

  1. NO-synthase inhibitors provide influence on protective effect of modified endotoxine diphosphoryl lipid A in a rat heart model of ischemic-reperfusion injury.

    PubMed

    Kuzelová, M; Mladonická, M; Bukovský, M; Dubnicková, M; Adameová, A; Svec, P

    2006-06-01

    The present study was designed to assess whether a protective effect of the modified diphosphoryl lipid A (modLA) against myocardial ischemia-reperfusion injury (IRI) in rats can be related to the mechanism involving inducible nitric oxide synthase (iNOS). Pre-treatment with modLA significantly reduced the duration of both ventricular tachycardia (p < 0.01) and ventricular fibrillation (p < 0.001) compared to controls. Under these conditions the incidence of animal death was reduced (p < 0.05). The beneficial effect of modLA was markedly attenuated by the prior administration of selective iNOS inhibitor S-methylisothiourea (SMT). In this animal group, mortality was significantly increased (p < 0.01) partially in consequence of sustained ventricular arrhythmias. These results indicate that induction of iNOS can be responsible for cardioprotection of modLA. PMID:16826982

  2. The myocardial infarct size-limiting and antiarrhythmic effects of acyl-CoA:cholesterol acyltransferase inhibitor VULM 1457 protect the hearts of diabetic-hypercholesterolaemic rats against ischaemia/reperfusion injury both in vitro and in vivo.

    PubMed

    Adameová, Adriana; Ravingerová, Tána; Svec, Pavel; Faberová, Viera; Kuzelová, Magdaléna

    2007-12-01

    The study was designed to characterise the influence of a novel acyl-CoA:cholesterol acyltransferase inhibitor, VULM 1457, on the severity of myocardial ischaemia-reperfusion injury in a model of diabetes mellitus and hypercholesterolaemia induced by co-administration of streptozotocin and a high fat-cholesterol diet. We used Langendorff-perfused rat hearts to measure the size of myocardial infarction after 30 min of regional ischaemia, followed by a 2-h reperfusion period, and open-chest rats were exposed to 6 min of ischaemia and 10 min of reperfusion to analyse ventricular arrhythmias. In addition to the high fat-cholesterol diet, VULM 1457 was administered to the diabetic-hypercholesterolaemic rats for 5 days. Decreased plasma and liver cholesterol levels and a significantly reduced occurrence of ventricular fibrillation (29% vs. 100%, P<0.01), determined via the mean number and duration of episodes (0.6+/-0.4 and 2.1+/-1.4 s vs. 2.8+/-0.8 and 53.5+/-14.4 s in diabetic-hypercholesterolaemic rats, both P<0.01), were observed in these animals. Lethal ventricular fibrillation was suppressed, and arrhythmia severity was also significantly decreased in these animals as compared to the non-treated animals (2.9+/-0.6 vs. 4.9+/-0.2; P<0.05). A smaller infarct size, normalised to the size of area at risk, was observed in the treated diabetic-hypercholesterolaemic group as compared to the non-treated group (16.3+/-1.9% vs. 37.3+/-3.1%; P<0.01). Aside from remarkable hypolipidaemic activity, VULM 1457 improved the overall myocardial ischaemia-reperfusion injury outcomes in the diabetic-hypercholesterolaemic rats by suppressing arrhythmogenesis as well as by reducing myocardial necrosis. PMID:17764671

  3. Head Injuries

    MedlinePlus

    ... before. Often, the injury is minor because your skull is hard and it protects your brain. But ... injuries can be more severe, such as a skull fracture, concussion, or traumatic brain injury. Head injuries ...

  4. Head Injuries

    MedlinePlus

    ... before. Usually, the injury is minor because your skull is hard and it protects your brain. But ... injuries can be more severe, such as a skull fracture, concussion, or traumatic brain injury. Head injuries ...

  5. Back Injuries

    MedlinePlus

    ... extending from your neck to your pelvis. Back injuries can result from sports injuries, work around the house or in the garden, ... back is the most common site of back injuries and back pain. Common back injuries include Sprains ...

  6. Head Injuries

    MedlinePlus

    ... of head injuries include bicycle or motorcycle wrecks, sports injuries, falls from windows (especially among children who live ... to watch for? When can I start playing sports again after a head injury? How can brain damage from a head injury ...

  7. Protective Effects of Phosphocreatine Administered Post-Treatment Combined With Ischemic Post-Conditioning on Rat Hearts With Myocardial Ischemia/Reperfusion Injury

    PubMed Central

    Zhang, Wenhua; Zhang, Huizhen; Xing, Yanqiu

    2015-01-01

    Background The aim of the study was to investigate the effects of phosphocreatine (PCr) post-treatment combined with ischemic post-conditioning on myocardial ischemia/reperfusion (I/R) injury in a rat model. Methods Forty Sprague-Dawley rats that had undergone 30 minutes ischemia and 120 minutes reperfusion were randomly divided into four groups (n = 10 in each group): the I/R group, the ischemia post-conditioning (IPost) group, the PCr group, and the IPost + PCr group. The activities of serum creatine kinase (CK), myeloperoxidase (MPO), and lactate dehydrogenase (LDH) were measured after 120 minutes of reperfusion. At the end of the experiment, serum levels of nuclear factor (NF)-κB and tumor necrosis factor (TNF)-α were detected, myocardial infarct size (IS) was measured by triphenyltetrazolium chloride staining, and myocardial expression of Bcl-2 and phosphorylated Akt (p-Akt) was determined by western blot. Results The IPost, PCr, and PCr + IPost groups had significantly lower IS than the I/R group (P < 0.05). The reductions in CK, LDH, and MPO release were consistent with the decrease in the myocardial IS (P < 0.05). Serum concentrations of TNF-α and NF-κB in the IPost, PCr, and PCr + IPost groups were significantly lower than those in the I/R group (P < 0.05). The levels of p-Akt and Bcl-2 in the IPost, PCr, and PCr + IPost groups were greater than those in the I/R group (P < 0.05). CK, LDH, MPO, NF-κB, TNF-α, p-Akt, Bcl-2 and IS were further enhanced in the IPost + PCr group (P < 0.05). Conclusions Post-treatment with PCr enhanced the protective effect of IPost on rat myocardium affected by I/R injury, possibly by inhibiting the inflammatory response and activating the phosphatidylinositol 3-kinase (PI-3K)/Akt/Bcl-2 signaling pathway. PMID:25699120

  8. Cell migration during heart regeneration in zebrafish.

    PubMed

    Tahara, Naoyuki; Brush, Michael; Kawakami, Yasuhiko

    2016-07-01

    Zebrafish possess the remarkable ability to regenerate injured hearts as adults, which contrasts the very limited ability in mammals. Although very limited, mammalian hearts do in fact have measurable levels of cardiomyocyte regeneration. Therefore, elucidating mechanisms of zebrafish heart regeneration would provide information of naturally occurring regeneration to potentially apply to mammalian studies, in addition to addressing this biologically interesting phenomenon in itself. Studies over the past 13 years have identified processes and mechanisms of heart regeneration in zebrafish. After heart injury, pre-existing cardiomyocytes dedifferentiate, enter the cell cycle, and repair the injured myocardium. This process requires interaction with epicardial cells, endocardial cells, and vascular endothelial cells. Epicardial cells envelope the heart, while endocardial cells make up the inner lining of the heart. They provide paracrine signals to cardiomyocytes to regenerate the injured myocardium, which is vascularized during heart regeneration. In addition, accumulating results suggest that local migration of these major cardiac cell types have roles in heart regeneration. In this review, we summarize the characteristics of various heart injury methods used in the research community and regeneration of the major cardiac cell types. Then, we discuss local migration of these cardiac cell types and immune cells during heart regeneration. Developmental Dynamics 245:774-787, 2016. © 2016 Wiley Periodicals, Inc. PMID:27085002

  9. Protective Effects of Kaempferol against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart via Antioxidant Activity and Inhibition of Glycogen Synthase Kinase-3β

    PubMed Central

    Zhou, Mingjie; Ren, Huanhuan; Han, Jichun; Wang, Wenjuan; Zheng, Qiusheng; Wang, Dong

    2015-01-01

    Objective. This study aimed to evaluate the protective effect of kaempferol against myocardial ischemia/reperfusion (I/R) injury in rats. Method. Left ventricular developed pressure (LVDP) and its maximum up/down rate (±dp/dtmax) were recorded as myocardial function. Infarct size was detected with 2,3,5-triphenyltetrazolium chloride staining. Cardiomyocyte apoptosis was determined using terminal deoxynucleotidyl nick-end labeling (TUNEL). The levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined using enzyme linked immunosorbent assay (ELISA). Moreover, total glycogen synthase kinase-3β (GSK-3β), phospho-GSK-3β (P-GSK-3β), precaspase-3, cleaved caspase-3, and cytoplasm cytochrome C were assayed using Western blot analysis. Results. Pretreatment with kaempferol significantly improved the recovery of LVDP and ±dp/dtmax, as well as increased the levels of SOD and P-GSK-3β and GSH/GSSG ratio. However, the pretreatment reduced myocardial infarct size and TUNEL-positive cell rate, as well as decreased the levels of cleaved caspase-3, cytoplasm cytochrome C, CK, LDH, MDA, and TNF-α. Conclusion. These results suggested that kaempferol provides cardioprotection via antioxidant activity and inhibition of GSK-3β activity in rats with I/R. PMID:26265983

  10. Heart regeneration.

    PubMed

    Breckwoldt, Kaja; Weinberger, Florian; Eschenhagen, Thomas

    2016-07-01

    Regenerating an injured heart holds great promise for millions of patients suffering from heart diseases. Since the human heart has very limited regenerative capacity, this is a challenging task. Numerous strategies aiming to improve heart function have been developed. In this review we focus on approaches intending to replace damaged heart muscle by new cardiomyocytes. Different strategies for the production of cardiomyocytes from human embryonic stem cells or human induced pluripotent stem cells, by direct reprogramming and induction of cardiomyocyte proliferation are discussed regarding their therapeutic potential and respective advantages and disadvantages. Furthermore, different methods for the transplantation of pluripotent stem cell-derived cardiomyocytes are described and their clinical perspectives are discussed. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel. PMID:26597703

  11. Hypoplastic left heart syndrome

    MedlinePlus

    HLHS; Congenital heart - hypoplastic left heart; Cyanotic heart disease - hypoplastic left heart ... Hypoplastic left heart is a rare type of congenital heart disease. It is more common in males than in females. As ...

  12. Penetrating cardiac injuries.

    PubMed

    Mittal, V; McAleese, P; Young, S; Cohen, M

    1999-05-01

    Our objective was to determine the influence of several clinical factors on the survival of patients with penetrating wounds to the heart. A retrospective review of 80 consecutive penetrating cardiac injuries treated in a Level II urban trauma center from 1980 through 1994 were examined. Thirty-six patients (45%) had gunshot wounds (including 1 shotgun wound), and 44 (55%) had stab wounds. Intervention consisted of emergency room (ER) or operating room thoracotomy. We measured the effect of several clinical factors on morbidity and patient survival. Survival rate was 17 of 36 (47%) in gunshot injuries and 35 of 44 (80%) in stab injuries, with an overall survival rate of 52 of 80 patients (65%). The average age was 24 years (range, 9-53), and there were 3 female patients. Twelve patients (15%) had multiple cardiac injuries, and 63 (79%) had other associated injuries. Fourteen patients (17%) presented with no blood pressure, and 55 (69%) were hypotensive on admission. ER thoracotomy was performed on 7 of 52 survivors (13%) and 24 of 28 nonsurvivors (86%). Survival after ER thoracotomy was 7 of 31 patients (22%). A selective approach is recommended, because ER thoracotomy has a limited role in penetrating cardiac injury. A high index of suspicion, prompt resuscitation, and immediate definitive surgical management resulted in a high survival rate for these frequently lethal injuries. PMID:10231214

  13. Heart Failure

    MedlinePlus

    ... blood the way it should. It can affect one or both sides of the heart. The weakening of the heart's pumping ability causes Blood and fluid to back up into the lungs The buildup of fluid in the feet, ankles and legs - called edema Tiredness and shortness of breath Common causes of ...

  14. Having Heart.

    PubMed

    Cochrane, Christine

    2015-01-01

    A heart comes in many forms. This article shares the experience of behavioral health nurses caring for a suicidal patient who needs a heart. As a team, the nurses and their patient shared the journey of what it takes to achieve an optimum quality of life with a left ventricular assist device (LVAD) while battling mental illness. PMID:26731919

  15. Retrograde heart perfusion: the Langendorff technique of isolated heart perfusion.

    PubMed

    Bell, Robert M; Mocanu, Mihaela M; Yellon, Derek M

    2011-06-01

    In the late 19th century, a number of investigators were working on perfecting isolated heart model, but it was Oscar Langendorff who, in 1895, pioneered the isolated perfused mammalian heart. Since that time, the Langendorff preparation has evolved and provided a wealth of data underpinning our understanding of the fundamental physiology of the heart: its contractile function, coronary blood flow regulation and cardiac metabolism. In more recent times, the procedure has been used to probe pathophysiology of ischaemia/reperfusion and disease states, and with the dawn of molecular biology and genetic manipulation, the Langendorff perfused heart has remained a stalwart tool in the study of the impact upon the physiology of the heart by pharmacological inhibitors and targeted deletion or up-regulation of genes and their impact upon intracellular signalling and adaption to clinically relevant stressful stimuli. We present here the basic structure of the Langendorff system and the fundamental experimental rules which warrant a viable heart preparation. In addition, we discuss the use of the isolated retrograde perfused heart in the model of ischaemia-reperfusion injury ex-vivo, and its applicability to other areas of study. The Langendorff perfusion apparatus is highly adaptable and this is reflected not only in the procedure's longevity but also in the number of different applications to which it has been turned. PMID:21385587

  16. Eye Injuries

    MedlinePlus

    The structure of your face helps protect your eyes from injury. Still, injuries can damage your eye, sometimes severely enough that you could lose your vision. Most eye injuries are preventable. If you play sports or ...

  17. Head Injuries

    MedlinePlus

    ... injuries internal head injuries, which may involve the skull, the blood vessels within the skull, or the brain Fortunately, most childhood falls or ... knock the brain into the side of the skull or tear blood vessels. Some internal head injuries ...

  18. Back Injuries

    MedlinePlus

    ... the most common site of back injuries and back pain. Common back injuries include Sprains and strains Herniated disks Fractured vertebrae These injuries can cause pain and limit your movement. Treatments vary but might ...

  19. Eye Injuries

    MedlinePlus

    ... of your face helps protect your eyes from injury. Still, injuries can damage your eye, sometimes severely enough that you could lose your vision. Most eye injuries are preventable. If you play sports or work ...

  20. Blast Injuries

    MedlinePlus

    ... Service Members & Veterans Family & Caregivers Medical Providers Blast Injuries U.S. Army photo by Sgt. Gustavo Olgiati How ... tertiary injury Does a blast cause different brain injuries than blunt trauma? There currently is no evidence ...

  1. Ocular Injury

    MedlinePlus

    ... usually occur from blunt trauma, such as a sports injury or a fall with injury to the nose ... of protective goggles at all times. Even in sports like baseball, eye injuries can be prevented by using batting helmets that ...

  2. Sports Injuries

    MedlinePlus

    ... sometimes you can injure yourself when you play sports or exercise. Accidents, poor training practices, or improper ... can also lead to injuries. The most common sports injuries are Sprains and strains Knee injuries Swollen ...

  3. The pathophysiology of heart failure.

    PubMed

    Kemp, Clinton D; Conte, John V

    2012-01-01

    Heart failure is a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return. This common condition affects over 5 million people in the United States at a cost of $10-38 billion per year. Heart failure results from injury to the myocardium from a variety of causes including ischemic heart disease, hypertension, and diabetes. Less common etiologies include cardiomyopathies, valvular disease, myocarditis, infections, systemic toxins, and cardiotoxic drugs. As the heart fails, patients develop symptoms which include dyspnea from pulmonary congestion, and peripheral edema and ascites from impaired venous return. Constitutional symptoms such as nausea, lack of appetite, and fatigue are also common. There are several compensatory mechanisms that occur as the failing heart attempts to maintain adequate function. These include increasing cardiac output via the Frank-Starling mechanism, increasing ventricular volume and wall thickness through ventricular remodeling, and maintaining tissue perfusion with augmented mean arterial pressure through activation of neurohormonal systems. Although initially beneficial in the early stages of heart failure, all of these compensatory mechanisms eventually lead to a vicious cycle of worsening heart failure. Treatment strategies have been developed based upon the understanding of these compensatory mechanisms. Medical therapy includes diuresis, suppression of the overactive neurohormonal systems, and augmentation of contractility. Surgical options include ventricular resynchronization therapy, surgical ventricular remodeling, ventricular assist device implantation, and heart transplantation. Despite significant understanding of the underlying pathophysiological mechanisms in heart failure, this disease causes significant morbidity and carries a 50% 5-year mortality. PMID:22227365

  4. Mechanisms of Cardiotoxicity and the Development of Heart Failure.

    PubMed

    Lee, Christopher S

    2015-12-01

    Cardiotoxicity is a broad term that refers to the negative effects of toxic substances on the heart. Cancer drugs can cause cardiotoxicity by effects on heart cells, thromboembolic events, and/or hypertension that can lead to heart failure. Rheumatoid arthritis biologics may interfere with ischemic preconditioning and cause/worsen heart failure. Long-term and heavy alcohol use can result in oxidative stress, apoptosis, and decreased contractile protein function. Cocaine use results in sympathetic nervous system stimulation of heart and smooth muscle cells and leads to cardiotoxicity and evolution of heart failure. The definition of cardiotoxicity is likely to evolve along with knowledge about detecting subclinical myocardial injury. PMID:26567492

  5. Heart CT scan

    MedlinePlus

    CAT scan - heart; Computed axial tomography scan - heart; Computed tomography scan - heart; Calcium scoring; Multi-detector CT scan - heart; Electron beam computed tomography - heart; Agaston score; Coronary calcium scan

  6. Coronary heart disease

    MedlinePlus

    Heart disease, Coronary heart disease, Coronary artery disease; Arteriosclerotic heart disease; CHD; CAD ... Coronary heart disease is the leading cause of death in the United States for men and women. Coronary heart ...

  7. Wine and heart health

    MedlinePlus

    Health and wine; Wine and heart disease; Preventing heart disease - wine; Preventing heart disease - alcohol ... more often just to lower your risk of heart disease. Heavier drinking can harm the heart and ...

  8. What Is Heart Failure?

    MedlinePlus

    ... page from the NHLBI on Twitter. What Is Heart Failure? Heart failure is a condition in which the heart can' ... force. Some people have both problems. The term "heart failure" doesn't mean that your heart has stopped ...

  9. Hearts Wish.

    ERIC Educational Resources Information Center

    Jones, Lethonee A.

    1989-01-01

    Investigates characteristics and themes in 102 drawings by sexually abused children. Themes of the drawings included genitalia, the absence of specific body parts, phallic symbols, inappropriate smiles, distorted body images, kinetic activity, prominent hands and fingers, and hearts. (RJC)

  10. Heart palpitations

    MedlinePlus

    Heart palpitations can be due to: Anxiety, stress, panic attack, or fear Caffeine intake Nicotine intake Cocaine or other illegal drugs Diet pills Exercise Fever However, some palpitations are due ...

  11. Heart Failure

    MedlinePlus

    ... together. About Rise Above HF Rise Above Heart Failure seeks to increase the dialogue about HF and improve the lives of people affected by the condition through awareness, education and support. Through the initiative, AHA strives to ...

  12. Heart Transplant

    MedlinePlus

    ... Doctors remove the patient's heart by transecting the aorta , the main pulmonary artery and the superior and ... sewing together the recipient and donor vena cavae, aorta, pulmonary artery and left atrium. In patients with ...

  13. Heart MRI

    MedlinePlus

    ... an imaging method that uses powerful magnets and radio waves to create pictures of the heart. It does ... radiation involved in MRI. The magnetic fields and radio waves used during the scan have not been shown ...

  14. Heart Attack

    MedlinePlus

    ... lower “bad” cholesterol (also called LDL, or low-density lipoprotein) levels and may help increase “good” cholesterol (also called HDL, or high-density lipoprotein). If you have had a heart attack, ...

  15. Heart pacemaker

    MedlinePlus

    ... may not get enough oxygen. Symptoms may be light-headedness, tiredness, fainting spells, and shortness of breath. Some pacemakers can be used to stop a heart rate that is too fast ( tachycardia ) ...

  16. Heart transplant

    MedlinePlus

    ... have symptoms. You must take drugs that prevent transplant rejection for the rest of your life. You will ... heart transplant. The main problem, as with other transplants, is rejection. If rejection can be controlled, survival increases to ...

  17. Heart MRI

    MedlinePlus

    ... severe kidney problems. People have been harmed in MRI machines when they did not remove metal objects from their clothes or when metal objects were left in the room by others. MRI is most often not recommended for traumatic injuries. ...

  18. Hypoxia and fetal heart development.

    PubMed

    Patterson, A J; Zhang, L

    2010-10-01

    Fetal hearts show a remarkable ability to develop under hypoxic conditions. The metabolic flexibility of fetal hearts allows sustained development under low oxygen conditions. In fact, hypoxia is critical for proper myocardial formation. Particularly, hypoxia inducible factor 1 (HIF-1) and vascular endothelial growth factor play central roles in hypoxia-dependent signaling in fetal heart formation, impacting embryonic outflow track remodeling and coronary vessel growth. Although HIF is not the only gene involved in adaptation to hypoxia, its role places it as a central figure in orchestrating events needed for adaptation to hypoxic stress. Although "normal" hypoxia (lower oxygen tension in the fetus as compared with the adult) is essential in heart formation, further abnormal hypoxia in utero adversely affects cardiogenesis. Prenatal hypoxia alters myocardial structure and causes a decline in cardiac performance. Not only are the effects of hypoxia apparent during the perinatal period, but prolonged hypoxia in utero also causes fetal programming of abnormality in the heart's development. The altered expression pattern of cardioprotective genes such as protein kinase c epsilon, heat shock protein 70, and endothelial nitric oxide synthase, likely predispose the developing heart to increased vulnerability to ischemia and reperfusion injury later in life. The events underlying the long-term changes in gene expression are not clear, but likely involve variation in epigenetic regulation. PMID:20712587

  19. Lisfranc injuries.

    PubMed

    Welck, M J; Zinchenko, R; Rudge, B

    2015-04-01

    Lisfranc injuries are commonly asked about in FRCS Orthopaedic trauma vivas. The term "Lisfranc injury" strictly refers to an injury where one or more of the metatarsals are displaced from the tarsus. The term is more commonly used to describe an injury to the midfoot centred on the 2nd tarsometatarsal joint. The injury is named after Jacques Lisfranc de St. Martin (1790-1847), a French surgeon and gynaecologist who first described the injury in 1815. 'Lisfranc injury' encompasses a broad spectrum of injuries, which can be purely ligamentous or involve the osseous and articular structures. They are often difficult to diagnose and treat, but if not detected and appropriately managed they can cause long-term disability. This review outlines the anatomy, epidemiology, classification, investigation and current evidence on management of this injury. PMID:25543185

  20. Pancreatic injury.

    PubMed

    Ahmed, Nasim; Vernick, Jerome J

    2009-12-01

    Injury to the pancreas, because of its retroperitoneal location, is a rare occurrence, most commonly seen with penetrating injuries (gun shot or stab wounds). Blunt trauma to the pancreas accounts for only 25% of the cases. Pancreatic injuries are associated with high morbidity and mortality due to accompanying vascular and duodenal injuries. Pancreatic injuries are not always easy to diagnose resulting in life threatening complications. Physical examination as well as serum amylase is not diagnostic following blunt trauma. Computed tomography (CT) scan can delineate the injury or transaction of the pancreas. Endoscopic retrograde pancreaticography (ERCP) is the main diagnostic modality for evaluation of the main pancreatic duct. Unrecognized ductal injury leads to pancreatic pseudocyst, fistula, abscess, and other complications. Management depends upon the severity of the pancreatic injury as well as associated injuries. Damage control surgery in hemodynamic unstable patients reduces morbidity and mortality. PMID:20016434

  1. Inhaled matters of the heart

    PubMed Central

    Zaky, Ahmed; Ahmad, Aftab; Dell’Italia, Louis J; Jahromi, Leila; Reisenberg, Lee Ann; Matalon, Sadis; Ahmad, Shama

    2015-01-01

    Inhalations of atmospheric pollutants, especially particulate matters, are known to cause severe cardiac effects and to exacerbate preexisting heart disease. Heart failure is an important sequellae of gaseous inhalation such as that of carbon monoxide. Similarly, other gases such as sulphur dioxide are known to cause detrimental cardiovascular events. However, mechanisms of these cardiac toxicities are so far unknown. Increased susceptibility of the heart to oxidative stress may play a role. Low levels of antioxidants in the heart as compared to other organs and high levels of reactive oxygen species produced due to the high energetic demand and metabolic rate in cardiac muscle are important in rendering this susceptibility. Acute inhalation of high concentrations of halogen gases is often fatal. Severe respiratory injury and distress occurs upon inhalation of halogens gases, such as chlorine and bromine; however, studies on their cardiac effects are scant. We have demonstrated that inhalation of high concentrations of halogen gases cause significant cardiac injury, dysfunction, and failure that can be critical in causing mortalities following exposures. Our studies also demonstrated that cardiac dysfunction occurs as a result of a direct insult independent of coexisting hypoxia, since it is not fully reversed by oxygen supplementation. Therefore, studies on offsite organ effects of inhaled toxic gases can impact development of treatment strategies upon accidental or deliberate exposures to these agents. Here we summarize the knowledge of cardiovascular effects of common inhaled toxic gases with the intent to highlight the importance of consideration of cardiac symptoms while treating the victims. PMID:26665179

  2. Basketball injuries.

    PubMed

    Newman, Joel S; Newberg, Arthur H

    2010-11-01

    Basketball injuries are most prevalent in the lower extremity, especially at the ankle and knee. Most basketball injuries are orthopedic in nature and commonly include ligament sprains, musculotendinous strains, and overuse injuries including stress fractures. By virtue of its excellent contrast resolution and depiction of the soft tissues and trabecular bone, magnetic resonance imaging has become the principal modality for evaluating many basketball injuries. In this article, commonly encountered basketball injuries and their imaging appearances are described. The epidemiology of basketball injuries across various age groups and levels of competition and between genders are reviewed. PMID:21094400

  3. Heart Failure

    MedlinePlus

    ... Tiredness and shortness of breath Common causes of heart failure are coronary artery disease, high blood pressure and diabetes. It is more common in people who are 65 years old or older, African Americans, people who are overweight, and people who have ...

  4. Heart Truth

    MedlinePlus

    ... about women’s risk for heart disease―the #1 killer of women in the United States―and share ... t Care What You Wear—It's the #1 Killer of Women ® are registered trademarks of U.S. ...

  5. Women's Heart Disease: Heart Attack Symptoms

    MedlinePlus

    ... this page please turn JavaScript on. Feature: Women's Heart Disease Heart Attack Symptoms Past Issues / Winter 2014 Table ... NHLBI has uncovered some of the causes of heart diseases and conditions, as well as ways to prevent ...

  6. After Heart Attack, New Threat: Heart Failure

    MedlinePlus

    ... of heart attack known as STEMI (ST elevation myocardial infarction). "Patients with ischemic heart disease are at the ... failure]. This includes those who have had a myocardial infarction, also called heart attack," Gho said. "Research studying ...

  7. Heart Health - Heart Disease: Symptoms, Diagnosis, Treatment

    MedlinePlus

    ... Bar Home Current Issue Past Issues Cover Story Heart Health Heart Disease: Symptoms, Diagnosis, Treatment Past Issues / Winter 2009 ... of this page please turn Javascript on. Most heart attacks happen when a clot in the coronary ...

  8. Heart Health: The Heart Truth Campaign 2009

    MedlinePlus

    ... Bar Home Current Issue Past Issues Cover Story Heart Health The Heart Truth Campaign 2009 Past Issues / Winter 2009 Table ... one of the celebrities supporting this year's The Heart Truth campaign. Both R&B singer Ashanti (center) ...

  9. Heart Health - Heart Disease: Symptoms, Diagnosis, Treatment

    MedlinePlus

    ... Issues Cover Story Heart Health Heart Disease: Symptoms, Diagnosis, Treatment Past Issues / Winter 2009 Table of Contents ... or both arms, the neck, jaw, or stomach. Diagnosis Key heart tests include: Electrocardiogram (ECG or EKG) — ...

  10. Transfixing cardiac injury with perforations in stomach, diaphragm and lung: unusual scenario in penetrating trauma

    PubMed Central

    Karigyo, Carlos Junior Toshiyuki; Fan, Otavio Goulart; Yoshida, Marcelo Miyazaki; Menescal, Roberto Jonathas; Tarasiewich, Marcos Jose

    2014-01-01

    A 23-year-old man suffered a penetrating injury caused by a metallic fragment thrown from a grass-cutting tool, resulting in perforating injuries in the stomach, diaphragm, heart, and lungs. PMID:24896170

  11. Spinal injury

    MedlinePlus

    ... head. Alternative Names Spinal cord injury; SCI Images Skeletal spine Vertebra, cervical (neck) Vertebra, lumbar (low back) Vertebra, thoracic (mid back) Vertebral column Central nervous system Spinal cord injury Spinal anatomy Two person roll - ...

  12. Corneal injury

    MedlinePlus

    ... as sand or dust Ultraviolet injuries: Caused by sunlight, sun lamps, snow or water reflections, or arc- ... a corneal injury if you: Are exposed to sunlight or artificial ultraviolet light for long periods of ...

  13. Inhalation Injuries

    MedlinePlus

    ... you can inhale that can cause acute internal injuries. Particles in the air from fires and toxic ... and lung diseases worse. Symptoms of acute inhalation injuries may include Coughing and phlegm A scratchy throat ...

  14. Pediatric heart surgery - discharge

    MedlinePlus

    ... reduced appetite Alternate Names Congenital heart surgery - discharge; Patent ductus arteriosus ligation - discharge; Hypoplastic left heart repair - ... of the aorta Congenital heart defect - corrective surgery Patent ductus arteriosus Pediatric heart surgery Tetralogy of Fallot ...

  15. Problem: Heart Valve Regurgitation

    MedlinePlus

    ... Pressure High Blood Pressure Tools & Resources Stroke More Problem: Heart Valve Regurgitation Updated:May 26,2016 What ... content was last reviewed May 2016. Heart Valve Problems and Disease • Home • About Heart Valves • Heart Valve ...

  16. Problem: Heart Valve Stenosis

    MedlinePlus

    ... Pressure High Blood Pressure Tools & Resources Stroke More Problem: Heart Valve Stenosis Updated:Aug 10,2016 About ... content was last reviewed May 2016. Heart Valve Problems and Disease • Home • About Heart Valves • Heart Valve ...

  17. Heart attack first aid

    MedlinePlus

    First aid - heart attack; First aid - cardiopulmonary arrest; First aid - cardiac arrest ... A heart attack occurs when the blood flow that carries oxygen to the heart is blocked. The heart muscle ...

  18. About Heart Attacks

    MedlinePlus

    ... survive. A heart attack occurs when the blood flow that brings oxygen to the heart muscle is severely reduced or ... survive. A heart attack occurs when the blood flow that brings oxygen to the heart muscle is severely reduced or ...

  19. Heart disease - resources

    MedlinePlus

    Resources - heart disease ... The following organizations are good resources for information on heart disease: American Heart Association -- www.heart.org Centers for Disease Control and Prevention -- www.cdc.gov/heartdisease

  20. What Causes Heart Block?

    MedlinePlus

    ... or inflammation of the heart muscle. Heart failure . Rheumatic (roo-MAT-ik) fever. Cardiomyopathy (KAR-de-o-mi-OP-a-the), or heart muscle diseases. Other diseases may increase the risk of heart ...

  1. Congenital heart disease

    MedlinePlus

    Congenital heart disease is a problem with the heart's structure and function that is present at birth. ... Congenital heart disease (CHD) can describe a number of different problems affecting the heart. It is the most common ...

  2. Heart CT scan

    MedlinePlus

    ... arteries to determine your risk for heart disease Congenital heart disease (heart problems that are present at birth) Problems ... Abnormal results may be due to: Aneurysm Congenital heart disease ... Narrowing of one or more coronary arteries (coronary artery ...

  3. Heart Attack Risk Assessment

    MedlinePlus

    ... Pressure Tools & Resources Stroke More Heart Attack Risk Assessment Updated:May 31,2016 We're sorry, but ... Can You Recognize a Heart Attack? Quiz Risk Assessment Patient Information Sheets: Heart Attack Heart Attack Personal ...

  4. Pediatric heart surgery

    MedlinePlus

    Heart surgery - pediatric; Heart surgery for children; Acquired heart disease; Heart valve surgery - children ... after the baby is born. For others, your child may be able to safely wait for months ...

  5. Cycling injuries.

    PubMed Central

    Cohen, G. C.

    1993-01-01

    Bicycle-related injuries have increased as cycling has become more popular. Most injuries to recreational riders are associated with overuse or improper fit of the bicycle. Injuries to racers often result from high speeds, which predispose riders to muscle strains, collisions, and falls. Cyclists contact bicycles at the pedals, seat, and handlebars. Each is associated with particular cycling injuries. Images Figure 1 Figure 3 Figure 4 Figure 5 PMID:8471908

  6. Orienteering injuries

    PubMed Central

    Folan, Jean M.

    1982-01-01

    At the Irish National Orienteering Championships in 1981 a survey of the injuries occurring over the two days of competition was carried out. Of 285 individual competitors there was a percentage injury rate of 5.26%. The article discusses the injuries and aspects of safety in orienteering. Imagesp236-ap237-ap237-bp238-ap239-ap240-a PMID:7159815

  7. Restart the heart.

    PubMed

    Klingberg, Karsten; Srivastava, David

    2016-01-01

    Early bystander cardiopulmonary resuscitation and rapid defibrillation are the most important factors for favourable outcomes after out of hospital cardiac arrest (OHCA)-as the new American Heart Association/European Resuscitation Council (AHA/ERC) guidelines emphasise. The patient in our case was a healthy young man who had a witnessed cardiac arrest due to a chest collision with the goalkeeper during a football match. Basic life support was immediately provided by his teammates until an automated external defibrillator was brought to the scene. Blunt cardiac injury (BCI) may result in injured myocardium or arrhythmias. Ventricular fibrillation due to BCI in absence of structural cardiac disease is one of the main causes of OHCA in young healthy athletes with high mortality rates. We demonstrate important aspects of the recently released guidelines on cardiac arrest and the chain of survival by the leading societies. PMID:26968838

  8. Life-threatening nail gun injuries.

    PubMed

    Beaver, A C; Cheatham, M L

    1999-12-01

    The use of pneumatic and explosive cartridge-activated nail guns is common in the construction industry. The ease and speed of nailing these tools afford enhance productivity at the cost of increased potential for traumatic injury. Although extremity injuries are most common, life-threatening injuries to the head, neck, chest, or abdomen and pelvis may occur. During a 20-month period, eight potentially life-threatening nail gun injuries were admitted to a Level I trauma center, including injuries to the brain, eye, neck, heart, lung, and femoral artery. Mechanism of injury included nail ricochet, nail gun misuse due to inadequate training, and successful suicide. Nail guns have significant potential for causing severe debilitating injury and death. These findings indicate a need for improved safety features and user education. The various types of nail guns, their ballistic potential, and techniques for operative management are discussed. PMID:10597056

  9. Heart Disease in Women

    MedlinePlus

    ... United States, 1 in 4 women dies from heart disease. In fact, coronary heart disease (CHD)—the most common type of heart ... heart information http://womenshealth.gov/publications/our-publications/fact-sheet/heart-disease.html New Heart Guidelines Released; Talk to ...

  10. Pediatric heart surgery

    MedlinePlus

    Heart surgery - pediatric; Heart surgery for children; Acquired heart disease; Heart valve surgery - children ... There are many kinds of heart defects. Some are minor, and others are more serious. Defects can occur inside the heart or in the large blood vessels ...

  11. Targeted Laser Ablation of the Zebrafish Larval Heart Induces Models of Heart Block, Valvular Regurgitation, and Outflow Tract Obstruction

    PubMed Central

    Matrone, Gianfranco; Maqsood, Sana; Taylor, Jonathan; Mullins, John J.; Tucker, Carl S.

    2014-01-01

    Abstract Mammalian models of cardiac disease have provided unique and important insights into human disease but have become increasingly challenging to produce. The zebrafish could provide inexpensive high-throughput models of cardiac injury and repair. We used a highly targeted laser, synchronized to fire at specific phases of the cardiac cycle, to induce regional injury to the ventricle, atrioventricular (AV) cushion, and bulbus arteriosus (BA). We assessed the impact of laser injury on hearts of zebrafish early larvae at 72 h postfertilization, to different regions, recording the effects on ejection fraction (EF), heart rate (HR), and blood flow at 2 and 24 h postinjury (hpi). Laser injury to the apex, midzone, and outflow regions of the ventricle resulted in reductions of the ventricle EF at 2 hpi with full recovery of function by 24 hpi. Laser injury to the ventricle, close to the AV cushion, was more likely to cause bradycardia and atrial–ventricular dysfunction, suggestive of an electrical conduction block. At 2 hpi, direct injury to the AV cushion resulted in marked regurgitation of blood from the ventricle to the atrium. Laser injury to the BA caused temporary outflow tract obstruction with cessation of ventricle contraction and circulation. Despite such damage, 80% of embryos showed complete recovery of the HR and function within 24 h of laser injury. Precision laser injury to key structures in the zebrafish developing heart provides a range of potentially useful models of hemodynamic overload, injury, and repair. PMID:25272304

  12. Transcriptional profiling of regenerating embryonic mouse hearts.

    PubMed

    Magarin, Manuela; Schulz, Herbert; Thierfelder, Ludwig; Drenckhahn, Jörg-Detlef

    2016-09-01

    The postnatal mammalian heart is considered a terminally differentiated organ unable to efficiently regenerate after injury. In contrast, we have recently shown a remarkable regenerative capacity of the prenatal heart using myocardial tissue mosaicism for mitochondrial dysfunction in mice. This model is based on inactivation of the X-linked gene encoding holocytochrome c synthase (Hccs) specifically in the developing heart. Loss of HCCS activity results in respiratory chain dysfunction, disturbed cardiomyocyte differentiation and reduced cell cycle activity. The Hccs gene is subjected to X chromosome inactivation, such that in females heterozygous for the heart conditional Hccs knockout approximately 50% of cardiac cells keep the defective X chromosome active and develop mitochondrial dysfunction while the other 50% remain healthy. During heart development the contribution of HCCS deficient cells to the cardiac tissue decreases from 50% at mid-gestation to 10% at birth. This regeneration of the prenatal heart is mediated by increased proliferation of the healthy cardiac cell population, which compensates for the defective cells allowing the formation of a fully functional heart by birth. Here we performed microarray RNA expression analyses on 13.5 dpc control and heterozygous Hccs knockout hearts to identify molecular mechanisms that drive embryonic heart regeneration. Array data have been deposited in the Gene Expression Omnibus (GEO) database under accession number GSE72054. PMID:27583204

  13. Head injury.

    PubMed

    Hureibi, K A; McLatchie, G R

    2010-05-01

    Head injury is one of the commonest injuries in sport. Most are mild but some can have serious outcomes. Sports medicine doctors should be able to recognise the clinical features and evaluate athletes with head injury. It is necessary during field assessment to recognise signs and symptoms that help in assessing the severity of injury and making a decision to return-to-play. Prevention of primary head injury should be the aim. This includes protective equipment like helmets and possible rule changes. PMID:20533694

  14. Heart Research

    NASA Technical Reports Server (NTRS)

    1991-01-01

    James Antaki and a group of researchers from the University of Pittsburgh School of Medicine used many elements of the Technology Utilization Program while looking for a way to visualize and track material points within the heart muscle. What they needed were tiny artificial "eggs" containing copper sulfate solution, small enough (about 2 mm in diameter) that they would not injure the heart, and large enough to be seen in Magnetic Resonance Imaging (MRI) images; they also had to be biocompatible and tough enough to withstand the beating of the muscle. The group could not make nor buy sufficient containers. After reading an article on microspheres in NASA Tech Briefs, and a complete set of reports on microencapsulation from the Jet Propulsion Laboratory (JPL), JPL put Antaki in touch with Dr.Taylor Wang of Vanderbilt University who helped construct the myocardial markers. The research is expected to lead to improved understanding of how the heart works and what takes place when it fails.

  15. Crosstalk between the heart and peripheral organs in heart failure

    PubMed Central

    Jahng, James Won Suk; Song, Erfei; Sweeney, Gary

    2016-01-01

    Mediators from peripheral tissues can influence the development and progression of heart failure (HF). For example, in obesity, an altered profile of adipokines secreted from adipose tissue increases the incidence of myocardial infarction (MI). Less appreciated is that heart remodeling releases cardiokines, which can strongly impact various peripheral tissues. Inflammation, and, in particular, activation of the nucleotide-binding oligomerization domain-like receptors with pyrin domain (NLRP3) inflammasome are likely to have a central role in cardiac remodeling and mediating crosstalk with other organs. Activation of the NLRP3 inflammasome in response to cardiac injury induces the production and secretion of the inflammatory cytokines interleukin (IL)-1β and IL-18. In addition to having local effects in the myocardium, these pro-inflammatory cytokines are released into circulation and cause remodeling in the spleen, kidney, skeletal muscle and adipose tissue. The collective effects of various cardiokines on peripheral organs depend on the degree and duration of myocardial injury, with systematic inflammation and peripheral tissue damage observed as HF progresses. In this article, we review mechanisms regulating myocardial inflammation in HF and the role of factors secreted by the heart in communication with peripheral tissues. PMID:26964833

  16. [Heart transplantation].

    PubMed

    Fukushima, Norihide; Matsuda, Hikaru

    2005-11-01

    While nearly 4,000 patients undergo heart transplantation (HTx) every year in the world, only 27 HTx were performed since February, 1999, because of very strict Organ Transplantation Law in Japan. All were treated with triple immunosuppressive regimen. Although two patients died of infection 4 months and 4 years after HTx, respectively, 23 were discharged and 16 returned to work or go to school. New immunosuppressive drugs, such as sirolimus and everolimus, treatment of presensitized patients before transplantation using cyclophosphamide and intravenous globulin infusion, compact implantable left ventricular assist supports and the future of pediatric HTx in Japan are discussed. PMID:16277260

  17. Isoproterenol effects evaluated in heart slices of human and rat in comparison to rat heart in vivo

    SciTech Connect

    Herrmann, Julia E.; Heale, Jason; Bieraugel, Mike; Ramos, Meg; Fisher, Robyn L.; Vickers, Alison E.M.

    2014-01-15

    Human response to isoproterenol induced cardiac injury was evaluated by gene and protein pathway changes in human heart slices, and compared to rat heart slices and rat heart in vivo. Isoproterenol (10 and 100 μM) altered human and rat heart slice markers of oxidative stress (ATP and GSH) at 24 h. In this in vivo rat study (0.5 mg/kg), serum troponin concentrations increased with lesion severity, minimal to mild necrosis at 24 and 48 h. In the rat and the human heart, isoproterenol altered pathways for apoptosis/necrosis, stress/energy, inflammation, and remodeling/fibrosis. The rat and human heart slices were in an apoptotic phase, while the in vivo rat heart exhibited necrosis histologically and further progression of tissue remodeling. In human heart slices genes for several heat shock 70 kD members were altered, indicative of stress to mitigate apoptosis. The stress response included alterations in energy utilization, fatty acid processing, and the up-regulation of inducible nitric oxide synthase, a marker of increased oxidative stress in both species. Inflammation markers linked with remodeling included IL-1α, Il-1β, IL-6 and TNFα in both species. Tissue remodeling changes in both species included increases in the TIMP proteins, inhibitors of matrix degradation, the gene/protein of IL-4 linked with cardiac fibrosis, and the gene Ccl7 a chemokine that induces collagen synthesis, and Reg3b a growth factor for cardiac repair. This study demonstrates that the initial human heart slice response to isoproterenol cardiac injury results in apoptosis, stress/energy status, inflammation and tissue remodeling at concentrations similar to that in rat heart slices. - Highlights: • Human response to isoproterenol induced cardiac injury evaluated in heart slices. • Isoproterenol altered apoptosis, energy, inflammation and remodeling pathways. • Human model verified by comparison to rat heart slices and rat heart in vivo. • Human and rat respond to isoproterenol

  18. Skiing Injuries

    PubMed Central

    Bartlett, L. H.

    1975-01-01

    In the broad spectrum of orthopedic skiing injuries, ‘second aid’ on the mountain and at the base by the physician is very important. All skiing physicians should carry minimal medical supplies, including narcotic medication. Diagnosis and treatment of injuries at the hospital are outlined. Most ski fractures of the tibia can be treated by conservative methods. A more aggressive approach to diagnosis and treatment of ligamentous injuries of the knee is recommended. PMID:20469236

  19. Gunshot injuries.

    PubMed

    Hinkle, J; Betz, S

    1995-05-01

    If current trends for this nation continue, by the year 2003 the number of people killed by firearms will exceed the number of people killed in motor vehicle accidents. Critical care practitioners must understand the mechanism of injury associated with firearm injuries to provide optimal care. This article reviews internal, exterior, and terminal ballistics, bullet design, wound classification, and initial assessment and treatment of firearm injuries. PMID:7743422

  20. Heart Health for Women

    MedlinePlus

    ... signs of a heart attack. 1. Eat a heart healthy diet. The nutrition facts on the food label can help you make ... heart health for women . (PDF 190KB) Get the facts about heart attacks in women . Learn More About Heart Disease: ...

  1. Diabetic Heart Disease

    MedlinePlus

    ... be coronary heart disease (CHD), heart failure, and diabetic cardiomyopathy. Diabetes by itself puts you at risk for heart disease. Other risk factors include Family history of heart disease Carrying extra ... Some people who have diabetic heart disease have no signs or symptoms of ...

  2. How the Heart Works

    MedlinePlus

    ... for the Public » Health Topics » How the Heart Works Explore How the Heart Works What Is... Anatomy Contraction Circulation Electrical System Heart ... Heart Disease Heart Valve Disease How the Lungs Work Send a link to NHLBI to someone by ...

  3. Rowing injuries.

    PubMed

    Rumball, Jane S; Lebrun, Constance M; Di Ciacca, Stephen R; Orlando, Karen

    2005-01-01

    Participation in the sport of rowing has been steadily increasing in recent decades, yet few studies address the specific injuries incurred. This article reviews the most common injuries described in the literature, including musculoskeletal problems in the lower back, ribs, shoulder, wrist and knee. A review of basic rowing physiology and equipment is included, along with a description of the mechanics of the rowing stroke. This information is necessary in order to make an accurate diagnosis and treatment protocol for these injuries, which are mainly chronic in nature. The most frequently injured region is the low back, mainly due to excessive hyperflexion and twisting, and can include specific injuries such as spondylolysis, sacroiliac joint dysfunction and disc herniation. Rib stress fractures account for the most time lost from on-water training and competition. Although theories abound for the mechanism of injury, the exact aetiology of rib stress fractures remains unknown. Other injuries discussed within, which are specific to ribs, include costochondritis, costovertebral joint subluxation and intercostal muscle strains. Shoulder pain is quite common in rowers and can be the result of overuse, poor technique, or tension in the upper body. Injuries concerning the forearm and wrist are also common, and can include exertional compartment syndrome, lateral epicondylitis, deQuervain's and intersection syndrome, and tenosynovitis of the wrist extensors. In the lower body, the major injuries reported include generalised patellofemoral pain due to abnormal patellar tracking, and iliotibial band friction syndrome. Lastly, dermatological issues, such as blisters and abrasions, and miscellaneous issues, such as environmental concerns and the female athlete triad, are also included in this article.Pathophysiology, mechanism of injury, assessment and management strategies are outlined in the text for each injury, with special attention given to ways to correct

  4. Epicardium-Derived Heart Repair

    PubMed Central

    Smits, Anke M.; Riley, Paul R.

    2016-01-01

    In the last decade, cell replacement therapy has emerged as a potential approach to treat patients suffering from myocardial infarction (MI). The transplantation or local stimulation of progenitor cells with the ability to form new cardiac tissue provides a novel strategy to overcome the massive loss of myocardium after MI. In this regard the epicardium, the outer layer of the heart, is a tractable local progenitor cell population for therapeutic pursuit. The epicardium has a crucial role in formation of the embryonic heart. After activation and migration into the developing myocardium, epicardial cells differentiate into several cardiac cells types. Additionally, the epicardium provides instructive signals for the growth of the myocardium and coronary angiogenesis. In the adult heart, the epicardium is quiescent, but recent evidence suggests that it becomes reactivated upon damage and recapitulates at least part of its embryonic functions. In this review we provide an update on the current knowledge regarding the contribution of epicardial cells to the adult mammalian heart during the injury response.

  5. Holes in the Heart

    MedlinePlus

    ... page from the NHLBI on Twitter. What Are Holes in the Heart? Holes in the heart are simple congenital (kon-JEN- ... the heart. However, some babies are born with holes in the upper or lower septum. A hole ...

  6. Pediatric heart surgery - discharge

    MedlinePlus

    ... discharge; Heart valve surgery - children - discharge; Heart surgery - pediatric - discharge; Heart transplant - pediatric - discharge ... Keane JF, Lock JE, Fyler DC, eds. Nadas' Pediatric Cardiology . 2nd ed. St. Louis, MO; WB Saunders; ...

  7. Right heart ventriculography

    MedlinePlus

    Angiography - right heart ... moved forward into the right side of the heart. As the catheter is advanced, the doctor can ... is injected into the right side of the heart. It helps the cardiologist determine the size and ...

  8. Left heart catheterization

    MedlinePlus

    Catheterization - left heart ... to help guide the catheters up into your heart and arteries. Dye will be injected into your ... in the blood vessels that lead to your heart. The catheter is then moved through the aortic ...

  9. What Causes Heart Failure?

    MedlinePlus

    ... the heart, leading to heart failure. High Blood Pressure Blood pressure is the force of blood pushing against the ... weaken your heart and lead to plaque buildup. Blood pressure is considered high if it stays at or ...

  10. Heart Attack Recovery FAQs

    MedlinePlus

    ... Pressure High Blood Pressure Tools & Resources Stroke More Heart Attack Recovery FAQs Updated:Aug 24,2016 Most people ... recovery. View an animation of a heart attack . Heart Attack Recovery Questions and Answers What treatments will I ...

  11. Heart Murmurs (For Kids)

    MedlinePlus

    ... than normal. You also might get an electrocardiogram (EKG), which measures electrical activity of the heart. None ... MORE ON THIS TOPIC The Heart Getting an EKG (Video) Your Heart & Circulatory System Mitral Valve Prolapse ...

  12. Congenital Heart Information Network

    MedlinePlus

    ... heart defects. Important Notice The Congenital Heart Information Network website is temporarily out of service. Please join ... and Uwe Baemayr for The Congenital Heart Information Network Exempt organization under Section 501(c)3. Copyright © ...

  13. Heart failure - home monitoring

    MedlinePlus

    ... Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice ... Cardiovascular Nursing; American Heart Association Council on Clinical ... Heart Association Council on Nutrition, Physical Activity, ...

  14. Heart failure - overview

    MedlinePlus

    ... Your heart muscle is stiff and does not fill up with blood easily. This is called diastolic heart failure. As the heart's pumping becomes less effective, blood may back up in other areas of the body. Fluid ...

  15. Heart and Down Syndrome

    MedlinePlus

    ... Associated Conditions » The Heart & Down Syndrome The Heart & Down Syndrome Abnormalities of the cardiovascular system are common in ... the Most Common Heart Defects in Children With Down Syndrome? The most common defects are Atrioventricular Septal Defect ( ...

  16. Sports Injuries

    MedlinePlus

    ... sometimes you can injure yourself when you play sports or exercise. Accidents, poor training practices, or improper gear can cause them. Some people get hurt because they are not in shape. Not warming up or stretching enough can also ... injuries are Sprains and strains Knee injuries Swollen ...

  17. Mending broken hearts: cardiac development as a basis for adult heart regeneration and repair

    PubMed Central

    Xin, Mei; Olson, Eric N.; Bassel-Duby, Rhonda

    2013-01-01

    As the adult mammalian heart has limited potential for regeneration and repair, the loss of cardiomyocytes during injury and disease can result in heart failure and death. The cellular processes and regulatory mechanisms involved in heart growth and development can be exploited to repair the injured adult heart through ‘reawakening’ pathways that are active during embryogenesis. Heart function has been restored in rodents by reprogramming non-myocytes into cardiomyocytes, by expressing transcription factors (GATA4, HAND2, myocyte-specific enhancer factor 2C (MEF2C) and T-box 5 (TBX5)) and microRNAs (miR-1, miR-133, miR-208 and miR-499) that control cardiomyocyte identity. Stimulating cardiomyocyte dedifferentiation and proliferation by activating mitotic signalling pathways involved in embryonic heart growth represents a complementary approach for heart regeneration and repair. Recent advances in understanding the mechanistic basis of heart development offer exciting opportunities for effective therapies for heart failure. PMID:23839576

  18. Rowing Injuries

    PubMed Central

    Hosea, Timothy M.; Hannafin, Jo A.

    2012-01-01

    Context: Rowing is one of the original modern Olympic sports and was one of the most popular spectator sports in the United States. Its popularity has been increasing since the enactment of Title IX. The injury patterns in this sport are unique because of the stress applied during the rowing stroke. Evidence Acquisition: This review summarizes the existing literature describing the biomechanics of the rowing stroke and rowing-related injury patterns. Data were obtained from previously published peer-reviewed literature through a search of the entire PubMed database (up to December, 2011) as well as from textbook chapters and rowing coaching manuals. Results: Rowing injuries are primarily overuse related. The knee, lumbar spine, and ribs are most commonly affected. The injury incidence is directly related to the volume of training and technique. Conclusion: Familiarity of the injury patterns and the biomechanical forces affecting the rowing athlete will aid in prompt diagnosis and appropriate management. PMID:23016093

  19. Volleyball injuries.

    PubMed

    Eerkes, Kevin

    2012-01-01

    There has been a significant increase in the numbers of people playing indoor and beach volleyball since the early 1980s and, consequently, an increase in injuries. Most injuries are related to repetitive jumping and hitting the ball overhead. The ankle is the most commonly injured joint, but the knee, shoulder, low back, and fingers also are vulnerable. The shoulder in particular is subject to extreme torque when hitting and jump serving the ball. Some injuries have a predilection for those playing on sand versus those playing in an indoor court. The clinician caring for volleyball players should be aware of the types of injuries these players sustain and how to help them return to play promptly and appropriately. This article reviews the specific injuries that are most common as a result of participating in the sport of volleyball. PMID:22965348

  20. Myocardial NF-κB activation is essential for zebrafish heart regeneration

    PubMed Central

    Karra, Ravi; Knecht, Anne K.; Kikuchi, Kazu; Poss, Kenneth D.

    2015-01-01

    Heart regeneration offers a novel therapeutic strategy for heart failure. Unlike mammals, lower vertebrates such as zebrafish mount a strong regenerative response following cardiac injury. Heart regeneration in zebrafish occurs by cardiomyocyte proliferation and reactivation of a cardiac developmental program, as evidenced by induction of gata4 regulatory sequences in regenerating cardiomyocytes. Although many of the cellular determinants of heart regeneration have been elucidated, how injury triggers a regenerative program through dedifferentiation and epicardial activation is a critical outstanding question. Here, we show that NF-κB signaling is induced in cardiomyocytes following injury. Myocardial inhibition of NF-κB activity blocks heart regeneration with pleiotropic effects, decreasing both cardiomyocyte proliferation and epicardial responses. Activation of gata4 regulatory sequences is also prevented by NF-κB signaling antagonism, suggesting an underlying defect in cardiomyocyte dedifferentiation. Our results implicate NF-κB signaling as a key node between cardiac injury and tissue regeneration. PMID:26472034

  1. Heart failure - medicines

    MedlinePlus

    CHF - medicines; Congestive heart failure - medicines; Cardiomyopathy - medicines; HF - medicines ... You will need to take most of your heart failure medicines every day. Some medicines are taken ...

  2. After Heart Attack, New Threat: Heart Failure

    MedlinePlus

    ... https://medlineplus.gov/news/fullstory_159007.html After Heart Attack, New Threat: Heart Failure 1 in 4 survivors develops this serious ... TUESDAY, May 24, 2016 (HealthDay News) -- Risk of heart failure appears high within a few years of ...

  3. Head injury - first aid

    MedlinePlus

    ... is shaken, is the most common type of traumatic brain injury. Scalp wounds. Skull fractures. Head injuries may cause ... of people who suffer head injuries are children. Traumatic brain injury (TBI) accounts for over 1 in 6 injury- ...

  4. Sequential Analysis of Autonomic Arousal and Self-Injurious Behavior

    ERIC Educational Resources Information Center

    Hoch, John; Symons, Frank; Sng, Sylvia

    2013-01-01

    There have been limited direct tests of the hypothesis that self-injurious behavior (SIB) regulates arousal. In this study, two autonomic biomarkers for physiological arousal (heart rate [HR] and the high-frequency [HF] component of heart rate variability [HRV]) were investigated in relation to SIB for 3 participants with intellectual…

  5. A new nonpenetrating ballistic injury.

    PubMed Central

    Carroll, A W; Soderstrom, C A

    1978-01-01

    A new, nonpenetrating ballistic injury mechanism involving individuals protected by soft body armor is described. Experimental studies using laboratory animals have demonstrated that despite stopping missile penetration, the heart, liver, spleen, and spinal cord are vulnerable to injury. The rapid jolting force of an impacting bullet is contrasted with the usually encountered mechanisms producing blunt trauma injury. The experimental methodology used to assess a 20% increase in survival probability and an 80% decrease in the need for surgical intervention with a new soft body armor is reviewed. Five cases of ballistic assaults on law enforcement personnel protected by soft body armor are presented. Four emphasize the potentially lifesaving qualities of the armor, while the fifth indicates the need for torso encircling design. Hospitalization should follow all assaults, regardless of the innocuous appearance of the skin lesion and the apparent well being on the assaulted individual. Therapeutic guidelines for patient management are suggested. Images Fig. 1. Fig. 2. Fig. 3. PMID:736653

  6. A new nonpenetrating ballistic injury.

    PubMed

    Carroll, A W; Soderstrom, C A

    1978-12-01

    A new, nonpenetrating ballistic injury mechanism involving individuals protected by soft body armor is described. Experimental studies using laboratory animals have demonstrated that despite stopping missile penetration, the heart, liver, spleen, and spinal cord are vulnerable to injury. The rapid jolting force of an impacting bullet is contrasted with the usually encountered mechanisms producing blunt trauma injury. The experimental methodology used to assess a 20% increase in survival probability and an 80% decrease in the need for surgical intervention with a new soft body armor is reviewed. Five cases of ballistic assaults on law enforcement personnel protected by soft body armor are presented. Four emphasize the potentially lifesaving qualities of the armor, while the fifth indicates the need for torso encircling design. Hospitalization should follow all assaults, regardless of the innocuous appearance of the skin lesion and the apparent well being on the assaulted individual. Therapeutic guidelines for patient management are suggested. PMID:736653

  7. Lightning Injuries

    MedlinePlus

    ... both chest compressions and artificial respiration. If an automated external defibrillator (AED) is available, it should be used (see Figure: Automated External Defibrillator: Jump-Starting the Heart ). A person ...

  8. Activation of EGFR/ERBB2 via Pathways Involving ERK1/2, P38 MAPK, AKT and FOXO Enhances Recovery of Diabetic Hearts from Ischemia-Reperfusion Injury

    PubMed Central

    Akhtar, Saghir; Yousif, Mariam H. M.; Chandrasekhar, Bindu; Benter, Ibrahim F.

    2012-01-01

    This study characterized the effects of diabetes and/or ischemia on epidermal growth factor receptor, EGFR, and/or erbB2 signaling pathways on cardiac function. Isolated heart perfusion model of global ischemia was used to study the effect of chronic inhibition or acute activation of EGFR/erbB2 signaling on cardiac function in a rat model of type-1 diabetes. Induction of diabetes with streptozotocin impaired recovery of cardiac function (cardiac contractility and hemodynamics) following 40 minutes of global ischemia in isolated hearts. Chronic treatment with AG825 or AG1478, selective inhibitors of erbB2 and EGFR respectively, did not affect hyperglycemia but led to an exacerbation whereas acute administration of the EGFR ligand, epidermal growth factor (EGF), led to an improvement in cardiac recovery in diabetic hearts. Diabetes led to attenuated dimerization and phosphorylation of cardiac erbB2 and EGFR receptors that was associated with reduced signaling via extracellular-signal-regulated kinase 1/2 (ERK1/2), p38 mitogen activated protein (MAP) kinase and AKT (protein kinase B). Ischemia was also associated with reduced cardiac signaling via these molecules whereas EGF-treatment opposed diabetes and/or ischemia induced changes in ERK1/2, p38 MAP kinase, and AKT-FOXO signaling. Losartan treatment improved cardiac function in diabetes but also impaired EGFR phosphorylation in diabetic heart. Co-administration of EGF rescued Losartan-mediated reduction in EGFR phosphorylation and significantly improved cardiac recovery more than with either agent alone. EGFR/erbB2 signaling is an important cardiac survival pathway whose activation, particularly in diabetes, ischemia or following treatment with drugs that inhibit this cascade, significantly improves cardiac function. These findings may have clinical relevance particularly in the treatment of diabetes-induced cardiac dysfunction. PMID:22720029

  9. Heart murmurs and other sounds

    MedlinePlus

    Chest sounds - murmurs; Heart sounds - abnormal; Murmur - innocent; Innocent murmur; Systolic heart murmur; Diastolic heart murmur ... The heart has four chambers: Two upper chambers (atria) Two lower chambers (ventricles) The heart has valves that close ...

  10. Who Needs a Heart Transplant?

    MedlinePlus

    ... from the NHLBI on Twitter. Who Needs a Heart Transplant? Most patients referred to heart transplant centers have ... for heart failure. Who Is Eligible for a Heart Transplant? The specialists at the heart transplant center will ...

  11. Corneal injury

    MedlinePlus

    ... at all times when using hand or power tools or chemicals, during high impact sports, or during other activities where you may get an eye injury. Wear sunglasses that screen ultraviolet light when you are ...

  12. Who Needs Heart Surgery?

    MedlinePlus

    ... disease (CHD) Fix heart valves that don't work well Control abnormal heart rhythms Place medical devices Replace a damaged heart with a healthy one If other treatments—such as lifestyle changes, medicines, and medical ... surgeon will work with you to decide whether you need heart ...

  13. Advanced Heart Failure

    MedlinePlus

    ... High Blood Pressure Tools & Resources Stroke More Advanced Heart Failure Updated:Oct 8,2015 When heart failure (HF) ... content was last reviewed on 04/06/2015. Heart Failure • Home • About Heart Failure • Causes and Risks for ...

  14. Broken Heart Syndrome

    MedlinePlus

    ... heart attacks are caused by blockages and blood clots forming in the coronary arteries, which supply the heart with blood. If these ... who experience broken heart syndrome have fairly normal coronary arteries, without severe blockages or clots. The heart cells are “stunned” by stress hormones ...

  15. Electric injury, Part II: Specific injuries.

    PubMed

    Fish, R M

    2000-01-01

    Electric injury can cause disruption of cardiac rhythm and breathing, burns, fractures, dislocations, rhabdomyolysis, eye and ear injury, oral and gastrointestinal injury, vascular damage, disseminated intravascular coagulation, peripheral and spinal cord injury, and Reflex Sympathetic Dystrophy. Secondary trauma from falls, fires, flying debris, and inhalation injury can complicate the clinical picture. Diagnostic and treatment considerations for electric injuries are described in this article, which is the second part of a three-part series on electric injuries. PMID:10645833

  16. Heart Procurement from a Donor on Venovenous ECMO Support.

    PubMed

    Singh, Gopal; Tsukashita, Masaki; Biscotti, Mauer; Costa, Joseph; Lambert, Daniel; Bacchetta, Matthew; Takayama, Hiroo

    2016-01-01

    We report the case of a 37-year-old woman with acute respiratory distress syndrome and became a candidate for organ donation after anoxic brain injury and was on a venovenous extracorporeal membrane oxygenation (VV-ECMO) support. On preoperative evaluation and gross examination, the donor's heart was acceptable for heart transplantation to a 62-year-old female patient with a history of nonischemic cardiomyopathy with a HeartMate II mechanical assist device. Orthotopic heart transplantation was successfully performed in the recipient. We report a case that suggests that the procurement of a heart from a donor on ECMO support can potentially expand the donor heart pool in carefully selected patients. PMID:26536537

  17. Aquatic Exercise and Heat-Related Injuries.

    ERIC Educational Resources Information Center

    Sova, Ruth

    1991-01-01

    Heat-related injuries in aquatics classes are possible, though 100 percent preventable. The article discusses heat-related syndromes; how bodies generate and dissipate heat; how elevated heart rates that burn calories differ from those that dissipate heat; and modification of exercise intensity to provide calorie-burning workouts without…

  18. Mitochondrial Metabolism in Aging Heart.

    PubMed

    Lesnefsky, Edward J; Chen, Qun; Hoppel, Charles L

    2016-05-13

    Altered mitochondrial metabolism is the underlying basis for the increased sensitivity in the aged heart to stress. The aged heart exhibits impaired metabolic flexibility, with a decreased capacity to oxidize fatty acids and enhanced dependence on glucose metabolism. Aging impairs mitochondrial oxidative phosphorylation, with a greater role played by the mitochondria located between the myofibrils, the interfibrillar mitochondria. With aging, there is a decrease in activity of complexes III and IV, which account for the decrease in respiration. Furthermore, aging decreases mitochondrial content among the myofibrils. The end result is that in the interfibrillar area, there is ≈50% decrease in mitochondrial function, affecting all substrates. The defective mitochondria persist in the aged heart, leading to enhanced oxidant production and oxidative injury and the activation of oxidant signaling for cell death. Aging defects in mitochondria represent new therapeutic targets, whether by manipulation of the mitochondrial proteome, modulation of electron transport, activation of biogenesis or mitophagy, or the regulation of mitochondrial fission and fusion. These mechanisms provide new ways to attenuate cardiac disease in elders by preemptive treatment of age-related defects, in contrast to the treatment of disease-induced dysfunction. PMID:27174952

  19. Oxidative Stress after Surgery on the Immature Heart

    PubMed Central

    Fudulu, Daniel; Angelini, Gianni

    2016-01-01

    Paediatric heart surgery is associated with increased inflammation and the production of reactive oxygen species. Use of the extracorporeal cardiopulmonary bypass during correction of congenital heart defects generates reactive oxygen species by various mechanisms: haemolysis, neutrophil activation, ischaemia reperfusion injury, reoxygenation injury, or depletion of the endogenous antioxidants. The immature myocardium is more vulnerable to reactive oxygen species because of developmental differences compared to the adult heart but also because of associated congenital heart diseases that can deplete its antioxidant reserve. Oxidative stress can be manipulated by various interventions: exogenous antioxidants, use of steroids, cardioplegia, blood prime strategies, or miniaturisation of the cardiopulmonary bypass circuit. However, it is unclear if modulation of the redox pathways can alter clinical outcomes. Further studies powered to look at clinical outcomes are needed to define the role of oxidative stress in paediatric patients. PMID:27123154

  20. Building and re-building the heart by cardiomyocyte proliferation.

    PubMed

    Foglia, Matthew J; Poss, Kenneth D

    2016-03-01

    The adult human heart does not regenerate significant amounts of lost tissue after injury. Rather than making new, functional muscle, human hearts are prone to scarring and hypertrophy, which can often lead to fatal arrhythmias and heart failure. The most-cited basis of this ineffective cardiac regeneration in mammals is the low proliferative capacity of adult cardiomyocytes. However, mammalian cardiomyocytes can avidly proliferate during fetal and neonatal development, and both adult zebrafish and neonatal mice can regenerate cardiac muscle after injury, suggesting that latent regenerative potential exists. Dissecting the cellular and molecular mechanisms that promote cardiomyocyte proliferation throughout life, deciphering why proliferative capacity normally dissipates in adult mammals, and deriving means to boost this capacity are primary goals in cardiovascular research. Here, we review our current understanding of how cardiomyocyte proliferation is regulated during heart development and regeneration. PMID:26932668

  1. Cardiorenal syndrome: a complex series of combined heart/kidney disorders.

    PubMed

    Goh, Ching Yan; Vizzi, Grazia; De Cal, Massimo; Ronco, Claudio

    2011-01-01

    Over the last decade, it has become increasingly clear that the cardiovascular and renal systems are interdependent. Primary disorders of either system have been shown to disturb the other system. As a result, a class of cardiorenal syndrome (CRS) has been identified where in a vicious cycle is established in which acute/chronic dysfunction of either the kidney or the heart exacerbates the loss of function in the other organ. The ADQI organization has proposed a classification derived from a consensus conference held in 2008. CRS is classified as a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other. The general definition has been expanded into five subtypes: CRS type 1 = acute worsening of heart function (acute heart failure-acute coronary syndrome) leading to kidney injury and/or dysfunction; CRS type 2 = chronic abnormalities in heart function (chronic heart failure-chronic heart disease) leading to kidney injury or dysfunction; CRS type 3 = acute worsening of kidney function (acute kidney injury) leading to heart injury and/or dysfunction; CRS type 4 = chronic kidney disease (chronic kidney disease) leading to heart injury, disease and/or dysfunction; and CRS type 5 = systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. A major problem with previous terminology was that it did not allow for identification of pathophysiological interactions occurring in the different types of combined heart/kidney disorders. The subdivision into different subtypes seems to provide a better approach to this syndrome. PMID:21921607

  2. Cold injuries.

    PubMed

    Long, William B; Edlich, Richard F; Winters, Kathryne L; Britt, L D

    2005-01-01

    Exposure to cold can produce a variety of injuries that occur as a result of man's inability to adapt to cold. These injuries can be divided into localized injury to a body part, systemic hypothermia, or a combination of both. Body temperature may fall as a result of heat loss by radiation, evaporation, conduction, and convection. Hypothermia or systemic cold injury occurs when the core body temperature has decreased to 35 degrees C (95 degrees F) or less. The causes of hypothermia are either primary or secondary. Primary, or accidental, hypothermia occurs in healthy individuals inadequately clothed and exposed to severe cooling. In secondary hypothermia, another illness predisposes the individual to accidental hypothermia. Hypothermia affects multiple organs with symptoms of hypothermia that vary according to the severity of cold injury. The diagnosis of hypothermia is easy if the patient is a mountaineer who is stranded in cold weather. However, it may be more difficult in an elderly patient who has been exposed to a cold environment. In either case, the rectal temperature should be checked with a low-reading thermometer. The general principals of prehospital management are to (1) prevent further heat loss, (2) rewarm the body core temperature in advance of the shell, and (3) avoid precipitating ventricular fibrillation. There are two general techniques of rewarming--passive and active. The mechanisms of peripheral cold injury can be divided into phenomena that affect cells and extracellular fluids (direct effects) and those that disrupt the function of the organized tissue and the integrity of the circulation (indirect effects). Generally, no serious damage is seen until tissue freezing occurs. The mildest form of peripheral cold injury is frostnip. Chilblains represent a more severe form of cold injury than frostnip and occur after exposure to nonfreezing temperatures and damp conditions. Immersion (trench) foot, a disease of the sympathetic nerves and blood

  3. Blast injury.

    PubMed

    de Candole, C A

    1967-01-28

    The shock wave generated by an explosion ("blast wave") may cause injury in any or all of the following: (1) direct impact on the tissues of variations in environmental pressure; (2) flying glass and other debris set in motion by it; (3) propulsion of the body. Injuries in the first category affect gas-containing organs (ears, lungs and intestines), and acute death is attributed to air forced into the coronary vessels via damaged pulmonary alveoli. It is estimated that overpressure sufficient to cause lung injury may occur up to five miles from a 20-megaton nuclear explosion. The greatest single hazard from blast is, however, flying glass, and serious wounding from this cause is possible up to 12 miles from an explosion of this magnitude. PMID:6015742

  4. Blast Injury

    PubMed Central

    de Candole, C. A.

    1967-01-01

    The shock wave generated by an explosion (“blast wave”) may cause injury in any or all of the following: (1) direct impact on the tissues of variations in environmental pressure; (2) flying glass and other debris set in motion by it; (3) propulsion of the body. Injuries in the first category affect gas-containing organs (ears, lungs and intestines), and acute death is attributed to air forced into the coronary vessels via damaged pulmonary alveoli. It is estimated that overpressure sufficient to cause lung injury may occur up to five miles from a 20-megaton nuclear explosion. The greatest single hazard from blast is, however, flying glass, and serious wounding from this cause is possible up to 12 miles from an explosion of this magnitude. PMID:6015742

  5. Spinal Cord Injury Map

    MedlinePlus

    ... on the severity of the injury. Tap this spinal column to see how the level of injury affects loss of function and control. Learn more about spinal cord injuries. A spinal cord injury affects the ...

  6. Eye Injuries at Home

    MedlinePlus

    ... Patient Stories Español Eye Health / Tips & Prevention Eye Injuries Sections Preventing Eye Injuries Recognizing and Treating Eye ... Sports Eye Injuries by the Numbers — Infographic Eye Injuries at Home Reviewed by: Brenda Pagan-Duran MD ...

  7. Cardiac injuries--a clinical and autopsy profile.

    PubMed

    Kulshrestha, P; Das, B; Iyer, K S; Sampath, K A; Sharma, M L; Rao, I M; Venugopal, P

    1990-02-01

    One hundred two patients sustaining cardiac injuries over a 4-year period were analysed to highlight the natural history of the cardiac injuries. There were 45 blunt, 36 stab, and 21 gunshot injuries. The injury involved the ventricle in 85, atrium in seven, pulmonary artery in five cases, and resulted in crush injury to the heart in the remaining five cases. Thirty-three patients (32.3%) died on the scene and 58 (56.9%) died during the transportation. Only 11 patients (10.8%) reached the hospital alive, and ten of these patients survived following thoracotomy and repair of the cardiac injury. The factors influencing the natural course of cardiac injury were analysed: 2.2% of patients with blunt cardiac trauma reached the hospital alive compared to 19.4% with stab and 14.3% with gunshot injuries; ventricular injuries had a greater prehospital mortality compared to atrial or pulmonary artery injuries; 11.3% of patients sustaining injury to right ventricle reached the hospital alive compared to 3% of those with left ventricular injuries. These data emphasize the need for rapid transport, immediate recognition, and aggressive surgical management, to make a favourable impact on the natural history of cardiac injuries. PMID:2304116

  8. Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATP-Sensitive Potassium Channel, Nitric Oxide, and Prostaglandins.

    PubMed

    Imani, Alireza; Khansari, Maryam; Azizi, Yaser; Rakhshan, Kamran; Faghihi, Mahdieh

    2015-08-01

    Postconditioning is a simple and safe strategy for cardioprotection and infarct size limitation. Our previous study showed that oxytocin (OT) exerts postconditioning effect on ischemic/reperfused isolated rat heart. The aim of this study was to investigate the involvement of OT receptor, mitochondrial ATP-sensitive potassium channel (mKATP), nitric oxide (NO) and cyclooxygenase (COX) pathways in OT postconditioning. Isolated rat hearts were divided into10 groups and underwent 30 min of regional ischemia followed by 120 min of reperfusion (n =6). In I/R (ischemia/reperfusion) group, ischemia and reperfusion were induced without any treatment. In OT group, oxytocin was perfused 5 min prior to beginning of reperfusion for 25 min. In groups 3-6, atosiban (oxytocin receptor blocker), L-NAME (N-Nitro-L-Arginine Methyl Ester, non-specific nitric oxide synthase inhibitor), 5-HD (5-hydroxydecanoate, mKATP inhibitor) and indomethacin (cyclooxygenase inhibitor) were infused prior to oxytocin administration. In others, the mentioned inhibitors were perfused prior to ischemia without oxytocin infusion. Infarct size, ventricular hemodynamic, coronary effluent, malondialdehyde (MDA) and lactate dehydrogenase (LDH) were measured at the end of reperfusion. OT perfusion significantly reduced infarct size, MDA and LDH in comparison with IR group. Atosiban, 5HD, L-NAME and indomethacin abolished the postconditioning effect of OT. Perfusion of the inhibitors alone prior to ischemia had no effect on infarct size, hemodynamic parameters, coronary effluent and biochemical markers as compared with I/R group. In conclusion, this study indicates that postconditioning effects of OT are mediated by activation of mKATP and production of NO and Prostaglandins (PGs). PMID:26545994

  9. Thioredoxin Reductase Was Nitrated in the Aging Heart After Myocardial Ischemia/Reperfusion

    PubMed Central

    Wang, Ke; Zhang, Jie; Wang, Xiaoliang; Liu, Xin; Zuo, Lin; Bai, Kehua; Shang, Jianyu; Ma, Lu; Liu, Teng; Wang, Li; Wang, Wen; Ma, Xinliang

    2013-01-01

    Abstract The age-related loss of anti-oxidant defense reduces recovery from myocardial ischemia/reperfusion injury (MI/R) in aged people. Our previous data showed that inactivation of thioredoxin (Trx) was involved in enhanced aging MI/R injury. Thioredoxin reductase (TrxR), the enzyme known to regulate Trx, is less efficient with age. The aim of the current study was to determine why TrxR activity was reduced and whether reduced TrxR activity contributed to enhanced aging MI/R injury. Both Trx and TrxR activity were decreased in the aging heart, and this difference was further amplified after MI/R. However, MI/R injury did not change TrxR expression between young and aging rats. Increased nitrogen oxide (NOx) but decreased nitric oxide (NO) bioavailability (decreased phosphorylated vasodilator-stimulated phosphoprotein) was observed in aging hearts. Peroxynitrite (ONOO−) was increased in aging hearts and was further amplified after MI/R. TrxR nitration in young and aging hearts was detected by immunoprecipitation (anti-nitrotyrosine) followed by immunoblotting (anti-TrxR). Compared with young hearts, TrxR nitration was increased in the aging hearts, and this was further intensified after MI/R. The ONOO− decomposition catalyst (FeTMPyp) reduced TrxR nitration and increased TrxR and Trx activity. More importantly, FeTMPyp attenuated the MI/R injury in aging hearts as evidenced by decreased caspase-3 and malondialdehyde (MDA) concentration and increased cardiac function. Increased ONOO− nitrated TrxR in the aging heart as a post-translational modification, which may be related to the enhanced MI/R injury of aging rats. Interventions that inhibit nitration and restore TrxR activity might be a therapy for attenuating enhanced MI/R injury in aging heart. PMID:23802942

  10. Heart failure overview

    MedlinePlus

    ... your heart contract at the same time. A defibrillator sends an electrical pulse to stop life-threatening ... heart rhythms. These people often receive an implanted defibrillator. When to Contact a Medical Professional Call your ...

  11. Overview of Heart Tumors

    MedlinePlus

    ... the heart. Most heart tumors are metastatic cancer. Did You Know... Noncancerous tumors can be as deadly ... slow the tumor's growth. Resources In This Article Did You Know 1 Did You Know... Table 2 ...

  12. Congenital heart disease

    MedlinePlus

    ... about genetic counseling and screening if you have a family history of cogenital heart disease. ... Fraser CD, Carberry KE. Congenital heart disease. In: Townsend CM ... Textbook of Cardiovascular Medicine . 10th ed. Philadelphia, PA: ...

  13. Heart failure - discharge

    MedlinePlus

    ... any drugs you may be taking for Diabetes, high blood pressure, or other medical conditions you have. ... of the arteries Heart failure - overview Heart pacemaker High blood pressure Implantable cardioverter-defibrillator Smoking - tips on ...

  14. Heart PET scan

    MedlinePlus

    Heart nuclear medicine scan; Heart positron emission tomography; Myocardial PET scan ... Udelson JE, Dilsizian V, Bonow RO. Nuclear cardiology. In: Mann DL, ... A Textbook of Cardiovascular Medicine . 10th ed. Philadelphia, ...

  15. Structure of the Heart

    MedlinePlus

    ... Central Nervous System Peripheral Nervous System Review Quiz Endocrine System Characteristics of Hormones Endocrine Glands & Their Hormones Pituitary & ... Thyroid & Parathyroid Glands Adrenal Gland Pancreas Gonads Other Endocrine Glands ... Cardiovascular System Heart Structure of the Heart Physiology of the ...

  16. Heart disease and intimacy

    MedlinePlus

    ... document from the American Heart Association and the ESC Council on Cardiovascular Nursing and Allied Professions (CCNAP). ... document from the American Heart Association and the ESC Council on Cardiovascular Nursing and Allied Professions (CCNAP). ...

  17. Right heart ventriculography

    MedlinePlus

    Angiography - right heart ... The catheter will be moved forward into the right side of the heart. As the catheter is advanced, the doctor can record pressures from the right atrium and right ventricle. Contrast material ("dye") is ...

  18. Heart Disease Risk Factors

    MedlinePlus

    ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke Prevention ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke Prevention ...

  19. Men and Heart Disease

    MedlinePlus

    ... this? Submit What's this? Submit Button Related CDC Web Sites Heart Disease Stroke High Blood Pressure Salt ... this? Submit What's this? Submit Button Related CDC Web Sites Heart Disease Stroke High Blood Pressure Salt ...

  20. Congenital Heart Defects

    MedlinePlus

    ... Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health. NIH: National Heart, Lung, and Blood Institute

  1. Hypothyroidism and Heart Disease

    MedlinePlus

    ... in Balance › Hypothyroidism and Heart Disease Fact Sheet Hypothyroidism and Heart Disease January 2014 Download PDFs English ... nervous system, body temperature, and weight. What is hypothyroidism and what are its symptoms? Hypothyroidism, also called ...

  2. Pericarditis - after heart attack

    MedlinePlus

    ... medlineplus.gov/ency/article/000166.htm Pericarditis - after heart attack To use the sharing features on this page, ... occur in the days or weeks following a heart attack. Causes Two types of pericarditis can occur after ...

  3. Adult Congenital Heart Association

    MedlinePlus

    ... survivable, manageable, yet in the routine years between infancy and adulthood, sometimes forgettable. The Adult Congenital Heart ... understand the continuum of the disease from its infancy. The Adult Congential Heart Association brings together valuable ...

  4. Types of Heart Block

    MedlinePlus

    ... Block Explore Heart Block What Is... Electrical System & EKG Results Types Causes Who Is at Risk Signs & ... the P and the R waves on the EKG (electrocardiogram). First-degree heart block may not cause ...

  5. Heart and Stroke Encyclopedia

    MedlinePlus

    ... Pressure Tools & Resources Stroke More The Heart and Stroke Encyclopedia Click a letter below to get a ... dozens of cardiovascular terms from our Heart and Stroke Encyclopedia and get links to in-depth information. ...

  6. Heart disease - risk factors

    MedlinePlus

    ... medlineplus.gov/ency/patientinstructions/000106.htm Heart disease - risk factors To use the sharing features on this ... may help you live a longer, healthier life. Risk Factors You Cannot Change Some of your heart ...

  7. Heart failure - tests

    MedlinePlus

    CHF - tests; Congestive heart failure - tests; Cardiomyopathy - tests; HF - tests ... An echocardiogram (Echo) is a test that uses sound waves to create a moving picture of the heart. The picture is much more detailed than a plain ...

  8. Heart failure - home monitoring

    MedlinePlus

    ... this page: //medlineplus.gov/ency/patientinstructions/000113.htm Heart failure - home monitoring To use the sharing features on ... body and the symptoms that tell you your heart failure is getting worse will help you stay healthier ...

  9. Getting a New Heart

    MedlinePlus

    ... is in place, the donor's main arteries—the aorta and pulmonary arteries—are sewn to yours. o ... heart and cause strokes and heart attacks. 4. Diabetes Mellitus Anti-rejection medications can cause diabetes. If ...

  10. Heart failure - discharge

    MedlinePlus

    ... a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: ... a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. ...

  11. Texas Heart Institute

    MedlinePlus

    ... Join us! James T. Willerson MD Cardiovascular Seminar Texas Heart Institute Journal Scientific Publications Library & Learning Resources ... Education 12th Annual Diabetes Symposium September 17, 2016 Texas Heart Institute Program Director: Mandeep Bajaj, MD Clinical ...

  12. Heart Rhythm Society

    MedlinePlus

    ... Search: Education & Meetings Scientific Sessions Certified Education Courses & Online Learning Heart Rhythm On Demand Co-Sponsored & Endorsed Events ... Education & Meetings less Scientific Sessions Certified Education Courses & Online Learning Heart Rhythm On Demand Co-Sponsored & Endorsed Events ...

  13. Cyanotic heart disease

    MedlinePlus

    ... or rhythms The treatment of choice for most congenital heart diseases is surgery to repair the defect . There are ... Some inherited factors may play a role in congenital heart disease. Many family members may be affected. If you ...

  14. Adult Congenital Heart Association

    MedlinePlus

    ... to ACHA Search The futures of adults with congenital heart disease made brighter by their pasts Get Involved 2016 ... conference theme is "The Changing Landscape of Adult Congenital Heart Disease." Join Us Help us improve the quality of ...

  15. Left heart catheterization

    MedlinePlus

    ... Bonow RO. Cardiac catheterization. In: Mann DL, Zipes DP, Libby P, eds. Braunwald's Heart Disease: A Textbook ... arteriography and intracoronary imaging In: Mann DL, Zipes DP, Libby P, eds. Braunwald's Heart Disease: A Textbook ...

  16. Heart and vascular services

    MedlinePlus

    ... gov/ency/article/007459.htm Heart and vascular services To use the sharing features on this page, ... blood vessels (arteries and veins). Heart and vascular services refers to the branch of medicine that focuses ...

  17. Heart bypass surgery - discharge

    MedlinePlus

    ... angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines ... Surgery. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice ...

  18. Coronary heart disease

    MedlinePlus

    ... adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice ... of the American Heart Association, American College of Cardiology, and American Society of Hypertension. Treatment of hypertension ...

  19. Heart valve surgery - discharge

    MedlinePlus

    ... summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.American College of Cardiology/American Heart Association Task Force on Practice Guidelines. ...

  20. Target Heart Rate Calculator

    MedlinePlus

    ... My Saved Articles » My ACS » + - Text Size Target Heart Rate Calculator Compute your best workout Enter your age ... is your age? years. How to Check Your Heart Rate Right after you stop exercising, take your pulse: ...

  1. Electrical Injuries

    MedlinePlus

    ... your injuries are depends on how strong the electric current was, what type of current it was, how it moved through your body, and how long you were exposed. Other factors include how ... you should see a doctor. You may have internal damage and not realize it.

  2. Inhalation Injuries

    MedlinePlus

    ... increase mortality 30% to 40% when patients with cutaneous burns and inhalation injury are compared with patients ... nasal hairs • Facial burns • Burns around the mouth • Mineral spirits – 104º F – paint thinner, brush cleaner. • Redness, ...

  3. A rigid barrier between the heart and sternum protects the heart and lungs against rupture during negative pressure wound therapy

    PubMed Central

    2011-01-01

    Objectives Right ventricular heart rupture is a devastating complication associated with negative pressure wound therapy (NPWT) in cardiac surgery. The use of a rigid barrier has been suggested to offer protection against this lethal complication, by preventing the heart from being drawn up and damaged by the sharp edges of the sternum. The aim of the present study was to investigate whether a rigid barrier protects the heart and lungs against injury during NPWT. Methods Sixteen pigs underwent median sternotomy followed by NPWT at -120 mmHg for 24 hours, in the absence (eight pigs) or presence (eight pigs) of a rigid plastic disc between the heart and the sternal edges. The macroscopic appearance of the heart and lungs was inspected after 12 and 24 hours of NPWT. Results After 24 hours of NPWT at -120 mmHg the area of epicardial petechial bleeding was 11.90 ± 1.10 cm2 when no protective disc was used, and 1.15 ± 0.19 cm2 when using the disc (p < 0.001). Heart rupture was observed in three of the eight animals treated with NPWT without the disc. Lung rupture was observed in two of the animals, and lung contusion and emphysema were seen in all animals treated with NPWT without the rigid disc. No injury to the heart or lungs was observed in the group of animals treated with NPWT using the rigid disc. Conclusion Inserting a rigid barrier between the heart and the sternum edges offers protection against heart rupture and lung injury during NPWT. PMID:21740574

  4. The zebrafish as a model of heart regeneration.

    PubMed

    Raya, Angel; Consiglio, Antonella; Kawakami, Yasuhiko; Rodriguez-Esteban, Concepcion; Izpisúa-Belmonte, Juan Carlos

    2004-01-01

    Regeneration is a complex biological process by which animals can restore the shape, structure and function of body parts lost after injury, or after experimental amputation. Only a few species of vertebrates display the capacity to regenerate body parts during adulthood. In the case of the heart, newts display a remarkable ability to regenerate large portions of myocardium after amputation, although the mechanisms underlying this process have not been addressed. Recently, it has been shown that adult zebrafish can also regenerate their hearts, thus offering new possibilities for experimentally approaching this fascinating biological phenomenon. The first insights into heart regeneration gained by studying this model organism are reviewed here. PMID:15671662

  5. Implantable Heart Aid

    NASA Technical Reports Server (NTRS)

    1984-01-01

    CPI's human-implantable automatic implantable defibrillator (AID) is a heart assist system, derived from NASA's space circuitry technology, that can prevent erratic heart action known as arrhythmias. Implanted AID, consisting of microcomputer power source and two electrodes for sensing heart activity, recognizes onset of ventricular fibrillation (VF) and delivers corrective electrical countershock to restore rhythmic heartbeat.

  6. Heart bypass surgery - discharge

    MedlinePlus

    ... Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest . 2012;141:e637S-e68S. Read More Angina Coronary heart disease Heart bypass surgery Heart failure - overview High blood cholesterol levels Smoking - ...

  7. Working Model Hearts

    ERIC Educational Resources Information Center

    Brock, David

    2009-01-01

    Despite student interest, the heart is often a poorly understood topic in biology. To help students understand this vital organ's physiology, the author created this investigation activity involving the mammalian heart and its role in the circulatory system. Students design, build, and demonstrate working artificial "hearts" to exhibit what they…

  8. The Heart of Coaching

    ERIC Educational Resources Information Center

    Docheff, Dennis M.; Gerdes, Dan

    2015-01-01

    This article challenges coaches to address the more personal, human elements of coaching--the HEART of coaching. While there is much research on numerous aspects of coaching, this article provides ideas that make a lasting impact on the hearts of athletes. Using HEART as an acronym, five elements of effective coaching are presented: Humility,…

  9. Heart bypass surgery

    MedlinePlus Videos and Cool Tools

    Heart bypass surgery begins with an incision made in the chest, with the breastbone cut exposing the heart. Next, a portion of the saphenous vein is ... used to bypass the blocked arteries in the heart. The venous graft is sewn to the aorta ...

  10. Heart Disease in Women

    MedlinePlus

    ... United States, 1 in 4 women dies from heart disease. The most common cause of heart disease in both men and women is narrowing ... the blood vessels that supply blood to the heart itself. This is called coronary artery disease, and ...

  11. Heart Valve Diseases

    MedlinePlus

    Your heart has four valves. Normally, these valves open to let blood flow through or out of your heart, and then shut to keep it from flowing ... close tightly. It's one of the most common heart valve conditions. Sometimes it causes regurgitation. Stenosis - when ...

  12. What Is Heart Surgery?

    MedlinePlus

    ... Links Related Topics Aneurysm Coronary Artery Bypass Grafting Heart Transplant Pacemakers Ventricular Assist Device Send a link to NHLBI to someone by E-MAIL | PRINT | SHARE this page from the ... Is Heart Surgery? Heart surgery is done to correct problems ...

  13. Heart bypass surgery

    MedlinePlus

    Heart bypass surgery creates a new route, called a bypass, for blood and oxygen to go around a blockage to reach your heart. ... heart is still beating. This is called off-pump coronary artery bypass, or OPCAB. To create the bypass graft: The doctor will take a ...

  14. Heart disease and depression

    MedlinePlus

    Heart disease and depression often go hand-in-hand. You are are more likely to feel sad or depressed after a heart attack ... heart disease. The good news is that treating depression may help improve both your mental and physical ...

  15. Heart Disease in Women

    MedlinePlus

    ... States, 1 in 4 women dies from heart disease. The most common cause of heart disease in both men and women is narrowing or ... the heart itself. This is called coronary artery disease, and it happens slowly over time. It's the ...

  16. How Is Heart Failure Diagnosed?

    MedlinePlus

    ... in a pocket, or hung around your neck. Nuclear Heart Scan A nuclear heart scan shows how well blood is flowing ... blood is reaching your heart muscle. During a nuclear heart scan, a safe, radioactive substance called a ...

  17. What Happens After Heart Surgery?

    MedlinePlus

    ANSWERS by heart Treatments + Tests What Happens After Heart Surgery? What are the ICU and CCU? In a ... doctors. This is where patients go after open-heart surgery or a heart attack. You’re watched around ...

  18. What Is a Heart Transplant?

    MedlinePlus

    ... from the NHLBI on Twitter. What Is a Heart Transplant? A heart transplant is surgery to remove a ... return to work for many different reasons. The Heart Transplant Process The heart transplant process starts when doctors ...

  19. Medications for Heart Valve Symptoms

    MedlinePlus

    ... Pressure Tools & Resources Stroke More Medications for Heart Valve Symptoms Updated:Aug 26,2015 How do medications ... was last reviewed on 03/26/14. Heart Valves Problems and Disease • Home • About Heart Valves • Heart ...

  20. Living with Heart Valve Disease

    MedlinePlus

    ... Clinical Trials Links Related Topics Congenital Heart Defects Endocarditis Heart Murmur How the Heart Works Mitral Valve ... your doctor if you have symptoms of infective endocarditis (IE). Symptoms of this heart infection include fever, ...

  1. Bioengineering Heart Muscle: A Paradigm for Regenerative Medicine

    PubMed Central

    Lui, Kathy O.; Tandon, Nina

    2012-01-01

    The idea of extending the lifetime of our organs is as old as humankind, fueled by major advances in organ transplantation, novel drugs, and medical devices. However, true regeneration of human tissue has becoming increasingly plausible only in recent years. The human heart has always been a focus of such efforts, given its notorious inability to repair itself following injury or disease. We discuss here the emerging bioengineering approaches to regeneration of heart muscle as a paradigm for regenerative medicine. Our focus is on biologically inspired strategies for heart regeneration, knowledge gained thus far about how to make a “perfect” heart graft, and the challenges that remain to be addressed for tissue-engineered heart regeneration to become a clinical reality. We emphasize the need for interdisciplinary research and training, as recent progress in the field is largely being made at the interfaces between cardiology, stem cell science, and bioengineering. PMID:21568715

  2. Living with Diabetic Heart Disease

    MedlinePlus

    ... Heart Disease » Living With Diabetic Heart Disease Explore Diabetic Heart Disease What Is... Causes Who Is at Risk Signs & Symptoms Diagnosis Treatments Prevention Living With Clinical Trials Links Related Topics Atherosclerosis Cardiomyopathy Coronary Heart Disease Heart Attack Heart Failure Send ...

  3. What Is Heart Valve Surgery?

    MedlinePlus

    ANSWERS by heart Treatments + Tests What Is Heart Valve Surgery? The four valves in your heart make sure that blood flows through your heart in the right direction. Heart valve surgery is done to replace or repair heart valves that Aortic ...

  4. Chronic treatment with trimetazidine reduces the upregulation of atrial natriuretic peptide in heart failure

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Trimetazidine (TMZ) is effective for the treatment of ischemic cardiomyopathy; however, little is known about the effect of TMZ in established injury-induced heart failure. When rats with established infarct-induced heart failure were treated for 12 weeks with TMZ there was no effect on left ventric...

  5. A RAT MODEL OF HEART FAILURE INDUCED BY ISOPROTERENOL AND A HIGH SALT DIET

    EPA Science Inventory

    Rat models of heart failure (HF) show varied pathology and time to disease outcome, dependent on induction method. We found that subchronic (4wk) isoproterenol (ISO) infusion in Spontaneously Hypertensive Heart Failure (SHHF) rats caused cardiac injury with minimal hypertrophy. O...

  6. Augmentation of Creatine in the Heart

    PubMed Central

    Russell, Angela J.; Lygate, Craig A.

    2015-01-01

    Creatine is a principle component of the creatine kinase (CK) phosphagen system common to all vertebrates. It is found in excitable cells, such as cardiomyocytes, where it plays an important role in the buffering and transport of chemical energy to ensure that supply meets the dynamic demands of the heart. Multiple components of the CK system, including intracellular creatine levels, are reduced in heart failure, while ischaemia and hypoxia represent acute crises of energy provision. Elevation of myocardial creatine levels has therefore been suggested as potentially beneficial, however, achieving this goal is not trivial. This mini-review outlines the evidence in support of creatine elevation and critically examines the pharmacological approaches that are currently available. In particular, dietary creatine-supplementation does not sufficiently elevate creatine levels in the heart due to subsequent down-regulation of the plasma membrane creatine transporter (CrT). Attempts to increase passive diffusion and bypass the CrT, e.g. via creatine esters, have yet to be tested in the heart. However, studies in mice with genetic overexpression of the CrT demonstrate proof-of-principle that elevated creatine protects the heart from ischaemia-reperfusion injury. This suggests activation of the CrT as a major unmet pharmacological target. However, translation of this finding to the clinic will require a greater understanding of CrT regulation in health and disease and the development of small molecule activators. PMID:26202199

  7. Augmentation of Creatine in the Heart

    PubMed Central

    Zervou, Sevasti; Whittington, Hannah J.; Russell, Angela J.; Lygate, Craig A.

    2016-01-01

    Creatine is a principle component of the creatine kinase (CK) phosphagen system common to all vertebrates. It is found in excitable cells, such as cardiomyocytes, where it plays an important role in the buffering and transport of chemical energy to ensure that supply meets the dynamic demands of the heart. Multiple components of the CK system, including intracellular creatine levels, are reduced in heart failure, while ischaemia and hypoxia represent acute crises of energy provision. Elevation of myocardial creatine levels has therefore been suggested as potentially beneficial, however, achieving this goal is not trivial. This mini-review outlines the evidence in support of creatine elevation and critically examines the pharmacological approaches that are currently available. In particular, dietary creatine-supplementation does not sufficiently elevate creatine levels in the heart due to subsequent down-regulation of the plasma membrane creatine transporter (CrT). Attempts to increase passive diffusion and bypass the CrT, e.g. via creatine esters, have yet to be tested in the heart. However, studies in mice with genetic overexpression of the CrT demonstrate proof-of-principle that elevated creatine protects the heart from ischaemia-reperfusion injury. This suggests activation of the CrT as a major unmet pharmacological target. However, translation of this finding to the clinic will require a greater understanding of CrT regulation in health and disease and the development of small molecule activators.

  8. Augmentation of Creatine in the Heart.

    PubMed

    Zervou, Sevasti; Whittington, Hannah J; Russell, Angela J; Lygate, Craig A

    2016-01-01

    Creatine is a principle component of the creatine kinase (CK) phosphagen system common to all vertebrates. It is found in excitable cells, such as cardiomyocytes, where it plays an important role in the buffering and transport of chemical energy to ensure that supply meets the dynamic demands of the heart. Multiple components of the CK system, including intracellular creatine levels, are reduced in heart failure, while ischaemia and hypoxia represent acute crises of energy provision. Elevation of myocardial creatine levels has therefore been suggested as potentially beneficial, however, achieving this goal is not trivial. This mini-review outlines the evidence in support of creatine elevation and critically examines the pharmacological approaches that are currently available. In particular, dietary creatine-supplementation does not sufficiently elevate creatine levels in the heart due to subsequent down-regulation of the plasma membrane creatine transporter (CrT). Attempts to increase passive diffusion and bypass the CrT, e.g. via creatine esters, have yet to be tested in the heart. However, studies in mice with genetic overexpression of the CrT demonstrate proof-of-principle that elevated creatine protects the heart from ischaemia-reperfusion injury. This suggests activation of the CrT as a major unmet pharmacological target. However, translation of this finding to the clinic will require a greater understanding of CrT regulation in health and disease and the development of small molecule activators. PMID:26202199

  9. Mitochondrial sirtuins in the heart.

    PubMed

    Bugger, Heiko; Witt, Constantin N; Bode, Christoph

    2016-09-01

    Sirtuins (SIRTs) are NAD(+)-dependent enzymes that catalyze deacylation of protein lysine residues. In mammals, seven sirtuins have been identified, SIRT1-7. SIRT3-5 are mainly or exclusively localized within mitochondria and mainly participate in the regulation of energy metabolic pathways. Since mitochondrial ATP regeneration is inevitably linked to the maintenance of cardiac pump function, it is not surprising that recent studies revealed a role for mitochondrial sirtuins in the regulation of myocardial energetics and function. In addition, mitochondrial sirtuins modulate the extent of myocardial ischemia reperfusion injury and the development of cardiac hypertrophy and failure. Thus, targeting mitochondrial sirtuins has been proposed as a novel approach to improve myocardial mitochondrial energetics, which is frequently impaired in cardiac disease and considered an important underlying cause contributing to several cardiac pathologies, including myocardial ischemia reperfusion injury and heart failure. In the current review, we present and discuss the available literature on mitochondrial sirtuins and their potential roles in cardiac physiology and disease. PMID:27295248

  10. Notch-independent RBPJ controls angiogenesis in the adult heart

    PubMed Central

    Díaz-Trelles, Ramón; Scimia, Maria Cecilia; Bushway, Paul; Tran, Danh; Monosov, Anna; Monosov, Edward; Peterson, Kirk; Rentschler, Stacey; Cabrales, Pedro; Ruiz-Lozano, Pilar; Mercola, Mark

    2016-01-01

    Increasing angiogenesis has long been considered a therapeutic target for improving heart function after injury such as acute myocardial infarction. However, gene, protein and cell therapies to increase microvascularization have not been successful, most likely because the studies failed to achieve regulated and concerted expression of pro-angiogenic and angiostatic factors needed to produce functional microvasculature. Here, we report that the transcription factor RBPJ is a homoeostatic repressor of multiple pro-angiogenic and angiostatic factor genes in cardiomyocytes. RBPJ controls angiogenic factor gene expression independently of Notch by antagonizing the activity of hypoxia-inducible factors (HIFs). In contrast to previous strategies, the cardiomyocyte-specific deletion of Rbpj increased microvascularization of the heart without adversely affecting cardiac structure or function even into old age. Furthermore, the loss of RBPJ in cardiomyocytes increased hypoxia tolerance, improved heart function and decreased pathological remodelling after myocardial infarction, suggesting that inhibiting RBPJ might be therapeutic for ischaemic injury. PMID:27357444

  11. [Survived stab to the heart in a schizophrenic man].

    PubMed

    Fieseler, Sybille; Zinka, Bettina; Kunz, Sebastian N

    2011-01-01

    Schizophrenia is associated with a significant risk of suicide. According to recent research, 10-15 % of all schizophrenic patients die by suicide. It is not uncommon that the victims show sharp force injuries, so that the forensic pathologist first has to differentiate between self-infliction and involvement of another person. The authors' case report presents a 68-year-old schizophrenic patient who committed suicide by jumping out of a window of his apartment located on the second floor after inflicting multiple stab wounds to his thoracic region. At autopsy, an older stab wound to the apex of the heart was detected. In the criminal investigation, a suicide attempt made 13 days before could be ascertained. As the patient did not want to be taken to a hospital at that time, the injury had never been examined or documented. Since there was no evidence suggesting homicide, the older stab to the heart was interpreted as a tentative injury. PMID:22039699

  12. Iatrogenic Transient Complete Heart Block in a Preexisting LBBB

    PubMed Central

    Kalamkar, Prachi; Bonnet, Christopher A.; Bajwa, Omer A.

    2016-01-01

    Catheter induced cardiac arrhythmia is a well-known complication encountered during pulmonary artery or cardiac catheterization. Injury to the cardiac conducting system often involves the right bundle branch which in a patient with preexisting left bundle branch block can lead to fatal arrhythmia including asystole. Such a complication during central venous cannulation is rare as it usually does not enter the heart. The guide wire or the cannula itself can cause such an injury during central venous cannulation. The length of the guide wire, its rigidity, and lack of set guidelines for its insertion make it theoretically more prone to cause such an injury. We report a case of LBBB that went into transient complete heart block following guide wire insertion during a central venous cannulation procedure. PMID:27478653

  13. Heart transplantation: review

    PubMed Central

    Mangini, Sandrigo; Alves, Bárbara Rubim; Silvestre, Odílson Marcos; Pires, Philippe Vieira; Pires, Lucas José Tachotti; Curiati, Milena Novaes Cardoso; Bacal, Fernando

    2015-01-01

    ABSTRACT Heart transplantation is currently the definitive gold standard surgical approach in the treatment of refractory heart failure. However, the shortage of donors limits the achievement of a greater number of heart transplants, in which the use of mechanical circulatory support devices is increasing. With well-established indications and contraindications, as well as diagnosis and treatment of rejection through defined protocols of immunosuppression, the outcomes of heart transplantation are very favorable. Among early complications that can impact survival are primary graft failure, right ventricular dysfunction, rejection, and infections, whereas late complications include cardiac allograft vasculopathy and neoplasms. Despite the difficulties for heart transplantation, in particular, the shortage of donors and high mortality while on the waiting list, in Brazil, there is a great potential for both increasing effective donors and using circulatory assist devices, which can positively impact the number and outcomes of heart transplants. PMID:26154552

  14. Tachycardia | Fast Heart Rate

    MedlinePlus

    ... Prevention & Treatment of High Blood Pressure High Blood Pressure Tools & Resources ... signals in the heart's upper chambers fire abnormally, which interferes with electrical signals coming from ...

  15. Heart Rate Monitors

    NASA Technical Reports Server (NTRS)

    1990-01-01

    Under a NASA grant, Dr. Robert M. Davis and Dr. William M. Portnoy came up with a new type of electrocardiographic electrode that would enable long term use on astronauts. Their invention was an insulated capacitive electrode constructed of a thin dielectric film. NASA subsequently licensed the electrode technology to Richard Charnitski, inventor of the VersaClimber, who founded Heart Rate, Inc., to further develop and manufacture personal heart monitors and to produce exercise machines using the technology for the physical fitness, medical and home markets. Same technology is on both the Home and Institutional Model VersaClimbers. On the Home Model an infrared heart beat transmitter is worn under exercise clothing. Transmitted heart rate is used to control the work intensity on the VersaClimber using the heart rate as the speedometer of the exercise. This offers advantages to a full range of users from the cardiac rehab patient to the high level physical conditioning of elite athletes. The company manufactures and markets five models of the 1*2*3 HEART RATE monitors that are used wherever people exercise to accurately monitor their heart rate. Company is developing a talking heart rate monitor that works with portable headset radios. A version of the heart beat transmitter will be available to the manufacturers of other aerobic exercise machines.

  16. Mitochondrial respiratory control and early defects of oxidative phosphorylation in the failing human heart.

    PubMed

    Lemieux, Hélène; Semsroth, Severin; Antretter, Herwig; Höfer, Daniel; Gnaiger, Erich

    2011-12-01

    Heart failure is a consequence of progressive deterioration of cardiac performance. Little is known about the role of impaired oxidative phosphorylation in the progression of the disease, since previous studies of mitochondrial injuries are restricted to end-stage chronic heart failure. The present study aimed at evaluating the involvement of mitochondrial dysfunction in the development of human heart failure. We measured the control of oxidative phosphorylation with high-resolution respirometry in permeabilized myocardial fibres from donor hearts (controls), and patients with no or mild heart failure but presenting with heart disease, or chronic heart failure due to dilated or ischemic cardiomyopathy. The capacity of the phosphorylation system exerted a strong limitation on oxidative phosphorylation in the human heart, estimated at 121 pmol O(2)s(-1)mg(-1) in the healthy left ventricle. In heart disease, a specific defect of the phosphorylation system, Complex I-linked respiration, and mass-specific fatty acid oxidation were identified. These early defects were also significant in chronic heart failure, where the capacities of the oxidative phosphorylation and electron transfer systems per cardiac tissue mass were decreased with all tested substrate combinations, suggesting a decline of mitochondrial density. Oxidative phosphorylation and electron transfer system capacities were higher in ventricles compared to atria, but the impaired mitochondrial quality was identical in the four cardiac chambers of chronic heart failure patients. Coupling was preserved in heart disease and chronic heart failure, in contrast to the mitochondrial dysfunction observed after prolonged cold storage of cardiac tissue. Mitochondrial defects in the phosphorylation system, Complex I respiration and mass-specific fatty acid oxidation occurred early in the development of heart failure. Targeting these mitochondrial injuries with metabolic therapy may offer a promising approach to delay

  17. Nerve Injuries in Athletes.

    ERIC Educational Resources Information Center

    Collins, Kathryn; And Others

    1988-01-01

    Over a two-year period this study evaluated the condition of 65 athletes with nerve injuries. These injuries represent the spectrum of nerve injuries likely to be encountered in sports medicine clinics. (Author/MT)

  18. Traumatic Brain Injury

    MedlinePlus

    ... Center PTACs Workspaces Log-in Search for: Traumatic Brain Injury A legacy resource from NICHCY Disability Fact ... in her. Back to top What is Traumatic Brain Injury? A traumatic brain injury (TBI) is an ...

  19. Eye Injuries at Work

    MedlinePlus

    ... Bureau of Labor Statistics, more than 20,000 workplace eye injuries happen each year. Injuries on the job often ... Occupational Safety and Health Administration (OSHA) reports that workplace eye injuries cost an estimated $300 million a year in ...

  20. Head injury. Second edition

    SciTech Connect

    Cooper, P.R.

    1987-01-01

    This book contains 22 chapters. Some of the chapter titles are: Radiographic Evaluation; Epidemiology of Head Injury; Emergency Care and Initial Evaluation; Skull Fracture and Traumatic Cerebrospinal Fluid Fistulas; Mild Head Injury; and Injuries of the Cranial Nerves.

  1. Traumatic Brain Injury

    MedlinePlus

    Traumatic brain injury (TBI) happens when a bump, blow, jolt, or other head injury causes damage to the brain. Every year, millions of people in the U.S. suffer brain injuries. More than half are bad enough that ...

  2. Spinal injury - resources

    MedlinePlus

    Resources - spinal injury ... The following organizations are good resources for information on spinal injury : National Institute of Neurological Disorders and Stroke -- www.ninds.nih.gov The National Spinal Cord Injury ...

  3. Wounds and Injuries

    MedlinePlus

    An injury is damage to your body. It is a general term that refers to harm caused by accidents, ... millions of people injure themselves every year. These injuries range from minor to life-threatening. Injuries can ...

  4. The effect of Ligustrum delavayanum on isolated perfused rat heart

    PubMed Central

    Stankovičová, Tatiana; Frýdl, Miroslav; Kubicová, Mária; Baróniková, Slávka; Nagy, Milan; Grančai, Daniel; Švec, Pavel

    2001-01-01

    BACKGROUND: Extract of ligustrum leaves (Ligustrum delavayanum Hariot [Oleaceae]) is well known in traditional Chinese medicine. One of the active components, oleuropein, displays vasodilating and hypotensive effects. OBJECTIVE: To analyze the effect of 0.008% lyophilized extract of ligustrum dissolved in 0.5% ethanol on heart function. ANIMALS AND METHODS: Experiments were done on isolated rat hearts perfused by the Langendorff method in control conditions and during ischemic-reperfusion injury. RESULTS: Application of ligustrum induced positive inotropic and vasodilating effects in spontaneously beating hearts. Pretreatment of the hearts with ligustrum reduced left ventricular diastolic pressure measured during reperfusion and improved left ventricular contraction compared with hearts without any pretreatment. Ligustrum significantly suppressed the incidence and duration of cardiac reperfusion arrhythmias, expressed as G-score, from 7.40±0.58 in nontreated rats to 1.97±0.50. DISCUSSION: Application of ligustrum or ethanol alone induced changes in coordination between atria and ventricles during ischemia-reperfusion injury. The ‘g-score’, a new parameter summing the incidence and duration of atrioventricular blocks, atrioventricular dissociation and cardiac arrest, is introduced. The g-scores with ligustrum pretreatment were higher during ischemia than during reperfusion. Ethanol significantly depressed myocardial contractility and coronary flow, and nonsignificantly decreased heart rate of isolated rat hearts. Electrical changes observed during coronary reperfusion in the presence of ethanol were accompanied by deterioration of contractile function. CONCLUSIONS: Ligustrum had a significant protective effect on rat myocardium against ischemic-reperfusion injury. Ethanol partially attenuated the protective effect of ligustrum. PMID:20428448

  5. Basketball Injuries: An Overview.

    ERIC Educational Resources Information Center

    Apple Jr., David F.

    1988-01-01

    This article discusses reasons for the increase in basketball-related injuries, describes common injuries, outlines steps for diagnosis and treatment, and offers recovery and prevention strategies. (IAH)

  6. Perioperative lung injury.

    PubMed

    Slinger, Peter

    2008-03-01

    Patients are at risk for several types of lung injury in the perioperative period. These injuries include atelectasis, pneumonia, pneumothorax, bronchopleural fistula, acute lung injury and acute respiratory distress syndrome. Anesthetic management can cause, exacerbate or ameliorate most of these injuries. Clinical research trends show that traditional protocols for perioperative mechanical ventilation, using large tidal volumes without positive end-expiratory pressure (PEEP) can cause a sub-clinical lung injury and this injury becomes clinically important when any additional lung injury is added. Lung-protective ventilation strategies using more physiologic tidal volumes and appropriate levels of PEEP can decrease the extent of this injury. PMID:18494396

  7. Dimensional analysis of heart rate variability in heart transplant recipients

    SciTech Connect

    Zbilut, J.P.; Mayer-Kress, G.; Geist, K.

    1987-01-01

    We discuss periodicities in the heart rate in normal and transplanted hearts. We then consider the possibility of dimensional analysis of these periodicities in transplanted hearts and problems associated with the record.

  8. Relaxin' the Heart: A Novel Therapeutic Modality.

    PubMed

    Raleigh, Juan M Valle; Toldo, Stefano; Das, Anindita; Abbate, Antonio; Salloum, Fadi N

    2016-07-01

    The peptide hormone relaxin has traditionally been linked to the maternal adaptation of the cardiovascular system during the first trimester of pregnancy. By promoting nitric oxide formation through different molecular signaling events, relaxin has been proposed as a pleiotropic and cardioprotective hormone in the setting of many cardiovascular diseases. In fact, preclinical studies were able to demonstrate that relaxin promotes vasodilatation and angiogenesis, ameliorates ischemia/reperfusion injury, and regulates extracellular matrix turnover and remodeling. In the RELAX-AHF phase 3 clinical trial, serelaxin (recombinant human relaxin) was shown to be safe, and it exerted survival benefits in patients with acute heart failure. RELAX-AHF-2 is currently ongoing, and it aims to address a larger population and evaluate harder clinical outcomes. Besides heart failure, acute myocardial infarction, peripheral arterial disease, and stable coronary disease could be target diseases for treatment with serelaxin in future clinical trials. PMID:26589290

  9. The stressed heart

    SciTech Connect

    Legato, M.J. )

    1987-01-01

    This book contains 16 papers. Some of the titles are: Regulation of gene expression in the normal and overloaded heart; Cell stress and the initiation of growth; Subcellular growth of cardiocytes during hypertrophy; Microcirculation is the stressed heart; and The biochemistry of myocardial failure.

  10. Inflammation and Heart Disease

    MedlinePlus

    ... Health • Watch, Learn & Live Animations Library Answers by Heart Fact Sheets Learn and live with our downloadable patient information sheets . Dozens of topics in a question-and-answer format that's brief, easy to follow and easy to read. ... Sodium and Salt 3 All About Heart Rate (Pulse) 4 What are the Symptoms of ...

  11. Heart imaging method

    DOEpatents

    Collins, H. Dale; Gribble, R. Parks; Busse, Lawrence J.

    1991-01-01

    A method for providing an image of the human heart's electrical system derives time-of-flight data from an array of EKG electrodes and this data is transformed into phase information. The phase information, treated as a hologram, is reconstructed to provide an image in one or two dimensions of the electrical system of the functioning heart.

  12. Mapping the Heart

    ERIC Educational Resources Information Center

    Hulse, Grace

    2012-01-01

    In this article, the author describes how her fourth graders made ceramic heart maps. The impetus for this project came from reading "My Map Book" by Sara Fanelli. This book is a collection of quirky, hand-drawn and collaged maps that diagram a child's world. There are maps of her stomach, her day, her family, and her heart, among others. The…

  13. Heart transplant - slideshow

    MedlinePlus

    ... this page: //medlineplus.gov/ency/presentations/100086.htm Heart transplant - series To use the sharing features on this ... A.M. Editorial team. Related MedlinePlus Health Topics Heart Transplantation A.D.A.M., Inc. is accredited by ...

  14. The total artificial heart

    PubMed Central

    Cook, Jason A.; Shah, Keyur B.; Quader, Mohammed A.; Cooke, Richard H.; Kasirajan, Vigneshwar; Rao, Kris K.; Smallfield, Melissa C.; Tchoukina, Inna

    2015-01-01

    The total artificial heart (TAH) is a form of mechanical circulatory support in which the patient’s native ventricles and valves are explanted and replaced by a pneumatically powered artificial heart. Currently, the TAH is approved for use in end-stage biventricular heart failure as a bridge to heart transplantation. However, with an increasing global burden of cardiovascular disease and congestive heart failure, the number of patients with end-stage heart failure awaiting heart transplantation now far exceeds the number of available hearts. As a result, the use of mechanical circulatory support, including the TAH and left ventricular assist device (LVAD), is growing exponentially. The LVAD is already widely used as destination therapy, and destination therapy for the TAH is under investigation. While most patients requiring mechanical circulatory support are effectively treated with LVADs, there is a subset of patients with concurrent right ventricular failure or major structural barriers to LVAD placement in whom TAH may be more appropriate. The history, indications, surgical implantation, post device management, outcomes, complications, and future direction of the TAH are discussed in this review. PMID:26793338

  15. Heart failure - palliative care

    MedlinePlus

    Chronic heart failure very often gets worse over time. Many people who have heart failure die of ... failure to take in enough calories and nutrients. Wasting of muscles and weight loss are part of the natural disease process. It can help to eat several small ...

  16. Coronary Heart Disease

    MedlinePlus

    ... by Mail Close www.diabetes.org > Living With Diabetes > Treatment and Care > Women Share: Print Page Text Size: A A ... heart-and-circulation, In this section Living With Diabetes Treatment and Care Women Coronary Heart Disease Sexual Health Women and ...

  17. Heart transplant - series (image)

    MedlinePlus

    ... The main problem, as with other transplants, is graft rejection. If rejection can be controlled, then survival can ... major problems are the same all major organ transplants face: a shortage of donor hearts rejection of the transplanted heart cost of the surgery ...

  18. Theory of heart

    SciTech Connect

    Glass, L. . Dept. of Physiology); Hunter, P. . Dept. of Engineering Science); McCulloch, A. )

    1991-01-01

    In recent years there has been a growth in interest in studying the heart from the perspective of the physical sciences: mechanics, fluid flow, electromechanics. This volume is the result of a workshop held in July 1989 at the Institute for Nonlinear Sciences at the University of California at San Diego that brought together scientists and clinicians with graduate students and postdoctoral fellows who share an interest in the heart. The chapters were prepared by the invited speakers as didactic reviews of their subjects but also include up-to-date results in their fields. Topics covered include the structure, mechanical properties, and function of the heart and the myocardium, electrical activity of the heart and myocardium, and mathematical models of heart function. Individual chapters are abstracted separately.

  19. Heart murmurs and other sounds

    MedlinePlus

    Chest sounds - murmurs; Heart sounds - abnormal; Murmur - innocent; Innocent murmur; Systolic heart murmur; Diastolic heart murmur ... classified ("graded") depending on how loud the murmur sounds with a stethoscope. The grading is on a ...

  20. Heart failure - fluids and diuretics

    MedlinePlus

    ... Clinical Cardiology; American Heart Association Council on Nutrition, Physical Activity, and Metabolism; American Heart Association Interdisciplinary Council on Quality of Care and Outcomes Research. State of the science: promoting self-care in persons with heart failure: ...

  1. Angioplasty and stent - heart - discharge

    MedlinePlus

    ... discharge; PTCA - discharge; Percutaneous transluminal coronary angioplasty - discharge; Heart artery dilatation - discharge ... the blood vessels that supply blood to your heart. You may have had a heart attack or ...

  2. Data and Statistics: Heart Failure

    MedlinePlus

    ... this? Submit What's this? Submit Button Related CDC Web Sites Heart Disease Stroke High Blood Pressure Salt ... to Prevent and Control Chronic Diseases Million Hearts® Web Sites with More Information About Heart Failure For ...

  3. Signs of a Heart Attack

    MedlinePlus

    ... attack Heart Health and Stroke Signs of a heart attack Related information Make the Call. Don't Miss ... to top More information on Signs of a heart attack Read more from womenshealth.gov Make the Call, ...

  4. Congenital heart defect - corrective surgery

    MedlinePlus

    ... born with one or more heart defects has congenital heart disease . Surgery is needed if the defect could harm ... 2008 Guidelines for the Management of Adults with Congenital Heart Disease: a report of the American College of Cardiology/ ...

  5. What Causes Heart Valve Disease?

    MedlinePlus

    ... Clinical Trials Links Related Topics Congenital Heart Defects Endocarditis Heart Murmur How the Heart Works Mitral Valve ... This rare but serious infection is called infective endocarditis . The germs can enter the bloodstream through needles, ...

  6. Lifestyle Changes for Heart Failure

    MedlinePlus

    ... about Alcohol and Heart Disease . Avoiding or limiting caffeine Consume only a moderate amount of caffeine per day, no more than a cup or two of coffee. Learn more about Caffeine and Heart Disease . Eating a heart-healthy diet ...

  7. Heart to heart - a custodian journal on grassroots ergonomics

    SciTech Connect

    Zalk, D. M., LLNL

    1998-03-04

    When we first requested to speak at the American Society of Safety Engineer`s Professional Development Conference in Seattle, Washington, the theme we had in mind for this program paper was quite different. It definitely was not anything like our title, `Heart to Heart` implies. It was more formal and traditional. Give you figures, diagrams and the like. But two years later, we have come to another conclusion, to tell you the story about how a group of custodians and health & safety professionals dreamed big dreams and they came true. In order to understand what occurred, we first need to start at the very beginning with the Custodian Quality Improvement Team (CQIT). This group had been formed by the Plant Engineering Department at the Lawrence Livermore National Laboratory (LLNL) located in Livermore, California. LLNL is operated by the University of California for The U.S.Department of Energy. It is the premier applied physics research laboratory in the world. Plant Engineering (PE) is much like a Public Works Department. PE has all of the crafts, such as plumbers and electricians, who do maintenance-type work, as well as the engineering and construction employees. PE maintain the utilities, constructs new buildings and takes care of old ones. They take of the roads and clean the buildings and landscape the campus. So the Custodian Shop and its some 150 employees is a member of the PE family so to speak. The CQIT had decided to investigate ways they could reduce the number of injuries they were having. They invited health and safety professionals, David Zalk (an Industrial Hygienist) and Jack Tolley (Safety Engineer) to consult with them about this. They are both Hazards Control Team 4 members at LLNL. They were both interested in ergonomics and suggested that an approach to reducing their injuries might lie in studying how the custodians actually do their work. David has extensive training in ergonomics, and Jack simply had a long-time interest in ergonomics for

  8. Acute kidney injury.

    PubMed

    Patschan, Daniel; Müller, Gerhard Anton

    2015-01-01

    Acute kidney injury is a frequent and serious complication in hospitalized patients. Mortality rates have not substantially been decreased during the last 20 years. In most patients AKI results from transient renal hypoperfusion or ischemia. The consequences include tubular cell dysfunction/damage, inflammation of the organ, and post-ischemic microvasculopathy. The two latter events perpetuate kidney damage in AKI. Clinical manifestations result from diminished excretion of water, electrolytes, and endogenous / exogenous waste products. Patients are endangered by cardiovascular complications such as hypertension, heart failure, and arrhythmia. In addition, the whole organism may be affected by systemic toxification (uremia). The diagnostic approach in AKI involves several steps with renal biopsy inevitable in some patients. The current therapy focuses on preventing further kidney damage and on treatment of complications. Different pharmacological strategies have failed to significantly improve prognosis in AKI. If dialysis treatment becomes mandatory, intermittent and continuous renal replacement therapies are equally effective. Thus, new therapies are urgently needed in order to reduce short- and long-term outcome in AKI. In this respect, stem cell-based regimens may offer promising perspectives. PMID:25618438

  9. Acute kidney injury

    PubMed Central

    Müller, Gerhard Anton

    2015-01-01

    Abstract: Acute kidney injury is a frequent and serious complication in hospitalized patients. Mortality rates have not substantially been decreased during the last 20 years. In most patients AKI results from transient renal hypoperfusion or ischemia. The consequences include tubular cell dysfunction/damage, inflammation of the organ, and post-ischemic microvasculopathy. The two latter events perpetuate kidney damage in AKI. Clinical manifestations result from diminished excretion of water, electrolytes, and endogenous / exogenous waste products. Patients are endangered by cardiovascular complications such as hypertension, heart failure, and arrhythmia. In addition, the whole organism may be affected by systemic toxification (uremia). The diagnostic approach in AKI involves several steps with renal biopsy inevitable in some patients. The current therapy focuses on preventing further kidney damage and on treatment of complications. Different pharmacological strategies have failed to significantly improve prognosis in AKI. If dialysis treatment becomes mandatory, intermittent and continuous renal replacement therapies are equally effective. Thus, new therapies are urgently needed in order to reduce short- and long-term outcome in AKI. In this respect, stem cell-based regimens may offer promising perspectives. PMID:25618438

  10. Lymphocytes and ischemia-reperfusion injury.

    PubMed

    Linfert, Douglas; Chowdhry, Tayseer; Rabb, Hamid

    2009-01-01

    Ischemia reperfusion injury (IRI) is a common and important clinical problem in many different organ systems, including kidney, brain, heart, liver, lung, and intestine. IRI occurs during all deceased donor organ transplants. IRI is a highly complex cascade of events that includes interactions between vascular endothelium, interstitial compartments, circulating cells, and numerous biochemical entities. It is well established that the innate immune system, such as complement, neutrophils, cytokines, chemokines, and macrophages participate in IRI. Recent data demonstrates an important role for lymphocytes, particularly T cells but also B cells in IRI. Lymphocytes not only participate in augmenting injury responses after IRI, but could also be playing a protective role depending on the cell type and stage of injury. Furthermore, lymphocytes appear to be participating in the healing response from IRI. These new data open the possibility for lymphocyte targeted therapeutics to improve the short and long term outcomes from IRI. PMID:19027612

  11. Angioplasty and stent placement - heart

    MedlinePlus

    ... angioplasty; Coronary artery angioplasty; Percutaneous transluminal coronary angioplasty; Heart artery dilatation ... to carefully guide the catheter up into your heart and arteries. Dye will be injected into your ...

  12. Targeting the Innate Immune Response to Improve Cardiac Graft Recovery after Heart Transplantation: Implications for the Donation after Cardiac Death.

    PubMed

    Toldo, Stefano; Quader, Mohammed; Salloum, Fadi N; Mezzaroma, Eleonora; Abbate, Antonio

    2016-01-01

    Heart transplantation (HTx) is the ultimate treatment for end-stage heart failure. The number of patients on waiting lists for heart transplants, however, is much higher than the number of available organs. The shortage of donor hearts is a serious concern since the population affected by heart failure is constantly increasing. Furthermore, the long-term success of HTx poses some challenges despite the improvement in the management of the short-term complications and in the methods to limit graft rejection. Myocardial injury occurs during transplantation. Injury initiated in the donor as result of brain or cardiac death is exacerbated by organ procurement and storage, and is ultimately amplified by reperfusion injury at the time of transplantation. The innate immune system is a mechanism of first-line defense against pathogens and cell injury. Innate immunity is activated during myocardial injury and produces deleterious effects on the heart structure and function. Here, we briefly discuss the role of the innate immunity in the initiation of myocardial injury, with particular focus on the Toll-like receptors and inflammasome, and how to potentially expand the donor population by targeting the innate immune response. PMID:27322252

  13. Targeting the Innate Immune Response to Improve Cardiac Graft Recovery after Heart Transplantation: Implications for the Donation after Cardiac Death

    PubMed Central

    Toldo, Stefano; Quader, Mohammed; Salloum, Fadi N.; Mezzaroma, Eleonora; Abbate, Antonio

    2016-01-01

    Heart transplantation (HTx) is the ultimate treatment for end-stage heart failure. The number of patients on waiting lists for heart transplants, however, is much higher than the number of available organs. The shortage of donor hearts is a serious concern since the population affected by heart failure is constantly increasing. Furthermore, the long-term success of HTx poses some challenges despite the improvement in the management of the short-term complications and in the methods to limit graft rejection. Myocardial injury occurs during transplantation. Injury initiated in the donor as result of brain or cardiac death is exacerbated by organ procurement and storage, and is ultimately amplified by reperfusion injury at the time of transplantation. The innate immune system is a mechanism of first-line defense against pathogens and cell injury. Innate immunity is activated during myocardial injury and produces deleterious effects on the heart structure and function. Here, we briefly discuss the role of the innate immunity in the initiation of myocardial injury, with particular focus on the Toll-like receptors and inflammasome, and how to potentially expand the donor population by targeting the innate immune response. PMID:27322252

  14. Electrical Injury-Induced Complete Atrioventricular Block: Is Permanent Pacemaker Required?

    PubMed Central

    Beton, Osman; Efe, Tolga Han; Kaya, Hakki; Bilgin, Murat; Dinc Asarcikli, Lale; Yilmaz, Mehmet Birhan

    2015-01-01

    A considerable percentage of electrical injuries occur as a result of work activities. Electrical injury can lead to various cardiovascular disorders: acute myocardial necrosis, myocardial ischemia, heart failure, arrhythmias, hemorrhagic pericarditis, acute hypertension with peripheral vasospasm, and anomalous, nonspecific ECG alterations. Ventricular fibrillation is the most common arrhythmia resulting from electrical injury and is the leading cause of death in electrical (especially low voltage alternating current) injury cases. Asystole, premature ventricular contractions, ventricular tachycardia, conduction disorders (various degrees of heart blocks, bundle-brunch blocks), supraventricular tachycardia, and atrial fibrillation are the other arrhythmic complications of electrical injury. Complete atrioventricular block has rarely been reported and permanent pacemaker was required for the treatment in some of these cases. Herein, we present a case of reversible complete atrioventricular block due to low voltage electrical injury in a young electrical technician. PMID:26839721

  15. Head Injuries in Children

    ERIC Educational Resources Information Center

    Pennington, Nicole

    2010-01-01

    School nurses play a crucial role in injury prevention and initial treatment when injuries occur at school. The role of school nurses includes being knowledgeable about the management of head injuries, including assessment and initial treatment. The school nurse must be familiar with the outcomes of a head injury and know when further evaluation…

  16. Thoracic injuries in professional rugby players: mechanisms of injury and imaging characteristics.

    PubMed

    Hayashi, Daichi; Roemer, Frank W; Kohler, Ryan; Guermazi, Ali; Gebers, Chris; De Villiers, Richard

    2014-07-01

    Professional rugby players are prone to traumatic thoracic injuries due to the use of minimal protective gear to cover the torso. In the 2007 Rugby World Cup, thoracic injuries occurred at a rate of 8.3 cases/1000 player-hours. CT and MRI play an important role in the diagnosis of these injuries. Vital internal organs, such as the heart, lungs, trachea, liver and large blood vessels lie within close proximity to the bony structures and what seems to be a simple rib fracture or clavicular dislocation can have potentially life-threatening complications that are not detected by conventional radiography. Cross-sectional imaging helps to determine the choice of treatment. Ultrasound offers a quick and dynamic imaging examination and allows high-resolution assessment of superficial tissues that complements conventional imaging. In this review article, we (1) presented data on incidence of thoracic injuries in professional rugby players; (2) described the anatomy of the joints comprising the thoracic cage and major muscles attached to the rib cage; (3) discussed indications and relevance for MRI and presented an optimised MRI protocol for assessment of suspected thoracic injury; and (4) illustrated various types of thoracic injuries seen in professional rugby players, including sternal contusion, retrosternal haematoma, manubriosternal disruption, sternoclavicular dislocation, rib fractures and injuries of the pectoralis major muscle. PMID:23962879

  17. Heart rate turbulence.

    PubMed

    Cygankiewicz, Iwona

    2013-01-01

    Heart rate turbulence (HRT) is a baroreflex-mediated biphasic reaction of heart rate in response to premature ventricular beats. Heart rate turbulence is quantified by: turbulence onset (TO) reflecting the initial acceleration of heart rate following premature beat and turbulence slope (TS) describing subsequent deceleration of heart rate. Abnormal HRT identifies patients with autonomic dysfunction or impaired baroreflex sensitivity due to variety of disorders, but also may reflect changes in autonomic nervous system induced by different therapeutic modalities such as drugs, revascularization, or cardiac resynchronization therapy. More importantly, impaired HRT has been shown to identify patients at high risk of all-cause mortality and sudden death, particularly in postinfarction and congestive heart failure patients. It should be emphasized that abnormal HRT has a well-established role in stratification of postinfarction and heart failure patients with relatively preserved left ventricular ejection fraction. The ongoing clinical trials will document whether HRT can be used to guide implantation of cardioverter-defibrillators in this subset of patients, not covered yet by ICD guidelines. This review focuses on the current state-of-the-art knowledge regarding clinical significance of HRT in detection of autonomic dysfunction and regarding the prognostic significance of this parameter in predicting all-cause mortality and sudden death. PMID:24215748

  18. Heart antibodies in cardiomyopathies.

    PubMed Central

    Trueman, T; Thompson, R A; Cummins, P; Littler, W A

    1981-01-01

    The reported frequency of circulating heart reactive antibodies in cardiomyopathies has varied and their significance is unknown. In this study such antibodies were sought in patients with primary congestive and hypertrophic cardiomyopathies and other heart diseases. Standard "single sandwich" and the more sensitive "double sandwich" indirect immunofluorescence techniques failed to disclose a significant difference between any cardiomyopathic group and controls in repeated experiments. With both techniques results were subject to considerable method-specific artefacts and observer variation. No published work associating heart antibodies detected by immunofluorescence methods with cariomyopathies adequately takes these into account. PMID:7028058

  19. Biomarkers of acute kidney injury and associations with short- and long-term outcomes

    PubMed Central

    Schaub, Jennifer A.; Parikh, Chirag R.

    2016-01-01

    Acute kidney injury is strongly associated with increased mortality and other adverse outcomes. Medical researchers have intensively investigated novel biomarkers to predict short- and long-term outcomes of acute kidney injury in many patient care settings, such as cardiac surgery, intensive care units, heart failure, and transplant. Future research should focus on leveraging this relationship to improve enrollment for clinical trials of acute kidney injury. PMID:27239295

  20. Pediatric Hand Injuries.

    PubMed

    Sullivan, Matthew A; Cogan, Charles J; Adkinson, Joshua M

    2016-01-01

    Pediatric hand injuries are extremely common. Although many hand injuries are adequately managed in the emergency department, some may need evaluation and treatment by a pediatric hand surgeon to ensure a good functional outcome. This article discusses the diagnosis and management of the most common pediatric hand maladies: fingertip injuries/amputation, tendon injuries, and phalangeal and metacarpal fractures. The plastic surgery nurse should be familiar with hand injuries that require intervention to facilitate efficient management and optimal postoperative care. PMID:27606586

  1. Heart to Heart Art: Empowering Homeless Children and Youth

    ERIC Educational Resources Information Center

    Shepard, Jerri; Booth, Deborah

    2009-01-01

    This article describes Heart to Heart Art, an after-school program developed for homeless children and youth at the YWCA in Spokane, Washington. Pre-service teacher candidates from a local university create meaningful activities that engage homeless students in visual art, music, drama, cooking, and community service. Heart to Heart Art was…

  2. Smoking Thickens Heart Wall, Leading to Heart Failure: Study

    MedlinePlus

    ... medlineplus.gov/news/fullstory_160932.html Smoking Thickens Heart Wall, Leading to Heart Failure: Study The more you smoke and the ... Sept. 13, 2016 (HealthDay News) -- Smoking leads to heart failure by causing thickened heart walls and reducing ...

  3. Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury

    PubMed Central

    Wu, Dongdong; Wang, Jun; Li, Hui; Xue, Mengzhou; Ji, Ailing; Li, Yanzhang

    2015-01-01

    Ischemia-reperfusion (I/R) injury is one of the major causes of high morbidity, disability, and mortality in the world. I/R injury remains a complicated and unresolved situation in clinical practice, especially in the field of solid organ transplantation. Hydrogen sulfide (H2S) is the third gaseous signaling molecule and plays a broad range of physiological and pathophysiological roles in mammals. H2S could protect against I/R injury in many organs and tissues, such as heart, liver, kidney, brain, intestine, stomach, hind-limb, lung, and retina. The goal of this review is to highlight recent findings regarding the role of H2S in I/R injury. In this review, we present the production and metabolism of H2S and further discuss the effect and mechanism of H2S in I/R injury. PMID:26064416

  4. Total Artificial Heart Implantation after Excision of Right Ventricular Angiosarcoma.

    PubMed

    Bruckner, Brian A; Abu Saleh, Walid K; Al Jabbari, Odeaa; Copeland, Jack G; Estep, Jerry D; Loebe, Matthias; Reardon, Michael J

    2016-06-01

    Primary cardiac sarcomas, although rare, are aggressive and lethal, requiring thorough surgical resection and adjuvant chemotherapy for the best possible outcome. We report the case of a 32-year-old woman who underwent total artificial heart implantation for right-sided heart failure caused by right ventricular angiosarcoma. For the first several weeks in intensive care, the patient recovered uneventfully. However, a postoperative liver biopsy indicated hepatocellular injury consistent with preoperative chemotherapy. She developed continuing liver failure, from which she died despite good cardiac function. PMID:27303244

  5. Multimodality imaging of foreign bodies in and around the heart.

    PubMed

    Illman, Jeffery E; Maleszewski, Joseph J; Byrne, Suzanne C; Gotway, Michael B; Kligerman, Seth J; Foley, Thomas A; Young, Phillip M; Bois, John P; Malik, Neera; Morris, Jonathan M; Araoz, Philip A

    2016-05-01

    Foreign objects are occasionally seen on computed tomography and could pose a diagnostic challenge to the radiologist and clinicians. It is important to recognize, characterize and localize these objects and determine their clinical significance. Most foreign objects in and around the heart are the result of direct penetrating injury or represent venous embolization to the heart. Foreign objects may cause symptoms and require prompt medical attention or maybe asymptomatic. Clinicians should be familiar with foreign objects that are encountered and understand treatment options. This paper looks at some of foreign objects that can be found and correlates with pathology where possible. PMID:27139781

  6. Total Artificial Heart Implantation after Excision of Right Ventricular Angiosarcoma

    PubMed Central

    Abu Saleh, Walid K.; Al Jabbari, Odeaa; Copeland, Jack G.; Estep, Jerry D.; Loebe, Matthias; Reardon, Michael J.

    2016-01-01

    Primary cardiac sarcomas, although rare, are aggressive and lethal, requiring thorough surgical resection and adjuvant chemotherapy for the best possible outcome. We report the case of a 32-year-old woman who underwent total artificial heart implantation for right-sided heart failure caused by right ventricular angiosarcoma. For the first several weeks in intensive care, the patient recovered uneventfully. However, a postoperative liver biopsy indicated hepatocellular injury consistent with preoperative chemotherapy. She developed continuing liver failure, from which she died despite good cardiac function. PMID:27303244

  7. Heart Murmurs and Your Child (For Parents)

    MedlinePlus

    ... Story" 5 Things to Know About Zika & Pregnancy Heart Murmurs and Your Child KidsHealth > For Parents > Heart ... to know how the heart works. How the Heart Works The normal heart has four chambers and ...

  8. Keeping Hearts Pumping

    NASA Technical Reports Server (NTRS)

    2002-01-01

    A collaboration between NASA, Dr. Michael DeBakey, Dr. George Noon, and MicroMed Technology, Inc., resulted in a life-saving heart pump for patients awaiting heart transplants. The MicroMed DeBakey VAD functions as a "bridge to heart transplant" by pumping blood throughout the body to keep critically ill patients alive until a donor heart is available. Weighing less than 4 ounces and measuring 1 inch by 3 inches, the pump is approximately one-tenth the size of other currently marketed pulsatile VADs. This makes it less invasive and ideal for smaller adults and children. Because of the pump's small size, less than 5 percent of the patients implanted developed device-related infections. It can operate up to 8 hours on batteries, giving patients the mobility to do normal, everyday activities.The MicroMed DeBakey VAD is a registered trademark of MicroMed Technology, Inc.

  9. Heart valve surgery

    MedlinePlus

    Valve replacement; Valve repair; Heart valve prosthesis; Mechanical valves, Prosthetic valves ... place. The main types of new valves are: Mechanical -- made of man-made materials, such as metal ( ...

  10. Heart PET scan

    MedlinePlus

    ... nuclear medicine scan; Heart positron emission tomography; Myocardial PET scan ... A PET scan requires a small amount of radioactive material (tracer). This tracer is given through a vein (IV), ...

  11. Heart bypass surgery

    MedlinePlus

    ... slow this process down, including: Not smoking Eating a heart-healthy diet Getting regular exercise Treating high blood pressure Controlling high blood sugar (if you have diabetes) and high cholesterol

  12. Heart valve surgery

    MedlinePlus

    ... occur, but this is rare. There is always a risk of infection. Talk to your doctor before having any type of medical procedure. The clicking of mechanical heart valves may be heard in the chest. This is normal.

  13. Heart, front view (image)

    MedlinePlus

    ... the heart. The vessels colored blue indicate the transport of blood with relatively low content of oxygen ... carbon dioxide. The vessels colored red indicate the transport of blood with relatively high content of oxygen ...

  14. Heart bypass surgery

    MedlinePlus Videos and Cool Tools

    ... of this great vein will be used to bypass the blocked arteries in the heart. The venous graft is sewn to the aorta and to the affected coronary artery past the blocked site. The internal mammary ...

  15. Heart Diseases and Disorders

    MedlinePlus

    ... very fast, but steady, heartbeat. Sick Sinus Syndrome ( SSS ) Sick sinus syndrome is not a disease, but ... the sinus node, is not working properly. In SSS , the heart rate can alternate between slow ( bradycardia ) ...

  16. Types of Heart Failure

    MedlinePlus

    ... to be made. Here we delve into the importance of shared decision making. This content was last ... heart failure. Popular Articles 1 Understanding Blood Pressure Readings 2 Sodium and Salt 3 Low Blood Pressure ...

  17. Classes of Heart Failure

    MedlinePlus

    ... to be made. Here we delve into the importance of shared decision making. HF Resources For Life ... heart failure. Popular Articles 1 Understanding Blood Pressure Readings 2 Sodium and Salt 3 Low Blood Pressure ...

  18. Heart failure - medicines

    MedlinePlus

    ACE inhibitors (angiotensin converting enzyme inhibitors) and ARBs (angiotensin II receptor blockers) work by opening blood vessels and lowering blood pressure. These medicines can: Reduce the work your heart has to do Help ...

  19. Target Heart Rates

    MedlinePlus

    ... a Healthy Heart Healthy Kids Our Kids Programs Childhood Obesity What is childhood obesity? Overweight in Children BMI in Children Is Childhood Obesity an Issue in Your Home? Addressing your Child's ...

  20. Alcohol and Heart Health

    MedlinePlus

    ... a Healthy Heart Healthy Kids Our Kids Programs Childhood Obesity What is childhood obesity? Overweight in Children BMI in Children Is Childhood Obesity an Issue in Your Home? Addressing your Child's ...

  1. Protein and Heart Health

    MedlinePlus

    ... a Healthy Heart Healthy Kids Our Kids Programs Childhood Obesity What is childhood obesity? Overweight in Children BMI in Children Is Childhood Obesity an Issue in Your Home? Addressing your Child's ...

  2. Caffeine and Heart Disease

    MedlinePlus

    ... a Healthy Heart Healthy Kids Our Kids Programs Childhood Obesity What is childhood obesity? Overweight in Children BMI in Children Is Childhood Obesity an Issue in Your Home? Addressing your Child's ...

  3. Meditation and Heart Health

    MedlinePlus

    ... a Healthy Heart Healthy Kids Our Kids Programs Childhood Obesity What is childhood obesity? Overweight in Children BMI in Children Is Childhood Obesity an Issue in Your Home? Addressing your Child's ...

  4. Stress and Heart Health

    MedlinePlus

    ... a Healthy Heart Healthy Kids Our Kids Programs Childhood Obesity What is childhood obesity? Overweight in Children BMI in Children Is Childhood Obesity an Issue in Your Home? Addressing your Child's ...

  5. Heart attack first aid

    MedlinePlus

    First aid - heart attack; First aid - cardiopulmonary arrest; First aid - cardiac arrest ... of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 ...

  6. Anatomy of the Heart

    MedlinePlus

    ... upper chambers, the right and left atria (AY-tree-uh), are shown in purple. The heart's lower chambers, the right and left ventricles (VEN-trih-kuls), are shown in red. Some of the main blood vessels (arteries and ...

  7. Heart valve surgery - discharge

    MedlinePlus

    ... Aspirin or clopidogrel (Plavix) or another blood thinner Warfarin (Coumadin). If you are taking warfarin, you will need to have regular blood tests. ... Instructions Aspirin and heart disease Clopidogrel (Plavix) Taking warfarin (Coumadin, Jantoven) - what to ask your doctor Taking ...

  8. Picturing the Heart

    MedlinePlus

    ... Information You are here Home » SCIENCE EDUCATION SCIENCE EDUCATION SCIENCE EDUCATION Science Topics Resource Links for General Public Resource ... Links for Students Glossary Picturing the Heart SCIENCE EDUCATION Science Topics Resource Links for General Public Resource ...

  9. American Heart Association

    MedlinePlus

    ... American Heart area Search by State SELECT YOUR LANGUAGE Español (Spanish) 简体中文 (Traditional Chinese) 繁体中文 (Simplified Chinese) Tiếng Việt (Vietnamese) Healthy Living Conditions Caregiver ...

  10. Stress and your heart

    MedlinePlus

    Coronary heart disease - stress; Coronary artery disease - stress ... Your body responds to stress on many levels. First, it releases stress hormones that make you breathe faster. Your blood pressure goes up. Your muscles ...

  11. Heart Truth for Latinas

    MedlinePlus

    ... for about a fifth. Latinas also have high rates of some factors that increase the risk of developing heart disease, such as diabetes, overweight and obesity, and physical inactivity. But there’s good news too: ...

  12. Is Heart Rate a Norepiphenomenon in Heart Failure?

    PubMed

    Hensey, Mark; O'Neill, James

    2016-09-01

    There has been an increased focus on heart rate as a target in the management of cardiovascular disease and more specifically in heart failure with preserved ejection fraction in recent years with several studies showing the benefit of a lower resting heart rate on outcomes. This review paper examines the pathophysiology behind the benefits of lowering heart rate in heart failure and also the evidence for and against the pharmacological agents available to achieve this. PMID:27457085

  13. Optical imaging of irradiated and non-irradiated hearts (Conference Presentation)

    NASA Astrophysics Data System (ADS)

    Bolin, Stephanie; Chen, Guanchu; Medhora, Meetha M.; Camara, Amadou K. S.; Ranji, Mahsa

    2016-03-01

    Objective: In this study, the metabolic state of the heart tissue is studied in a rodent model of ischemia and reperfusion (IR) in rats exposed to irradiation injury using a cryofluorescence imaging technique. Mitochondrial metabolic state is evaluated by autofluorescence of mitochondrial metabolic coenzymes NADH and FAD. The redox ratio (NADH/FAD) is used as a biochemical/metabolic marker of oxidative stress, before, during and after IR. Materials and methods: Hearts were extracted from non-irradiated (control) and irradiated rats (Irr) given 15 Gy whole thorax irradiation rats (WTI). After 35 days, before the onset of radiation pneumonitis, these two groups of hearts were subjected to one of three treatments; Time control (TC; hearts perfused for the duration of the protocol without ischemia or IR), 25 minutes ischemia with no reperfusion and 25 minutes ischemia followed by 60 minutes reperfusion (IR). Hearts were removed from the Langendorff perfusion system and immediately snap frozen in liquid N2 to preserve the metabolic state after injury; 3-dimensional (3D) cryo-fluorescent imager was used to obtain in fixed time NADH and FAD fluorescence images and their distribution across the entire ventricles. In this study, a 30-μm axial resolution was used resulting in 550 cross-section images per heart. The 3D images of the redox ratio and their respective histograms were calculated in the six groups of hearts. Results: We compared the mean values of the redox ratio in each group, which demonstrate a reduced mitochondrial redox state in both irradiated and non-irradiated ischemic hearts and an oxidized mitochondrial redox state for both irradiated and non-irradiated ischemia-reperfusion hearts compared to control hearts. For non-irradiated hearts, ischemia and IR injuries resulted respectively in 61% increase and 54% decrease in redox ratio when compared with TC. For irradiated hearts, ischemia and IR injuries resulted respectively in 90% increase and 50% decrease

  14. Music and the heart.

    PubMed

    Koelsch, Stefan; Jäncke, Lutz

    2015-11-21

    Music can powerfully evoke and modulate emotions and moods, along with changes in heart activity, blood pressure (BP), and breathing. Although there is great heterogeneity in methods and quality among previous studies on effects of music on the heart, the following findings emerge from the literature: Heart rate (HR) and respiratory rate (RR) are higher in response to exciting music compared with tranquilizing music. During musical frissons (involving shivers and piloerection), both HR and RR increase. Moreover, HR and RR tend to increase in response to music compared with silence, and HR appears to decrease in response to unpleasant music compared with pleasant music. We found no studies that would provide evidence for entrainment of HR to musical beats. Corresponding to the increase in HR, listening to exciting music (compared with tranquilizing music) is associated with a reduction of heart rate variability (HRV), including reductions of both low-frequency and high-frequency power of the HRV. Recent findings also suggest effects of music-evoked emotions on regional activity of the heart, as reflected in electrocardiogram amplitude patterns. In patients with heart disease (similar to other patient groups), music can reduce pain and anxiety, associated with lower HR and lower BP. In general, effects of music on the heart are small, and there is great inhomogeneity among studies with regard to methods, findings, and quality. Therefore, there is urgent need for systematic high-quality research on the effects of music on the heart, and on the beneficial effects of music in clinical settings. PMID:26354957

  15. Heart Rate Monitor

    NASA Technical Reports Server (NTRS)

    1984-01-01

    In the mid 70's, NASA saw a need for a long term electrocardiographic electrode suitable for use on astronauts. Heart Rate Inc.'s insulated capacitive electrode is constructed of thin dielectric film applied to stainless steel surface, originally developed under a grant by Texas Technical University. HRI, Inc. was awarded NASA license and continued development of heart rate monitor for use on exercise machines for physical fitness and medical markets.

  16. Congenital Heart Defects and CCHD

    MedlinePlus

    ... heart. Heart valves. These open and close to control blood flow to and from the heart. Arteries and veins. Arteries are blood vessels that carry blood away from the heart to the body. Veins are blood vessels that carry blood from ...

  17. How Is Heart Failure Treated?

    MedlinePlus

    ... have surgery or as a long-term treatment. Heart transplant . A heart transplant is an operation in which a person’s diseased ... with a healthy heart from a deceased donor. Heart transplants are done as a life-saving measure for ...

  18. Devices in Heart Failure

    PubMed Central

    Munir, Shahzeb M.; Bogaev, Roberta C.; Sobash, Ed; Shankar, K. J.; Gondi, Sreedevi; Stupin, Igor V.; Robertson, Jillian; Brewer, M. Alan; Casscells, S. Ward; Delgado, Reynolds M.; Ahmed, Amany

    2008-01-01

    Congestive heart failure has long been one of the most serious medical conditions in the United States; in fact, in the United States alone, heart failure accounts for 6.5 million days of hospitalization each year. One important goal of heart-failure therapy is to inhibit the progression of congestive heart failure through pharmacologic and device-based therapies. Therefore, there have been efforts to develop device-based therapies aimed at improving cardiac reserve and optimizing pump function to meet metabolic requirements. The course of congestive heart failure is often worsened by other conditions, including new-onset arrhythmias, ischemia and infarction, valvulopathy, decompensation, end-organ damage, and therapeutic refractoriness, that have an impact on outcomes. The onset of such conditions is sometimes heralded by subtle pathophysiologic changes, and the timely identification of these changes may promote the use of preventive measures. Consequently, device-based methods could in the future have an important role in the timely identification of the subtle pathophysiologic changes associated with congestive heart failure. PMID:18612451

  19. Ophthalmic thermal injuries.

    PubMed

    Lipshy, K A; Wheeler, W E; Denning, D E

    1996-06-01

    Reflex lid closure often protects the eyes during facial burns. Although corneal burns are uncommon, other ophthalmic injuries occur more frequently. Ophthalmic burns are usually associated with marked facial damage and possible inhalation injury. Failure to recognize and appropriately treat ophthalmic burns can lead to catastrophic sequelae. We performed a 2-year survey of all facial burns in our burn unit. Forty-four patients with thermal facial burns were identified. Sixteen patients had ophthalmic injuries. Corneal injury was detected in 13 per cent (2/16). Intubation was required in 43.75 per cent (7/16) of patients with ophthalmic injuries. Mortality was 25 per cent (4/16). We conclude that patients with facial burns severe enough to cause ophthalmic injuries may be associated with other lethal injuries, and a high index of suspicion should be maintained until all lethal injuries are ruled out. All ophthalmic injuries should be evaluated by an ophthalmologist. PMID:8651533

  20. Cardioprotection in ischaemia–reperfusion injury: novel mechanisms and clinical translation

    PubMed Central

    Altamirano, Francisco; Wang, Zhao V; Hill, Joseph A

    2015-01-01

    Abstract In recent decades, robust successes have been achieved in conquering the acutely lethal manifestations of heart disease. Nevertheless, the prevalence of heart disease, especially heart failure, continues to rise. Among the precipitating aetiologies, ischaemic disease is a leading cause of heart failure. In the context of ischaemia, the myocardium is deprived of oxygen and nutrients, which elicits a cascade of events that provokes cell death. This ischaemic insult is typically coupled with reperfusion, either spontaneous or therapeutically imposed, wherein blood supply is restored to the previously ischaemic tissue. While this intervention limits ischaemic injury, it triggers a new cascade of events that is also harmful, viz. reperfusion injury. In recent years, novel insights have emerged regarding mechanisms of ischaemia–reperfusion injury, and some hold promise as targets of therapeutic relevance. Here, we review a select number of these pathways, focusing on recent discoveries and highlighting prospects for therapeutic manipulation for clinical benefit. PMID:26173176

  1. The continuing evolution of the Langendorff and ejecting murine heart: new advances in cardiac phenotyping

    PubMed Central

    Liao, Ronglih; Podesser, Bruno K.

    2012-01-01

    The isolated retrograde-perfused Langendorff heart and the isolated ejecting heart have, over many decades, resulted in fundamental discoveries that form the underpinnings of our current understanding of the biology and physiology of the heart. These two experimental methodologies have proven invaluable in studying pharmacological effects on myocardial function, metabolism, and vascular reactivity and in the investigation of clinically relevant disease states such as ischemia-reperfusion injury, diabetes, obesity, and heart failure. With the advent of the genomics era, the isolated mouse heart preparation has gained prominence as an ex vivo research tool for investigators studying the impact of gene modification in the intact heart. This review summarizes the historical development of the isolated heart and provides a practical guide for the establishment of the Langendorff and ejecting heart preparations with a particular emphasis on the murine heart. In addition, current applications and novel methods of recording cardiovascular parameters in the isolated heart preparation will be discussed. With continued advances in methodological recordings, the isolated mouse heart preparation will remain physiologically relevant for the foreseeable future, serving as an integral bridge between in vitro assays and in vivo approaches. PMID:22636675

  2. Neuropathophysiology of Brain Injury.

    PubMed

    Quillinan, Nidia; Herson, Paco S; Traystman, Richard J

    2016-09-01

    Every year in the United States, millions of individuals incur ischemic brain injury from stroke, cardiac arrest, or traumatic brain injury. These acquired brain injuries can lead to death or long-term neurologic and neuropsychological impairments. The mechanisms of ischemic and traumatic brain injury that lead to these deficiencies result from a complex interplay of interdependent molecular pathways, including excitotoxicity, acidotoxicity, ionic imbalance, oxidative stress, inflammation, and apoptosis. This article reviews several mechanisms of brain injury and discusses recent developments. Although much is known from animal models of injury, it has been difficult to translate these effects to humans. PMID:27521191

  3. Cardiac arrhythmias associated with spinal cord injury

    PubMed Central

    Hector, Sven Magnus; Biering-Sørensen, Tor; Krassioukov, Andrei; Biering-Sørensen, Fin

    2013-01-01

    Context/Objectives To review the current literature to reveal the incidence of cardiac arrhythmias and its relation to spinal cord injury (SCI). Methods Data source: MEDLINE database, 304 hits, and 32 articles were found to be relevant. The relevant articles all met the inclusion criteria: (1) contained original data (2) on cardiac arrhythmias (3) in humans with (4) traumatic SCI. Results In the acute phase of SCI (1–14 days after injury) more cranial as well as more severe injuries seemed to increase the incidence of bradycardia. Articles not covering the first 14 days after injury, thus describing the chronic phase of SCI, showed that individuals with SCI did not have a higher incidence of cardiac arrhythmias compared with able-bodied controls. Furthermore, their heart rate did not differ significantly. Penile vibro-stimulation was the procedure investigated most likely to cause bradycardia, which in turn was associated with episodes of autonomic dysreflexia. The incidence of bradycardia was found to be 17–77% for individuals with cervical SCI. For individuals with thoracolumbar SCI, the incidence was 0–13%. Conclusion Bradycardia was commonly seen in the acute stage after SCI as well as during procedures such as penile vibro-stimulation and tracheal suction. These episodes of bradycardia were seen more often in individuals with cervical injuries. Longitudinal studies with continuous electrocardiogram recordings are needed to uncover the true relation between cardiac arrhythmias and SCI. PMID:24090076

  4. Heart Alterations after Domoic Acid Administration in Rats

    PubMed Central

    Vieira, Andres C.; Cifuentes, José Manuel; Bermúdez, Roberto; Ferreiro, Sara F.; Castro, Albina Román; Botana, Luis M.

    2016-01-01

    Domoic acid (DA) is one of the best known marine toxins, causative of important neurotoxic alterations. DA effects are documented both in wildlife and experimental assays, showing that this toxin causes severe injuries principally in the hippocampal area. In the present study we have addressed the long-term toxicological effects (30 days) of DA intraperitoneal administration in rats. Different histological techniques were employed in order to study DA toxicity in heart, an organ which has not been thoroughly studied after DA intoxication to date. The presence of DA was detected by immunohistochemical assays, and cellular alterations were observed both by optical and transmission electron microscopy. Although histological staining methods did not provide any observable tissue damage, transmission electron microscopy showed several injuries: a moderate lysis of myofibrils and loss of mitochondrial conformation. This is the first time the association between heart damage and the presence of the toxin has been observed. PMID:26978401

  5. Applying the Principles of Homicide by Heart Attack.

    PubMed

    Hlavaty, Leigh; Sung, LokMan

    2016-06-01

    Homicide by heart attack is a well-established model in forensic pathology that describes death elicited during or immediately after a criminal act where a threat or fear of physical injury is present. After its introduction nearly 4 decades ago, the principle has undergone a handful of modifications but still maintains its core concepts. All cases of this nature during a 20-year period at the Wayne County Medical Examiner's Office were compared and contrasted for demographics, circumstances and scene investigation, and autopsy and toxicology findings. Of the cases fulfilling the previously established criteria for homicide by heart attack, more than 80% displayed significant changes because of hypertension. This finding coincides with the high prevalence of hypertension in our urban population and highlights the significance of this disease. Also present were minor external and internal injuries in select cases, which reinforce the understanding that physical contact between the decedent and assailant does not preclude this diagnosis. PMID:27049661

  6. Incidence of syndesmotic injury.

    PubMed

    Vosseller, J Turner; Karl, John W; Greisberg, Justin K

    2014-03-01

    Injury to the tibiofibular syndesmosis can occur with ankle sprain or fracture. The incidence of syndesmotic injury has not been specifically studied at a population level. Data on syndesmotic injury were obtained from the Healthcare Cost and Utilization Project (HCUP), a federal-state-private partnership. It is administered by the Agency for Healthcare Research and Quality, a division of the US Department of Health and Human Services. Two HCUP databases were queried for 8 states: the State Inpatient Database and the State Emergency Department Database. The first 6 International Classification of Diseases, Ninth Edition (ICD-9) code diagnoses were searched for codes that are used for syndesmotic injury (ie, 845.03). These data, along with data from the 2010 US census, were used to yield incidence rates for syndesmosis injury, as well as for various demographic groups. National estimates of injury totals were also calculated. In the 8 states, there were a total of 1821 syndesmotic injuries. Given the population of these states, the incidence rate of syndesmotic injury was 2.09 syndesmotic injuries per 100,000 person-years. This incidence correlates to an estimated 6445 syndesmotic injuries per year in the United States. These data provide some baseline numbers as to the incidence of syndesmotic injury in the United States. Although the incidence was low relative to some other injuries, the fact that syndesmotic injuries tend to occur in younger patients may have a greater effect in terms of productive years of life lost. PMID:24762148

  7. Hand Injuries and Disorders

    MedlinePlus

    ... the wrist, often making your fingers feel numb Injuries that result in fractures, ruptured ligaments and dislocations ... deformity Tendinitis - irritation of the tendons Disorders and injuries of your fingers and thumb

  8. Rotator Cuff Injuries

    MedlinePlus

    ... cuff are common. They include tendinitis, bursitis, and injuries such as tears. Rotator cuff tendons can become ... cuff depends on age, health, how severe the injury is, and how long you've had the ...

  9. What Are Sports Injuries?

    MedlinePlus

    ... 06:02 Size: 11.7 MB November 2014 What Are Sports Injuries? Fast Facts: An Easy-to- ... Research Is Being Done on Treating Sports Injuries? What’s the Difference Between an Acute and a Chronic ...

  10. Head injury - first aid

    MedlinePlus

    ... medlineplus.gov/ency/article/000028.htm Head injury - first aid To use the sharing features on this page, ... a concussion can range from mild to severe. First Aid Learning to recognize a serious head injury and ...

  11. Head Injury Prevention Tips

    MedlinePlus

    Head Injury Prevention Tips American Association of Neurological Surgeons 5550 Meadowbrook Drive, Rolling Meadows, IL 60008-3852 ... defined as a blow or jolt to the head or a penetrating head injury that disrupts the ...

  12. Injuries in classical ballet.

    PubMed

    Quirk, R

    1984-11-01

    The specialised medical knowledge about dancers' injuries is negligible compared with that which surrounds sports medicine. The author discusses his experience in the management of more than 2000 injuries sustained by dancers of classical ballet. PMID:6151832

  13. Spinal Cord Injuries

    MedlinePlus

    Your spinal cord is a bundle of nerves that runs down the middle of your back. It carries signals back ... forth between your body and your brain. A spinal cord injury disrupts the signals. Spinal cord injuries usually ...

  14. Leg Injuries and Disorders

    MedlinePlus

    ... can damage your legs. Common leg injuries include sprains and strains, joint dislocations, and fractures. These injuries can affect the entire leg, or just the foot, ankle, knee, or hip. Certain diseases also lead to leg ...

  15. Hip Injuries and Disorders

    MedlinePlus

    ... or falling can all sometimes lead to hip injuries. These include Strains Bursitis Dislocations Fractures Certain diseases also lead to hip injuries or problems. Osteoarthritis can cause pain and limited ...

  16. Brachial Plexus Injuries

    MedlinePlus

    ... Diversity Find People About NINDS NINDS Brachial Plexus Injuries Information Page Synonym(s): Erb's Palsy Table of Contents ( ... done? Clinical Trials Organizations What are Brachial Plexus Injuries? The brachial plexus is a network of nerves ...

  17. Arm Injuries and Disorders

    MedlinePlus

    ... of muscles, joints, tendons and other connective tissue. Injuries to any of these parts of the arm ... a fall or an accident. Types of arm injuries include Tendinitis and bursitis Sprains Dislocations Broken bones ...

  18. Brachial Plexus Injuries

    MedlinePlus

    ... to the shoulder, arm, and hand. Brachial plexus injuries are caused by damage to those nerves. Symptoms ... sensation in the arm or hand Brachial plexus injuries can occur as a result of shoulder trauma, ...

  19. Facial Injuries and Disorders

    MedlinePlus

    Face injuries and disorders can cause pain and affect how you look. In severe cases, they can affect sight, ... your nose, cheekbone and jaw, are common facial injuries. Certain diseases also lead to facial disorders. For ...

  20. Teeth Injuries (For Parents)

    MedlinePlus

    ... Things to Know About Zika & Pregnancy First Aid: Teeth Injuries KidsHealth > For Parents > First Aid: Teeth Injuries ... or young child injures the gums or baby teeth: Apply pressure to the area (if it's bleeding) ...