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Sample records for acute atropine intoxication

  1. Vagolytic atropine attenuates cerebral vasodilation response during acute orthostatic hypotension

    PubMed Central

    Choi, Woo-Jong; Lee, Kichang; Kim, Young-Kug; Song, Kyo-Joon; Jeong, Sung-Moon

    2015-01-01

    Background Atropine is an anticholinergic drug which is commonly used in clinical practice. The effect of parasympathetic block with atropine on dynamic cerebrovascular regulation remains unclear. This study was aimed to identify effects of vagolytic atropine on cerebrovascular response during acute orthostatic hypotension in humans. Methods Continuous middle cerebral blood flow velocity (CBFV, transcranial Doppler) and arterial blood pressure (ABP, Finometer) were measured during a sit-to-stand procedure in 10 healthy subjects with placebo and vagolytic (10 µg/kg) doses of atropine. Cerebral vascular tone was assessed by cerebrovascular resistance (CVR = ABP / CBFV). Dynamic cerebral autoregulation was also assessed by transfer function analysis of ABP and CBFV. Results During the standing session, ABP fell to a similar extent in both groups by an average of 23 to 25 mmHg (26% to 29%). CBFV also fell in all subjects but significantly more in vagolytic atropine (-15.0 ± 7.0 cm/s) compared with placebo (-12.0 ± 5.8 cm/s, P < 0.05). CVR was decreased significantly in the placebo group during posture change (1.56 ± 0.44 vs. 1.38 ± 0.38, P < 0.05), in contrast, lesser decreased in the atropine group (1.60 ± 0.50 vs. 1.53 ± 0.42, P = 0.193). Transfer function coherence in the very-low-frequency range was significantly increased in the atropine group during the standing session (0.55 ± 0.14), compared with the sitting session (0.45 ± 0.14, P = 0.006). Conclusions These data present that vagolytic atropine attenuates cerebral vasodilation response to acute orthostatic hypotension, suggesting the use of atropine may need care in patients with cerebrovascular disease with vagal impairment. PMID:26634084

  2. Clinical cases in acute intoxication.

    PubMed

    Smith, Sean B; Maguire, Jennifer; Mauck, Karen F

    2009-12-01

    Over 2.5 million accidental and intentional drug-related poisonings are reported annually in the United States. Early diagnosis and management of patients who present with acute intoxication can significantly reduce both morbidity and mortality. The initial evaluation of patients with suspected or proven intoxications should focus on hemodynamic stability, mental status, and respiratory function. However, early recognition of toxic ingestion is paramount to implementing life-saving treatments. Important historical clues are often found in a social history that considers intravenous drug use, alcohol use, and any access or exposure to illicit substances. A patient's medication list should also be scrutinized for psychoactive or sedative medications, such as tricyclic antidepressants or opioids. In this article we present case-based discussions of the specific diagnosis and management of 5 commonly occurring acute intoxication syndromes. PMID:20877175

  3. Acute bromadiolone intoxication.

    PubMed

    Grobosch, Thomas; Angelow, Boris; Schönberg, Lena; Lampe, Dagmar

    2006-05-01

    A 55-year-old man came to the hospital with a bleeding wound on his tongue. The coating of his tongue was green, and his sputum was red. Because an increased international normalized ratio-value was measured, a blood sample was sent to our laboratory with the suspicion of coumarin intoxication. Liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) analysis confirmed the poisoning was by bromadiolone, with its maximum serum concentration at 440 microg/L. The analysis of further samples resulted in a calculated elimination half-life of 140 h. The analytical method described was developed for the determination and quantitation of bromadialone using LC-MS. This method is suitable for the simultaneous identification and quantitation of 10 indirect anticoagulants in human serum, which include five superwarfarins (brodifacoum, bromadiolone, difenacoum, difethialone, and flocoumafen) as rodenticides licenced in Germany and five other vitamin K antagonists (acenocoumarol, coumatetralyl, coumachlor, phenprocoumon, and warfarin). The method is based on an acidic (pH 4.2) liquid-liquid extraction followed by LC-ESI-MS analysis. Analytical separation was carried out using an Atlantis C18 column (2.1 x 20 mm, 3 microm). The mobile phase consisted of methanol/0.1% formic acid; the flow rate was 0.6 mL/min, and the time needed for analysis was 5 min. The lower limit of quantitation was 5 microg/L (signal-to-noise > 10). PMID:16803669

  4. Acute arsenic intoxication from environmental arsenic exposure

    SciTech Connect

    Franzblau, A.; Lilis, R. )

    1989-11-01

    Reports of acute arsenic poisoning arising from environmental exposure are rare. Two cases of acute arsenic intoxication resulting from ingestion of contaminated well water are described. These patients experienced a variety of problems: acute gastrointestinal symptoms, central and peripheral neurotoxicity, bone marrow suppression, hepatic toxicity, and mild mucous membrane and cutaneous changes. Although located adjacent to an abandoned mine, the well water had been tested for microorganisms only and was found to be safe. Regulations for testing of water from private wells for fitness to drink are frequently nonexistent, or only mandate biologic tests for microorganisms. Well water, particularly in areas near mining activity, should be tested for metals.

  5. Neuromuscular Functions on Experimental Acute Methanol Intoxication

    PubMed Central

    Moral, Ali Reşat; Çankayalı, İlkin; Sergin, Demet; Boyacılar, Özden

    2015-01-01

    Objective The incidence of accidental or suicidal ingestion of methyl alcohol is high and methyl alcohol intoxication has high mortality. Methyl alcohol intoxication causes severe neurological sequelae and appears to be a significant problem. Methyl alcohol causes acute metabolic acidosis, optic neuropathy leading to permanent blindness, respiratory failure, circulatory failure and death. It is metabolised in the liver, and its metabolite formic acid has direct toxic effects, causing oxidative stress, mitochondrial damage and increased lipid peroxidation associated with the mechanism of neurotoxicity. Methanol is known to cause acute toxicity of the central nervous system; however, the effects on peripheral neuromuscular transmission are unknown. In our study, we aimed to investigate the electrophysiological effects of experimentally induced acute methanol intoxication on neuromuscular transmission in the early period (first 24 h). Methods After approval by the Animal Experiment Ethics Committee of Ege University, the study was carried out on 10 Wistar rats, each weighing about 200 g. During electrophysiological recordings and orogastric tube insertion, the rats were anaesthetised using intra-peritoneal (IP) injection of ketamine 100 mg kg−1 and IP injection of xylazine 10 mg kg−1. The rats were given 3 g kg−1 methyl alcohol by the orogastric tube. Electrophysiological measurements from the gastrocnemius muscle were compared with baseline. Results Latency measurements before and 24 h after methanol injection were 0.81±0.11 ms and 0.76±0.12 ms, respectively. CMAP amplitude measurements before and 24 h after methanol injection were 9.85±0.98 mV and 9.99±0.40 mV, respectively. CMAP duration measurements before and 24 h after methanol injection were 9.86±0.03 ms and 9.86±0.045 ms, respectively. Conclusion It was concluded that experimental methanol intoxication in the acute phase (first 24 h) did not affect neuromuscular function. PMID:27366524

  6. [Action of analeptics in acute alcoholic intoxication].

    PubMed

    Bender, K I; Bobrova, L A

    1978-01-01

    Tests conducted on rabbits in a state of acute ethanol poisoning (2.5 g/kg per os) of a medium degree demonstrated that caffein (10 mg/kg) and bemegride (5 mg/kg) introduced one time intravenously at the height of alcoholic intoxication raise the activity of aerobic oxidative processes, but fail to eliminate metabolic acidosis and do not accelerate the excretion of ethanol. Unlike caffein, bemegride shows a tendency toward respiratory compensation of metabolic acidosis and lowers the activity of the alcohol-dehydrogenase. PMID:26595

  7. Acute Alcohol Intoxication-Induced Microvascular Leakage

    PubMed Central

    Doggett, Travis M.; Breslin, Jerome W.

    2014-01-01

    Background Alcohol intoxication can increase inflammation and worsen injury, yet the mechanisms involved are not clear. We investigated whether acute alcohol intoxication elevates microvascular permeability, and investigated potential signaling mechanisms in endothelial cells that may be involved. Methods Conscious rats received a 2.5 g/kg alcohol bolus via gastric catheters to produce acute intoxication. Microvascular leakage of intravenously administered FITC-albumin from the mesenteric microcirculation was assessed by intravital microscopy. Endothelial-specific mechanisms were studied using cultured endothelial cell monolayers. Transendothelial electrical resistance (TER) served as an index of barrier function, before and after treatment with alcohol or its metabolite acetaldehyde. Pharmacologic agents were used to test the roles of alcohol metabolism, oxidative stress, p38 mitogen-activated protein (MAP) kinase, myosin light chain kinase (MLCK), rho kinase (ROCK), and exchange protein activated by cAMP (Epac). VE-cadherin localization was investigated to assess junctional integrity. Rac1 and RhoA activation were assessed by ELISA assays. Results Alcohol significantly increased FITC-albumin extravasation from the mesenteric microcirculation. Alcohol also significantly decreased TER and disrupted VE-cadherin organization at junctions. Acetaldehyde significantly decreased TER, but inhibition of ADH or application of a superoxide dismutase mimetic failed to prevent alcohol-induced decreases in TER. Inhibition of p38 MAP kinase, but not MLCK or ROCK, significantly attenuated the alcohol-induced barrier dysfunction. Alcohol rapidly decreased GTP-bound Rac1 but not RhoA during the drop in TER. Activation of Epac increased TER, but did not prevent alcohol from decreasing TER. However, activation of Epac after initiation of alcohol-induced barrier dysfunction quickly resolved TER to baseline levels. Conclusions Our results suggest that alcohol intoxication increases

  8. Acute pancreatitis and acute renal failure complicating doxylamine succinate intoxication.

    PubMed

    Lee, Yang Deok; Lee, Soo Teik

    2002-06-01

    Doxylamine succinate is an antihistaminic drugwith additional hypnotic, anticholinergic and local anesthetic effects first described in 1948. In Korea and many other countries, it is a common-over-the counter medication frequently involved in overdoses. Clinical symtomatology of doxylamine succinate overdose includes somnolence, coma, seizures, mydriasis, tachycardia, psychosis, and rhabdomyolysis. A serious complication may be rhabdomyolysis with subsequent impairment of renal function and acute renal failure. We report a case of acute renal failure and acute pancreatitis complicating a doxylamine succinate intoxication. PMID:12046971

  9. Acute ethanol intoxication and the trauma patient: hemodynamic pitfalls.

    PubMed

    Bilello, John; McCray, Victor; Davis, James; Jackson, Lascienya; Danos, Leigh Ann

    2011-09-01

    Many trauma patients are acutely intoxicated with alcohol. Animal studies have demonstrated that acute alcohol intoxication inhibits the normal release of epinephrine, norepinephrine, and vasopressin in response to acute hemorrhage. Ethanol also increases nitric oxide release and inhibits antidiuretic hormone secretion. This article studies the effects of alcohol intoxication (measured by blood alcohol level, BAL) on the presentation and resuscitation of trauma patients with blunt hepatic injuries. A retrospective registry and chart review was conducted of all patients who presented with blunt liver injuries at an ACS-verified, level I trauma center. Data collected included admission BAL, systolic blood pressure, hematocrit, International Normalized Ratio (INR), liver injury grade, Injury Severity Score (ISS), intravenous fluid and blood product requirements, base deficit, and mortality. From September 2002 to May 2008, 723 patients were admitted with blunt hepatic injuries. Admission BAL was obtained in 569 patients, with 149 having levels >0.08%. Intoxicated patients were more likely to be hypotensive on admission (p = 0.01) despite a lower liver injury grade and no significant difference in ISS. There was no significant difference in the percent of intoxicated patients requiring blood transfusion. However, when blood was given, intoxicated patients required significantly more units of packed red blood cells (PRBC) than their nonintoxicated counterparts (p = 0.01). Intoxicated patients also required more intravenous fluid during their resuscitation (p = 0.002). Alcohol intoxication may impair the ability of blunt trauma patients to compensate for acute blood loss, making them more likely to be hypotensive on admission and increasing their PRBC and intravenous fluid requirements. All trauma patients should have BAL drawn upon admission and their resuscitation should be performed with an understanding of the physiologic alterations associated with acute alcohol

  10. [Acute lethal alcohol intoxication (author's transl)].

    PubMed

    Kringsholm, B

    1976-01-01

    In 14,744 autopsy cases from an 18-year period 92 cases (of which 7 were ruled out because of decomposition were observed in which death was supposed to be due to direct acute alcoholic intoxication. In the police reports 81 persons were designated as chronic alcoholics or abusers of spirits. The blood alcohol level ranged between 2.04 and 4.92 o/oo. The cases studied were divided into two groups, one with low and the other with high lethal alcohol level. Fatty liver and cirrhosis were found with identical frequency in the two groups, whereas cardiac hypertrophy of obscure origin occurred markedly more often in the group with low lethal blood alcohol level. On the basis the possible mechanism of death in the cases with cardiac hypertrophy is discussed. Finally, the relation between the blood and urine alcohol concentrations observed in 72 cases is discussed. On the assumption that the water phase of the blood was 75 per cent of the total blood, death occurred in the persons without cardiac hypertrophy with fairly identical frequency either in the phase of absorption or the phase of elimination, whereas in the persons with cardiac hypertrophy death most often occurred in the phase of absorption. These statements should, however, be taken with some reservation, partly because the water phase of the blood may vary considerably post mortem (60-90 per cent) and partly because the urine alcohol concentration depends on serval variable factors. PMID:137612

  11. Behavioral assessment of NIH Swiss mice acutely intoxicated with tetramethylenedisulfotetramine.

    PubMed

    Flannery, Brenna M; Silverman, Jill L; Bruun, Donald A; Puhger, Kyle R; McCoy, Mark R; Hammock, Bruce D; Crawley, Jacqueline N; Lein, Pamela J

    2015-01-01

    Tetramethylenedisulfotetramine (TETS) is a potent convulsant poison that is thought to trigger seizures by inhibiting the function of the type A gamma-aminobutyric acid receptor (GABAAR). Acute intoxication with TETS can cause vomiting, convulsions, status epilepticus (SE) and even death. Clinical case reports indicate that individuals who survive poisoning may exhibit long-term neuropsychological issues and cognitive deficits. Therefore, the objective of this research was to determine whether a recently described mouse model of acute TETS intoxication exhibits persistent behavioral deficits. Young adult male NIH Swiss mice received a seizure-inducing dose of TETS (0.15mg/kg, ip) and then were rescued from lethality by administration of diazepam (5mg/kg, ip) approximately 20min post-TETS-exposure. TETS-intoxicated mice typically exhibited 2 clonic seizures prior to administration of diazepam with no subsequent seizures post-diazepam injection as assessed using behavioral criteria. Seizures lasted an average of 72s. Locomotor activity, anxiety-like and depression-relevant behaviors and cognition were assessed at 1week, 1month and 2months post-TETS exposure using open field, elevated-plus maze, light↔dark transitions, tail suspension, forced swim and novel object recognition tasks. Interestingly, preliminary validation tests indicated that NIH Swiss mice do not respond to the shock in fear conditioning tasks. Subsequent evaluation of hot plate and tail flick nociception tasks revealed that this strain exhibits significantly decreased pain sensitivity relative to age- and sex-matched C57BL/6J mice, which displayed normal contextual fear conditioning. NIH Swiss mice acutely intoxicated with TETS exhibited no significant anxiety-related, depression-relevant, learning or memory deficits relative to vehicle controls at any of the time points assessed with the exception of significantly increased locomotor activity at 2months post-TETS intoxication. The general absence

  12. Antagonists for acute oral cadmium chloride intoxication

    SciTech Connect

    Basinger, M.A.; Jones, M.M.; Holscher, M.A.; Vaughn, W.K.

    1988-01-01

    An examination has been carried out on the relative efficacy of a number of chelating agents when acting as antagonists for oral cadmium chloride intoxication in mice. The compounds were administered orally after the oral administration of cadmium chloride at 1 mmol/kg. Of the compounds examined, several were useful in terms of enhancing survival, but by far the most effective in both enhancing survival and leaving minimal residual levels of cadmium in the liver and the kidney, was meso-2,3-dimercaptosuccinic acid (DMSA). Several polyaminocarboxylic acids also enhanced survival. The most effective of these in reducing liver and kidney levels of cadmium were diethylenetriaminepentaacetic acid (DTPA), trans-1,2-diaminocyclohexane-N,N,N'N'-tetraacetic acid (CDTA), and triethylenetetraminehexaacetic acid (TTHA). D-Penicillamine (DPA) was found to promote survival but also led to kidney cadmium levels higher than those found in the controls. Sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) was as effective in promoting survival as DMSA but left levels of cadmium in the kidney and liver that were approximately four times greater than those found with DMSA.

  13. Death due to acute tetrachloroethylene intoxication in a chronic abuser.

    PubMed

    Amadasi, Alberto; Mastroluca, Lavinia; Marasciuolo, Laura; Caligara, Marina; Sironi, Luca; Gentile, Guendalina; Zoja, Riccardo

    2015-05-01

    Volatile substances are used widespread, especially among young people, as a cheap and easily accessible drug. Tetrachloroethylene is one of the solvents exerting effects on the central nervous system with experiences of disinhibition and euphoria. The case presented is that of a 27-year-old female, found dead by her father at home with cotton swabs dipped in the nostrils. She was already known for this type of abuse and previously admitted twice to the hospital for nonfatal acute poisonings. The swabs were still soaked in tetrachloroethylene. Toxicological and histological investigations demonstrated the presence of an overlap between chronic intake of the substance (with high concentrations in sites of accumulation, e.g., the adipose tissue, and contemporary tissue damage, as histologically highlighted) and acute intoxication as final cause of death, with a concentration of 158 mg/L in cardiac blood and 4915 mg/kg in the adipose tissue. No other drugs or medicines were detected in body fluids or tissues, and to our knowledge, this is the highest concentration ever detected in forensic cases. This peculiar case confirms the toxicity of this substance and focuses on the importance of complete histological and toxicological investigations in the distinction between chronic abuse and acute intoxication. PMID:25605280

  14. [Cardioprotective effect of GABA derivatives in acute alcohol intoxication].

    PubMed

    Perfilova, V N; Tiurenkov, I N; Berestovitskaia, V M; Vasil'eva, O S

    2006-01-01

    Cardioprotective properties of GABA analogs under conditions of acute alcoholic intoxication have been studied using the following functional tests: volume loads, tests for adrenoreactivity, and maximum isometric load. The experiments showed that a 32% aqueous ethanol solution intraperitoneally injected in a dose of 8 g/kg produces a cardiotoxic action, which is manifested by a decrease in the inotropic reserve in load tests. Citrocard (50 mg/kg), phenibut (50 mg/kg), and piracetam (200 mg/kg) prevent the alcohol-induced myocardium injury, as shown by the heart contractility retained on a higher level in the test group than in the control group. PMID:16995433

  15. Characteristic manifestations of acute paint thinner-intoxicated children.

    PubMed

    Agin, Khosrow; Hassanian-Moghaddam, Hossein; Shadnia, Shahin; Rahimi, Hamid Reza

    2016-07-01

    In this study, we evaluated the acute clinical and para-clinical abnormalities arising from paint thinner (PT) poisoning in children. Data were collected from 2008 to 2013, and sourced from the medical records of PT-intoxicated children and through questionnaires. A total of 42 children were enrolled in the study. The mean age was 37.2±2.4 months. The participants ranged from10 to 96 months of age; with a median age of 3 months; and a modal age of 24 months. The sex ratio in the study was 22 males (64.9%) to 20 females (35.1%). Clinical biochemistry results of participants revealed the significant presence of alkaline phosphatase (ALP, 569.25±151.58U/L), and lactate dehydrogenase (LDH, 576.14±164.97 IU/L). Arterial blood gas (ABG) analysis was also carried out. Chest X-ray predominantly revealed right side alveolar air space consolidation. These results confirmed hepatotoxicity and pneumonia in PT-intoxicated children. The study also revealed that positive outcomes were achieved in patients with early treatment and management. In addition, the current finding confirmed the timely transfer of the victim to the poisoning center. PMID:27235798

  16. [Mitochondrial dysfunction and compensatory mechanisms in liver cells during acute carbon tetrachloride-induced rat intoxication].

    PubMed

    Zavodnik, I B

    2015-01-01

    Electron-transport chain and redox-balance of mitochondria are important targets that are damaged during intoxication. The aim of the present work was to estimate the role of impairments in cellular bioenergetic function in the development of liver damage during acute carbon tetrachloride intoxication in rats and to elucidate possible compensatory mechanisms. Acute CCl4-induced rat intoxication (0.8 g/kg or 4 g/kg) resulted in considerable impairments of respiratory and synthetic mitochondrial functions; their manifestations depended on the dose of the toxic agent and the duration of the intoxication increased and accompanied by complete uncoupling of oxidation and phosphorylation processes in liver mitochondria. The intoxication induced considerable liver damage and accumulation of NO in blood plasma and liver tissue. The changes of some parameters of liver mitochondrial functional activity demonstrate an oscillative pattern, reflecting compensatory mechanisms during intoxication that involved increased reduced glutathione level and enhanced succinate dehydrogenase activity. PMID:26716745

  17. Effectiveness of chelation therapy with time after acute uranium intoxication

    SciTech Connect

    Domingo, J.L.; Ortega, A.; Llobet, J.M.; Corbella, J. )

    1990-01-01

    The effect of increasing the time interval between acute uranium exposure and chelation therapy was studied in male Swiss mice. Gallic acid, 4,5-dihydroxy-1,3- benzenedisulfonic acid (Tiron), diethylenetriaminepentaacetic acid (DTPA), and 5-aminosalicylic acid (5-AS) were administered ip at 0, 0.25, 1, 4, and 24 hr after sc injection of 10 mg/kg of uranyl acetate dihydrate. Chelating agents were given at doses equal to one-fourth of their respective LD50 values. Daily elimination of uranium into urine and feces was determined for 4 days after which time the mice were killed, and the concentration of uranium was measured in kidney, spleen, and bone. The excretion of uranium was especially rapid in the first 24 hr. Treatment with Tiron or gallic acid at 0, 0.25, or 1 hr after uranium exposure significantly increased the total excretion of the metal. In kidney and bone, only administration of Tiron at 0, 0.25, or 1 hr after uranium injection, or gallic acid at 1 hr after uranium exposure significantly reduced tissue uranium concentrations. Treatment at later times (4 to 24 hr) did not increase the total excretion of the metal and did not decrease the tissue uranium concentrations 4 days after uranyl acetate administration. The results show that the length of time before initiating chelation therapy for acute uranium intoxication greatly influences the effectiveness of this therapy.

  18. Hematobiochemical alterations of acute chlorpyriphos intoxication in indigenous chicken

    PubMed Central

    Begum, Shameem Ara; Upadhyaya, Tirtha Nath; Baruah, Gautam Kumar; Rahman, Taibur; Pathak, Debesh Chandra; Sarma, Kabita; Bora, Rumi Saikia

    2015-01-01

    Aim: The present investigation was undertaken to elaborate hematobiochemical alterations of acute chlorpyriphos (CPF) toxicity in indigenous chicken. Since there is no available literature on the detailed hematobiochemical changes of CPF in indigenous chicken, hence, the present study was designed to establish toxicological effect of CPF on blood biochemical parameters of indigenous chicken which are at a great risk of exposure to pesticides. These will help physiologist, pathologist, and poultry scientists for effective production strategy as well as disease control regime. Materials and Methods: The birds were divided into two major Groups I and II. Group I served as control and Group II was treated with CPF (36 mg/kg). Blood samples were assayed for hemoglobin (Hb), total erythrocyte count (TEC), total leukocyte count (TLC), differential leukocyte count, and biochemical constituents such as alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), cholinesterase (CHE), total protein, and uric acid. Results: Hb, TEC, and TLC levels increased significantly (p<0.01) in toxin fed birds, whereas, lymphocyte percent decreased significantly, and heterophil percent increased significantly. Serum ALP, AST, ALT, and uric acid increased significantly in CPF treated birds. Decreased serum CHE values were observed in CPF fed group. The protein level remained almost same. Uric acid level was found to be increased significantly in the treated group compared to control. Conclusion: The results indicated that acute CPF intoxication produce changes in hematology and biochemical constituents of the treated birds. PMID:27065642

  19. Risk of Acute Kidney Injury and Long-Term Outcome in Patients With Acetaminophen Intoxication

    PubMed Central

    Chen, Yu-Guang; Lin, Cheng-Li; Dai, Ming-Shen; Chang, Ping-Ying; Chen, Jia-Hong; Huang, Tzu-Chuan; Wu, Yi-Ying; Kao, Chia-Hung

    2015-01-01

    Abstract Acetaminophen (APAP) intoxication is a common cause of hepatic toxicity and life-threatening hepatic failure. However, few studies have investigated the possible association between APAP intoxication and acute kidney injury (AKI). We constructed a retrospective cohort study to clarify the relationship between APAP intoxication and the risk of AKI. We identified patients with APAP intoxication and selected a comparison cohort that was 1:4 frequency matched according to age, sex, and year of APAP intoxication diagnosis from the Taiwan National Health Insurance Research Database from 1998 to 2010. We analyzed the risks of AKI for patients with APAP intoxication by using Cox proportional hazards regression models. In this study, 2914 patients with APAP intoxication and 11,656 controls were included. The overall risks of developing AKI were 2.41-fold in the patients with APAP intoxication compared with the comparison cohort. After we excluded APAP intoxication patients with coexisting AKI and hepatic failure/hepatitis, the overall risks of developing AKI were still 2.22-fold in the patients with APAP intoxication. There were 2 patients who had end-stage renal disease (ESRD) following APAP intoxication-related AKI. Limitations include retrospective review, selection bias, and absence of data on detail medications used, laboratory investigations and dosage of APAP intoxication. Our long-term cohort study results showed that AKI is a possible adverse effect among patients with APAP intoxication, regardless of whether patients have presented with hepatic toxicity. However, additional studies are necessary to clarify whether such patients can progress to ESRD. PMID:26579812

  20. NUTRITIONAL THERAPY IN THE TREATMENT OF ACUTE CORROSIVE INTOXICATION IN ADULTS

    PubMed Central

    Chibishev, Andon; Markoski, Velo; Smokovski, Ivica; Shikole, Emilija; Stevcevska, Aleksandra

    2016-01-01

    Introduction: Acute intoxications with corrosive substances can cause severe chemical injuries of the upper gastrointestinal tract, most often located in the mouth, pharynx, esophagus, stomach and duodenum. If a patient survives the acute phase of intoxication, regenerative response may result in esophageal and/or gastric stenosis, and increased risk of esophageal and gastric cancer. Such intoxication may be fatal due to perforation or tracheal necrosis. Enteral nutrition is a nutritional method when nutritional substances are administered through specially designed tubing placed through the nose or percutaneously, directly into the GIT. Aim: The aim of this study is to describe the methods of artificial nutrition in patients with acute corrosive intoxications and the importance of nutritional support in the treatment of these intoxications. Discussion: Nutrition in the treatment of acute corrosive intoxications is one of the most important therapeutic processes that largely contribute to faster recovery of the post-corrosive injuries of upper GIT, stabilization of biologic, immunologic and metabolic parameters, and reduction of length of stay in hospital Aim of the treatment of acute corrosive intoxications is to prevent perforation and progressive fibrosis, and esophageal and gastric stenosis. There are different and often conflicting positions, on the conservative treatment of acute corrosive intoxications in adults. Such treatment mainly consists of anti-secretory treatment, antibiotics and intensive hyper-alimentation, aiming to prevent late post-corrosive intoxications. Conclusion: It is considered that nutritional support plays a major role in maintenance of metabolic processes and prevention of severe metabolic complications that could additionally aggravate the condition and impair the treatment. PMID:27047272

  1. Bath salt intoxication causing acute kidney injury requiring hemodialysis.

    PubMed

    Regunath, Hariharan; Ariyamuthu, Venkatesh Kumar; Dalal, Pranavkumar; Misra, Madhukar

    2012-10-01

    Traditional bath salts contain a combination of inorganic salts like Epsom salts, table salt, baking soda, sodium metaphosphate, and borax that have cleansing properties. Since 2010, there have been rising concerns about a new type of substance abuse in the name of "bath salts." They are beta-ketone amphetamine analogs and are derivates of cathinone, a naturally occurring amphetamine analog found in the "khat" plant (Catha edulis). Effects reported with intake included increased energy, empathy, openness, and increased libido. Serious adverse effects reported with intoxication included cardiac, psychiatric, and neurological signs and symptoms. Not much is known about the toxicology and metabolism of these compounds. They inhibit monoamine reuptake (dopamine, nor epinephrine, etc.) and act as central nervous system stimulants with high additive and abuse potential because of their clinical and biochemical similarities to effects from use of cocaine, amphetamine, and 3,4-methylenedioxy-N-methylamphetamine. Deaths associated with use of these compounds have also been reported. We report a case of acute kidney injury associated with the use of "bath salt" pills that improved with hemodialysis. PMID:23036036

  2. Nitrite as an antidote for acute hydrogen sulfide intoxication

    SciTech Connect

    Beck, J.F.; Bradbury, C.M.; Connors, A.J.; Donini, J.C.

    1981-11-01

    The detoxification of hydrogen sulfide (H/sub 2/S) by a heme catalyzed oxidation was examined as part of an on-going study of H/sub 2/S toxicity. Interlocking O/sub 2/ absorption and sulfide depletion data indicate that both oxyhemoglobin and methemoglobin are effective catalytic agents. Although the latter is more efficacious, the life time of excess sulfide in the presence of oxygen and either of the above is of the order of minutes. It has also been established that the formation of methemoglobin following nitrite administration occurs preferentially under oxygen poor conditions. Under an atmospheric or oxygen enriched environment, which favors sulfide depletion, the nitrite retards sulfide oxidation. Thus nitrite as an antidote for acute H/sub 2/S intoxication can only be effective within the first few minutes after the exposure, at which time resuscitation and/or ventilation of the victim is likely to produce conditions in which the nitrite actually slows sulfide removal.

  3. Spatiotemporal pattern of neuronal injury induced by DFP in rats: A model for delayed neuronal cell death following acute OP intoxication

    SciTech Connect

    Li Yonggang; Lein, Pamela J.; Liu Cuimei; Bruun, Donald A.; Tewolde, Teclemichael; Ford, Gregory; Ford, Byron D.

    2011-06-15

    Organophosphate (OP) neurotoxins cause acute cholinergic toxicity and seizures resulting in delayed brain damage and persistent neurological symptoms. Testing novel strategies for protecting against delayed effects of acute OP intoxication has been hampered by the lack of appropriate animal models. In this study, we characterize the spatiotemporal pattern of cellular injury after acute intoxication with the OP diisopropylfluorophosphate (DFP). Adult male Sprague-Dawley rats received pyridostigmine (0.1 mg/kg, im) and atropine methylnitrate (20 mg/kg, im) prior to DFP (9 mg/kg, ip) administration. All DFP-treated animals exhibited moderate to severe seizures within minutes after DFP injection but survived up to 72 h. AChE activity was significantly depressed in the cortex, hippocampus, subcortical brain tissue and cerebellum at 1 h post-DFP injection and this inhibition persisted for up to 72 h. Analysis of neuronal injury by Fluoro-Jade B (FJB) labeling revealed delayed neuronal cell death in the hippocampus, cortex, amygdala and thalamus, but not the cerebellum, starting at 4 h and persisting until 72 h after DFP treatment, although temporal profiles varied between brain regions. At 24 h post-DFP injection, the pattern of FJB labeling corresponded to TUNEL staining in most brain regions, and FJB-positive cells displayed reduced NeuN immunoreactivity but were not immunopositive for astrocytic (GFAP), oligodendroglial (O4) or macrophage/microglial (ED1) markers, demonstrating that DFP causes a region-specific delayed neuronal injury mediated in part by apoptosis. These findings indicate the feasibility of this model for testing neuroprotective strategies, and provide insight regarding therapeutic windows for effective pharmacological intervention following acute OP intoxication. - Research Highlights: > DFP induced neuronal FJB labeling starting at 4-8 h after treatment > The pattern of DFP-induced FJB labeling closely corresponded to TUNEL staining > FJB

  4. [Histomorphometric characteristic of human brain in acute alcoholic intoxication].

    PubMed

    Shormanov, S V; Shormanova, N S

    2005-01-01

    Different brain sections were studied in 20 subjects, who died of ethanol intoxication and in 14 subjects who died of injuries of the heart and main vessels, in order to detect histological changes in the brain and for the purpose of defining spatial and quantitative ratios between cerebral tissue structures in alcoholic intoxication. Different histological, stereometric and morphometric tools were made use of. It was demonstrated that, in alcoholic intoxication, there occur severe disorders of the circulation with affection of vessels in the brain; there are also dystrophic and necrotic changes in neurocytes, glial cells and white substance. The square of neurons shrinks due to death of some of them in the cortex of hemispheres, thalamus and cerebellum. As for the medulla, they are more resistant, there, to ethanol. The diameter of capillaries in the studied brain sections diminishes due to a reduced tonus of cerebral arteries; the quantity of such vessels increases within a standard area, which is conditioned by the compensatory opening of reserve capillaries. All this can be important in dealing with issues of thanatogenesis and of forensic medical diagnosis in death of alcoholic intoxication. PMID:15881135

  5. [Role of hemodialysis in the management of acute lithium intoxication].

    PubMed

    Maghraoui, Jaouad El; Kabbali, Nadia; Arrayhani, Mohamed; Houssaini, Tarik Sqalli

    2016-01-01

    We report the case of a 47-years old patient, traited with lithium for manic-depressive psychosis over a period of twenty and admitted to hospital with a disorder of consciousness after suicide attempt with lithium overdose (ingestion of 30 tablets of Téralithe(®) LP 400, delayed action galenic forms corresponding to 12 g of lithium carbonate), clinically improved after three hemodialysis sessions. This study illustrates the therapeutic role of hemodialysis in voluntary intoxications with extended release lithium even a week after the ingestion and the therapeutic insufficiency of a single hemodialysis session. PMID:27583091

  6. From divination to madness: features of acute intoxication with Salvia use

    PubMed Central

    Winslow, Munidasa; Mahendran, Rathi

    2014-01-01

    Salvia divinorum is a psychoactive botanical plant that is increasingly used for the ‘legal’ highs that it can produce. It is readily available for purchase on the Internet, and most abusers are unaware of the toxicity and abuse potential associated with its use. As the use of novel compounds among abusers is not uncommon, physicians need to increase their awareness and recognition of these new substances. Herein, we report a case of an acute presentation of Salvia intoxication. PMID:24763842

  7. The Anion Gap is a Predictive Clinical Marker for Death in Patients with Acute Pesticide Intoxication.

    PubMed

    Lee, Sun-Hyo; Park, Samel; Lee, Jung-Won; Hwang, Il-Woong; Moon, Hyung-Jun; Kim, Ki-Hwan; Park, Su-Yeon; Gil, Hyo-Wook; Hong, Sae-Yong

    2016-07-01

    Pesticide formulation includes solvents (methanol and xylene) and antifreeze (ethylene glycol) whose metabolites are anions such as formic acid, hippuric acid, and oxalate. However, the effect of the anion gap on clinical outcome in acute pesticide intoxication requires clarification. In this prospective study, we compared the anion gap and other parameters between surviving versus deceased patients with acute pesticide intoxication. The following parameters were assessed in 1,058 patients with acute pesticide intoxication: blood chemistry (blood urea nitrogen, creatinine, glucose, lactic acid, liver enzymes, albumin, globulin, and urate), urinalysis (ketone bodies), arterial blood gas analysis, electrolytes (Na(+), K(+), Cl(-) HCO3 (-), Ca(++)), pesticide field of use, class, and ingestion amount, clinical outcome (death rate, length of hospital stay, length of intensive care unit stay, and seriousness of toxic symptoms), and the calculated anion gap. Among the 481 patients with a high anion gap, 52.2% had a blood pH in the physiologic range, 35.8% had metabolic acidosis, and 12.1% had acidemia. Age, anion gap, pesticide field of use, pesticide class, seriousness of symptoms (all P < 0.001), and time lag after ingestion (P = 0.048) were significant risk factors for death in univariate analyses. Among these, age, anion gap, and pesticide class were significant risk factors for death in a multiple logistic regression analysis (P < 0.001). In conclusions, high anion gap is a significant risk factor for death, regardless of the accompanying acid-base balance status in patients with acute pesticide intoxication. PMID:27366016

  8. The Anion Gap is a Predictive Clinical Marker for Death in Patients with Acute Pesticide Intoxication

    PubMed Central

    2016-01-01

    Pesticide formulation includes solvents (methanol and xylene) and antifreeze (ethylene glycol) whose metabolites are anions such as formic acid, hippuric acid, and oxalate. However, the effect of the anion gap on clinical outcome in acute pesticide intoxication requires clarification. In this prospective study, we compared the anion gap and other parameters between surviving versus deceased patients with acute pesticide intoxication. The following parameters were assessed in 1,058 patients with acute pesticide intoxication: blood chemistry (blood urea nitrogen, creatinine, glucose, lactic acid, liver enzymes, albumin, globulin, and urate), urinalysis (ketone bodies), arterial blood gas analysis, electrolytes (Na+, K+, Cl- HCO3-, Ca++), pesticide field of use, class, and ingestion amount, clinical outcome (death rate, length of hospital stay, length of intensive care unit stay, and seriousness of toxic symptoms), and the calculated anion gap. Among the 481 patients with a high anion gap, 52.2% had a blood pH in the physiologic range, 35.8% had metabolic acidosis, and 12.1% had acidemia. Age, anion gap, pesticide field of use, pesticide class, seriousness of symptoms (all P < 0.001), and time lag after ingestion (P = 0.048) were significant risk factors for death in univariate analyses. Among these, age, anion gap, and pesticide class were significant risk factors for death in a multiple logistic regression analysis (P < 0.001). In conclusions, high anion gap is a significant risk factor for death, regardless of the accompanying acid-base balance status in patients with acute pesticide intoxication. PMID:27366016

  9. Generalized chorea due to delayed encephalopathy after acute carbon monoxide intoxication

    PubMed Central

    Sung, Yueh-Feng; Chen, Ming-Hua; Peng, Giia-Sheun; Lee, Jiunn-Tay

    2015-01-01

    Movement disorder due to delayed encephalopathy after carbon monoxide (CO) intoxication is uncommon. Generalized chorea, presenting as an initial symptom of delayed encephalopathy, is extremely rare. We describe a 60-year-old woman, who had completely recovered from acute CO poisoning, developed mental and behavioral changes, urinary incontinence and generalized chorea 2 weeks thereafter. T2-weighted brain magnetic resonance imaging showed extensive hyperintensity of the bilateral periventricular and subcortical white matter and the globus pallidus. Brain single-photon emission computed tomography (SPECT) with technetium-99 ethylene cysteine dimer showed inhomogeneous perfusion in the cerebral cortex, with decreased uptake in bilateral frontal regions. Delayed encephalopathy after acute CO intoxication was diagnosed, and the symptoms gradually improved after hyperbaric oxygen therapy (HBOT). This case report demonstrates that generalized chorea may be one of the initial presenting symptoms of delayed encephalopathy after acute CO intoxication. We hypothesize that the generalized chorea in our patient may have been caused by the subcortical white matter lesions, which most likely interrupted the basal ganglia-thalamocortical circuits and that HBOT may be the treatment of choice for such patients. PMID:25745326

  10. Generalized chorea due to delayed encephalopathy after acute carbon monoxide intoxication.

    PubMed

    Sung, Yueh-Feng; Chen, Ming-Hua; Peng, Giia-Sheun; Lee, Jiunn-Tay

    2015-01-01

    Movement disorder due to delayed encephalopathy after carbon monoxide (CO) intoxication is uncommon. Generalized chorea, presenting as an initial symptom of delayed encephalopathy, is extremely rare. We describe a 60-year-old woman, who had completely recovered from acute CO poisoning, developed mental and behavioral changes, urinary incontinence and generalized chorea 2 weeks thereafter. T2-weighted brain magnetic resonance imaging showed extensive hyperintensity of the bilateral periventricular and subcortical white matter and the globus pallidus. Brain single-photon emission computed tomography (SPECT) with technetium-99 ethylene cysteine dimer showed inhomogeneous perfusion in the cerebral cortex, with decreased uptake in bilateral frontal regions. Delayed encephalopathy after acute CO intoxication was diagnosed, and the symptoms gradually improved after hyperbaric oxygen therapy (HBOT). This case report demonstrates that generalized chorea may be one of the initial presenting symptoms of delayed encephalopathy after acute CO intoxication. We hypothesize that the generalized chorea in our patient may have been caused by the subcortical white matter lesions, which most likely interrupted the basal ganglia-thalamocortical circuits and that HBOT may be the treatment of choice for such patients. PMID:25745326

  11. Intravenous Lipid Emulsion Therapy for Acute Synthetic Cannabinoid Intoxication: Clinical Experience in Four Cases

    PubMed Central

    Aksel, Gökhan; Güneysel, Özlem; Taşyürek, Tanju; Kozan, Ergül; Çevik, Şebnem Eren

    2015-01-01

    There is no specific antidote for intoxication with synthetic cannabinoids. In this case series, we considered the efficiency of intravenous lipid emulsion therapy in four cases, who presented to emergency department with synthetic cannabinoid (bonzai) intoxication. The first patient had a GCS of 3 and a left bundle branch block on electrocardiography. The electrocardiography revealed sinus rhythm with normal QRS width after the treatment. The second patient had bradycardia, hypotension, and a GCS of 14. After intravenous lipid emulsion therapy, the bradycardia resolved, and the patient's GCS improved to 15. The third patient presented with a GCS of 8, and had hypotension and bradycardia. After the treatment, not only did the bradycardia resolve, but also the GCS improved to 15. The fourth patient, whose electrocardiography revealed accelerated junctional rhythm, had a GCS of 13. The patient's rhythm was sinus after the treatment. Cardiovascular recovery was seen in all four cases, and neurological recovery was also seen in three of them. Based on the fact that intravenous lipid emulsion is beneficial in patients intoxicated with lipophilic drugs, unstable patients presenting to the emergency department with acute synthetic cannabinoid intoxication may be candidates for intravenous lipid emulsion treatment. PMID:26078891

  12. Does acute alcohol intoxication cause transaminase elevations in children and adolescents?

    PubMed

    Binder, Christoph; Knibbe, Karoline; Kreissl, Alexandra; Repa, Andreas; Thanhaeuser, Margarita; Greber-Platzer, Susanne; Berger, Angelika; Jilma, Bernd; Haiden, Nadja

    2016-03-01

    Several long-term effects of alcohol abuse in children and adolescents are well described. Alcohol abuse has severe effects on neurodevelopmental outcome, such as learning disabilities, memory deficits, and decreased cognitive performance. Additionally, chronic alcohol intake is associated with chronic liver disease. However, the effects of acute alcohol intoxication on liver function in children and adolescents are not well characterized. The aim of this study was to determine if a single event of acute alcohol intoxication has short-term effects on liver function and metabolism. All children and adolescents admitted to the Department of Pediatrics and Adolescent Medicine between 2004 and 2011 with the diagnosis "acute alcohol intoxication" were included in this retrospective analysis. Clinical records were evaluated for age, gender, alcohol consumption, blood alcohol concentration, symptoms, and therapy. Blood values of the liver parameters, CK, creatinine, LDH, AP, and the values of the blood gas analysis were analyzed. During the 8-year study period, 249 children and adolescents with the diagnosis "acute alcohol intoxication" were admitted, 132 (53%) girls and 117 (47%) boys. The mean age was 15.3 ± 1.2 years and the mean blood alcohol concentration was 0.201 ± 0.049%. Girls consumed significantly less alcohol than boys (64 g vs. 90 g), but reached the same blood alcohol concentration (girls: 0.199 ± 0.049%; boys: 0.204 ± 0.049%). The mean values of liver parameters were in normal ranges, but AST was increased in 9.1%, ALT in 3.9%, and γGT in 1.4%. In contrast, the mean value of AST/ALT ratio was increased and the ratio was elevated in 92.6% of all patients. Data of the present study showed significant differences in the AST/ALT ratio (p < 0.01) in comparison to a control group. Data of the present study indicate that there might be an effect of acute alcohol intoxication on transaminase levels. The AST/ALT ratio seems to reflect the damage in hepatocytes

  13. Acute arsine intoxication as a consequence of metal burnishing operations.

    PubMed

    Romeo, L; Apostoli, P; Kovacic, M; Martini, S; Brugnone, F

    1997-09-01

    The report concerns a 30-year-old factory worker, employed in a small galvanizing plant for over ten years in the burnishing, copper- and nickel-plating of small metal articles for the shoe industry. Acute arsine poisoning was attributed to the use of a dilute solution of CuSO4 (3%), HCl (32%), and As2O3 (2%) for burnishing metal (Fe-Zn) shoelace eyelet holes, in the absence of local exhaust ventilation and with no respiratory protection. Arsine caused severe intravascular hemolysis with a rapid drop in hematocrit and hemoglobin levels. Other body organs were involved as a result of the hypoxic effect of anemia and hemolysis, or as a direct toxic effect of the arsine itself. Our experience confirms that exchange transfusion is capable of rapidly arresting the adverse effects of arsine. The importance of preventive measures and worker information to avoid acute arsine poisoning is emphasized. PMID:9219649

  14. Acute Methamphetamine Intoxication: Brain Hyperthermia, Blood-Brain Barrier and Brain Edema

    PubMed Central

    Kiyatkin, Eugene A.; Sharma, Hari S.

    2011-01-01

    Methamphetamine (METH) is a powerful and often abused stimulant with potent addictive and neurotoxic properties. While it is generally assumed that multiple chemical substances released in the brain following METH-induced metabolic activation (or oxidative stress) are primary factors underlying damage of neural cells, in this work we will present data suggesting a role of brain hyperthermia and associated leakage of the brain-blood barrier (BBB) in acute METH-induced toxicity. First, we show that METH induces a dose-dependent brain and body hyperthermia, which is strongly potentiated by associated physiological activation and in warm environments that prevent proper heat dissipation to the external environment. Second, we demonstrate that acute METH intoxication induces robust, widespread but structure-specific leakage of the BBB, acute glial activation, and increased water content (edema), which are related to drug-induced brain hyperthermia. Third, we document widespread morphological abnormalities of brain cells, including neurons, glia, epithelial and endothelial cells developing rapidly during acute METH intoxication. These structural abnormalities are tightly related to the extent of brain hyperthermia, leakage of the BBB, and brain edema. While it is unclear whether these rapidly developed morphological abnormalities are reversible, this study demonstrates that METH induces multiple functional and structural perturbations in the brain, determining its acute toxicity and possibly contributing to neurotoxicity. PMID:19897075

  15. Effect of acute ammonia intoxication on cerebral metabolism in rats with portacaval shunts.

    PubMed Central

    Hindfelt, B; Plum, F; Duffy, T E

    1977-01-01

    Rats were made chronically hyperammonemic by portal-systemic shunting and, 8 wk later, were subjected to acute ammonia intoxication by the intraperitoneal injection of 5.2 mmol/kg of ammonium acetate. In free-ranging animals, ammonia treatment induced a brief period of precoma (10-15 min) that progressed into deep, anesthetic coma lasting for several hours and was associated with a high mortality. In paralyzed, artificially ventilated animals that were lightly anesthetized with nitrous oxide, acute ammonia intoxication caused major disturbances of cerebral carbohydrate, amino acid, and energy metabolism that correlated in time with the change in functional state. At 10 min after injection (precoma), the concentrations of most glycolytic intermediates were increased, as was the lactate/pyruvate ratio. Citrate declined, despite a twofold rise in pyruvate, suggesting that the conversion of pyruvate to citrate had been impaired. Concentrations of phosphocreatine, and of the putative neurotransmitters, glutamate and aspartate, declined during precoma, but the concentrations of the adenine nucleotides in the cerebral hemispheres, cerebellum, and brain stem remained within normal limits. At 60 min after injection (coma), ATP declined in all regions of brain; the reduction in total high-energy phosphates was most notable in the brain stem. The findings indicate that cerebral dysfunction in chronic, relapsing ammonia intoxication is not due to primary energy failure. Rather, it is suggested that ammonia-induced depletion of glutamic and aspartic acids, and inhibition of the malate-asparate hydrogen shuttle are the dominant neurochemical lesions. PMID:838855

  16. [Pharmacological correction of toxic liver damage in patients with heavy forms of acute ethanol intoxication].

    PubMed

    Shikalova, I A; Shilov, V V; Vasil'ev, S A; Batotsyrenov, B V; Loladze, A T

    2012-01-01

    The efficiency of using remaxol and ademethionine in the therapy of patients with heavy acute alcohol intoxication on the background of toxic liver damage has been studied. The administration of remaxol led to improvement of the clinical treatment of alcohol intoxication, which is manifested by a decrease in the rate and duration of delirium tremens (from 33.9 to 10.8%), frequency of secondary lung disorders (from 18.5 to 3.1%), duration of stay in hospital (from 7.3 +/- 0.6 to 5.6 +/- 0.3 days), and total therapy duration (from 11.8 +/- 1.05 to 5.6 +/- 0.3 days). The results of biochemical investigations confirmed that remaxol and ademethionine provide effective treatment of the toxic liver damage. Remaxol decreases the degree of metabolic disorders to a greater extent than does ademethionine. PMID:22702109

  17. The emergency care of cocaine intoxications.

    PubMed

    Vroegop, M P; Franssen, E J; van der Voort, P H J; van den Berg, T N A; Langeweg, R J; Kramers, C

    2009-04-01

    Cocaine is frequently used, especially among adolescents and by men between the age of 25 and 44. Many of them are able to use cocaine in normal day-to-day life, without any problems. Reduced prices of cocaine and other recreational drugs such as MDMA (ecstasy) and gamma hydroxybutyrate (GHB) has led to an increased incidence of intoxications with these drugs. Since the production of cocaine is illegal, it may be impure and mixtures with other drugs such as atropine may occur. The treatment of patients with an acute cocaine intoxication can be complicated. Combination of cocaine with other drugs results in clinical pictures which are difficult to discriminate and that may have important consequences for treatment. PMID:19581655

  18. The Assessment of Electroencephalographic Changes and Memory Disturbances in Acute Intoxications with Industrial Poisons

    PubMed Central

    Chalupa, B.; Synková, J.; Ševčík, M.

    1960-01-01

    A report is given of the results of the electroencephalogram (EEG) and of an experimental memory examination in a group of 22 cases of acute carbon monoxide and solvents poisoning of varying severity. An abnormal EEG recording, most often in the form of theta activity 5-6 sec., was found in 12 patients; memory disturbances were found in 13 cases. There was correlation between the results of the two examinations as well as with the clinical classification of the degree of intoxication. The methods are suitable for the solving of various theoretical and practical questions in industrial toxicology. PMID:13692202

  19. Tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 Levels in Patients with Acute Paraquat Intoxication

    PubMed Central

    Seok, Su-Jin; Kim, Su-Ji; Gil, Hyo-Wook; Yang, Jong-Oh; Lee, Eun-Young

    2011-01-01

    To investigate the effects of reactive oxygen species (ROS) on tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) plasma levels, and their possible implications on clinical outcome, we measured tPA and PAI-1 levels in 101 patients with acute paraquat (PQ) intoxication. The control group consisted of patients who ingested non-PQ pesticides during the same period. tPA and PAI-1 levels were higher in the PQ group than in the controls. PQ levels were significantly correlated with ingested amount, timelag to hospital, tPA level, and hospitalization duration. tPA levels were correlated with PAI-1, fibrin degradation product (FDP), and D-dimer. D-dimer levels were lower in the PQ group than in the controls. Univariate analysis indicated the following significant determinants of death: age, ingested amount, PQ level, timelag to hospital, serum creatinine, lipase, pH, pCO2, HCO3-, WBC, FDP, PAI-1, and tPA. However, multivariate analysis indicated that only PQ level was significant independent factor predicting death. In conclusion, tPA and PAI-1 levels were higher, while D-dimer levels were lower in the PQ group than in the controls, implying that ROS stimulate tPA and PAI-1, but PAI-1 activity overrides tPA activity in this setting. Decreased fibrinolytic activity appears to be one of the clinical characteristics of acute PQ intoxication. PMID:21468253

  20. Fatal acute alcohol intoxication in an ALDH2 heterozygote: a case report.

    PubMed

    Yamamoto, H; Tanegashima, A; Hosoe, H; Fukunaga, T

    2000-08-14

    On an evening in November, a 25-year-old man was found dead in his bedroom. There were many empty snap-out sheets for flunitrazepam tablets in the trash at his bedside. He had been beaten by a gang of young people earlier in the morning of the same day. At the medico-legal autopsy, although there were many bruises and/or abrasions on the whole body, only slight subdural hemorrhage was observed, and none of them was thought to be the cause of death. Flunitrazepam and its metabolites were not detected in his body fluid by gas chromatography-mass spectrometry (GC-MS). Marked lung edema and a severe congestion of organs were observed. His blood alcohol concentration from the femoral vein was 2.00 mg/ml. Fatal cases of acute alcohol intoxication usually have shown higher alcohol concentration (2.25-6.23 mg/ml). Although the genotype of aldehyde dehydrogenase 2 (ALDH2) has not previously been mentioned as a contributing factor in determining the cause of death, in this case the genotype of ALDH2 was ALDH2*1/2 and thus is important. Those who possess the ALDH2*2 gene show high concentrations of acetaldehyde (AcH) at even comparatively lower alcohol levels. Consequently, the cause of death was considered to be acute alcohol intoxication including AcH poisoning. PMID:10940605

  1. Cerebral blood flow changes with acute cocaine intoxication: clinical correlations with SPECT, CT, and MRI.

    PubMed

    Mena, I; Giombetti, R J; Miller, B L; Garrett, K; Villanueva-Meyer, J; Mody, C; Goldberg, M A

    1994-01-01

    In summary, these data suggest that widespread primary or secondary cerebral vasoconstriction is common in patients with neurological complications from cocaine. In most patients, SPECT showed wide-spread hypoperfusion in regions that had no clear clinical significance (e.g., the periventricular area). In many, the SPECT was performed more than 24 hours after the onset of neurological symptomatology. These findings raise several questions. It has been assumed that these SPECT changes in patients with acute neurological symptoms are temporary, although it will be important to determine whether these areas of hypoperfusion persist after symptoms have abated. Recently, Holman and colleagues (1991) found multifocal and deep areas of hypoperfusion with SPECT in 16 of 18 patients with a history of chronic cocaine abuse. Although most of the subjects tested positive for cocaine, several had abstained from cocaine use for weeks prior to the study. All 18 subjects had neuropsychological deficits, 13 mild and 5 moderate. Similarly, Pascual-Leone and colleagues (1991) have shown that CT scan atrophy strongly correlates with the duration of cocaine abuse, suggesting that brain injury may occur with continued use of cocaine. It is the authors' concern that cocaine abuse might produce permanent changes in cerebral perfusion. In conclusion, brain SPECT was found to be a useful procedure in the evaluation of acute cocaine intoxication. Brain SPECT revealed focal cortical lesions not seen on head CT or MRI, which corresponded to clinical deficits. In addition, [99mTc]HMPAO brain SPECT had a characteristic scalloped appearance, and this may be a marker for acute intoxication with cocaine. This study further supports the contention that cocaine causes neurological disease by its vasoconstrictive action. PMID:7603541

  2. Acute alcohol intoxication and suicide: a gender-stratified analysis of the National Violent Death Reporting System

    PubMed Central

    Kaplan, Mark S; McFarland, Bentson H; Huguet, Nathalie; Conner, Kenneth; Caetano, Raul; Giesbrecht, Norman; Nolte, Kurt B

    2013-01-01

    Objectives Although it is well known that people with alcohol dependence are at a markedly elevated risk for suicide, much less is known about the role of acute alcohol use in suicidal behaviours. The primary aims of this epidemiological study were to assess the prevalence and factors associated with acute alcohol intoxication among 57 813 suicide decedents in 16 states. Methods Data from the restricted National Violent Death Reporting System 2003–2009 for male and female suicide decedents aged 18 years and older were analysed by multiple logistic regression to compare decedents with and without acute alcohol intoxication (defined as blood alcohol concentration (BAC) ≥0.08 g/dl). Results Among men, those who were younger, American Indian/Alaska Native, Hispanic, veterans, of lower educational attainment, deceased from a self-inflicted firearm injury or hanging/suffocation and residing in rural areas were more likely to have been intoxicated at the time of death. Among women, the factors associated with a BAC ≥0.08 g/dl were younger age, being American Indian/Alaska Native, and using a firearm, hanging/suffocation or falling as method of death. Conclusions In both men and women, alcohol intoxication was associated with violent methods of suicide and declined markedly with age, suggesting that addressing risks associated with acute alcohol use may be of the greatest aid in the prevention of violent suicides among young and middle age adults. PMID:22627777

  3. Are there biomedical criteria to assess an acute carbon dioxide intoxication by a volcanic emission?

    NASA Astrophysics Data System (ADS)

    Stupfel, Maurice; Le Guern, François

    1989-11-01

    On August 21, 1987, more than 1800 people, thousands of head of cattle and countless wild animals, including birds, were killed by a gas release which occurred during about 4 hours at the lake in the crater Iwi at Nyos in Cameroon; plant life was mostly unaffected. An international inquiry was performed by British, French, Italian, Japanese and U.S. volcanologists and physicians to determine what had been the cause of this disaster. An international conference organised by United Nations Educational Scientific, and Cultural Organisation (U.N.E.S.C.O.), the Cameroon Government and the U.N. Economic Commission for Africa held in Yaoundé March, 1987 concluded: 'that the cause of sudden death was suffocation (asphyxia) in a carbon dioxide atmosphere' The medical findings have been explained by asphyxia caused by carbon dioxide. The presence of other volcanic gases, e.g. hydrogen sulfide, cannot be ruled out' (Sigvaldason, 1989, this issue). This paper reviews what is mainly known about an acute carbon dioxide intoxication in order to disprove or confirm the diagnosis and helps to interpret the field observations and testimonies to provide a basis to discuss the prevention of such an intoxication.

  4. Acute multiple focal neuropathies and delayed postanoxic encephalopathy after alcohol intoxication

    PubMed Central

    Wang, Wei-Che; Yang, Hsiu-Chun; Chen, Yao-Jen

    2015-01-01

    Acute-onset alcohol-associated neuropathy is only occasionally reported, and delayed postanoxic encephalopathy is rare. Here, we report a male who developed acute multiple focal neuropathies and later delayed postanoxic encephalopathy after alcohol intoxication. He had hypoxia and rhabdomyolysis, presenting with acute renal failure initially, and cardiopulmonary support, including mechanical ventilation, led to improvement of the patient at the acute stage. He suffered from bilateral hand numbness and mild weakness of the right lower limb thereafter. Nerve-conduction study revealed no pickup of compound muscle action potential or sensory nerve action potential in the bilateral ulnar nerve, but showed attenuated amplitude of compound muscle action potential in the right femoral nerve. Multiple focal neuropathies were suspected, and he received outpatient rehabilitation after being discharged. However, the patient developed gradual onset of weakness in four limbs and cognitive impairment 23 days after the hypoxia event. Brain computed tomography showed low attenuation over bilateral globus pallidus, and brain magnetic resonance imaging disclosed diffuse increased signal intensity on T2-weighted images and fluid-attenuated inversion recovery in bilateral white matter. He was admitted again under the impression of delayed postanoxic brain injury. Supportive treatment and active rehabilitation were given. He had gradual improvement in motor and functional status after rehabilitation. He could walk with festinating gait under supervision, and needed only minimal assistance in performing activities of daily living approximately 1 year later. PMID:26229472

  5. Assessment of Expression of Genes Coding GABAA Receptors during Chronic and Acute Intoxication of Laboratory Rats with Ethanol.

    PubMed

    Osechkina, N S; Ivanov, M B; Nazarov, G V; Batotsyrenova, E G; Lapina, N V; Babkin, A V; Berdinskikh, I S; Melekhova, A S; Voitsekhovich, K O; Lisitskii, D S; Kashina, T V

    2016-02-01

    Expression of genes encoding the individual subunits of ionotropic GABAA receptor was assessed after acute and chronic intoxication of rats with ethanol. The chronic 1-month-long exposure to ethanol signifi cantly decreased (by 38%) expression of Gabrb1 gene in the hippocampus. Acute exposure to ethanol elevated expression of genes Gabrb1 (by 1.7 times), Gabra1 (by 3.8 times), and Gabra4 (by 6.5 times), although it diminished expression of Gabra2 gene by 1.4 times. In preliminarily alcoholized rats, acute intoxication with ethanol enhanced expression of genes Gabrb1 and Gabra5 by 1.7 and 8.7 times, respectively. There was neither acute nor chronic effect of ethanol on expression of gene Gabra3. PMID:26902358

  6. Acute phenytoin intoxication in a 4-year-old mimicking viral meningoencephalitis

    PubMed Central

    Shukla, Amlin; Sankar, Jhuma; Verma, Ankit; Dubey, Nandkishore

    2013-01-01

    We report here the case of a 4-year-old female preschooler who presented to the emergency department with generalised tonic-clonic convulsions and history of vomiting, irritability and dysarthria of short duration. On examination she was found to be responsive only to painful stimulus, had terminal neck stiffness and bilateral extensor plantars. In view of her clinical presentation, an initial diagnosis of viral meningoencephalitis was made in the emergency room and the child treated accordingly. On subsequent transfer to the intensive care unit (ICU), the parents revealed additional history of an elder sibling taking phenytoin for seizures. Therefore, a suspicion of acute phenytoin toxicity was made and phenytoin levels sent for confirmation. Her serum phenytoin level was 80 μgm/mL (normal: 10–20). The child was managed conservatively and discharged after 5 days of hospitalisation. We chose to report this case to highlight the unusual presentation of this rare intoxication. PMID:23814089

  7. Differential effects of naltrexone on cardiac, subjective and behavioural reactions to acute ethanol intoxication

    PubMed Central

    Peterson, Jordan B.; Conrod, Patricia; Vassileva, Jasmin; Gianoulakis, Christina; Pihl, Robert O.

    2006-01-01

    Objective Alcohol may have psychomotor stimulant properties during the rising limb of the blood alcohol curve at commonly self-administered doses. Increased heart rate (HR) immediately after alcohol consumption may serve as an indicator or marker of such properties, which appear to be potentially opiate-mediated and dopamine-dependent. Naltrexone, an opiate antagonist, has been used successfully in the treatment of alcoholism and may produce its therapeutic effects through its effects on alcohol metabolism or by blocking alcohol's rewarding effects. We hypothesized that, if naltrexone blocks the psychomotor stimulant properties of ethanol, then it would decrease or eliminate the HR increase associated with acute alcohol intoxication and that this would be independent of any effect on alcohol metabolism. Methods Twenty male subjects were administered placebo and alcohol (1.0 mL 95% USP ethanol/kg body weight) in a laboratory setting on one day and naltrexone (50 mg) and alcohol on another (counterbalanced). We assessed all subjects for a change in HR and for a subjective and behavioural response from 35 to 170 minutes after drug or alcohol administration. Results The placebo and alcohol mix produced a significant mean HR increase from baseline (F1,95 = 46.01, p < 0.0001, Cohen's d = 0.62), while naltrexone and alcohol did not (nonsignificant). The significant effects of naltrexone on blood alcohol level did not account for the effect of naltrexone on alcohol-induced HR change but did account for alterations in subjective and behavioural response to alcohol. Conclusions Naltrexone appears to substantially reduce the HR increase that is characteristic of alcohol intoxication. This finding appears to lend moderate support to the notions that, first, naltrexone has differential effects on alcohol reactions and, second, that it specifically blocks the acute psychomotor stimulant properties of alcohol. PMID:17136216

  8. A Heart too Drunk to Drive; AV Block following Acute Alcohol Intoxication.

    PubMed

    van Stigt, Arthur H; Overduin, Ruben J; Staats, Liza C; Loen, Vera; van der Heyden, Marcel A G

    2016-02-29

    Acute excessive alcohol consumption is associated with heart rhythm disorders like atrial fibrillation but also premature ventricular contractions, collectively known as the "holiday heart syndrome". More rarely but clinically significant are reports of atrioventricular (AV) conduction disturbances in binge drinkers with no underlying heart disease or chronic alcohol consumption. To obtain better insights into common denominators and the potential underlying mechanisms we collected and compared individual case reports of AV block following acute alcohol intoxication in otherwise healthy people. By screening PubMed, Google Scholar, Scopus and JSTOR, fifteen cases were found of which eight were sufficiently documented for full analysis. Blood alcohol levels ranged from 90 to 958 mg/dl (19 to 205 mM). Second and third degree AV block was observed most (6/8) albeit that in two of these patients a vagal stimulus led to deterioration from first into higher order AV block. In all cases, patients reverted to normal sinus rhythm upon becoming sober again. Mildly lowered body temperature (35.9 ± 0.5°C) was observed but can be excluded as a major cause of conduction blockade. We hypothesize that ethanol induced partial inhibition of calcium and potentially also sodium currents in conductive tissue structures may be one of the mechanisms of conduction slowing and block that may become exaggerated upon increased vagal tone. An impairment of gap junction function cannot be excluded as a contributing factor. In conclusion, cases of documented alcohol induced AV block are very rare but events can occur at relatively low serum alcohol levels which should prompt to awareness of this phenomenon in alcohol intoxicated patients. PMID:26875557

  9. Event-level associations between affect, alcohol intoxication, and acute dependence symptoms: Effects of urgency, self-control, and drinking experience

    PubMed Central

    Simons, Jeffrey S.; Dvorak, Robert D.; Batien, Bryan D.; Wray, Tyler B.

    2012-01-01

    This study used experience sampling to examine within-person associations between positive affect, anxiety, sadness, and hostility and two outcomes: alcohol intoxication and acute dependence symptoms. We examined the role of urgency, premeditation, and perseverance in predicting the alcohol outcomes and tested whether the affective associations varied as a function of urgency. Participants completed baseline assessments and 21 days of experience sampling on PDAs. Hypotheses were partially confirmed. Positive affect was positively, and sadness inversely, associated with intoxication. Hostility was associated with intoxication for men but not women. Negative urgency moderated the association between anxiety and intoxication, making it stronger. However, positive urgency did not moderate the effect of positive affect. Heavier drinkers exhibited the greatest number of symptoms, yet the association between intoxication and acute signs of alcohol disorder were attenuated among these individuals. Results support the use of experience sampling to study acute signs and symptoms of high risk drinking and dependence. PMID:20685044

  10. Marijuana intoxication

    MedlinePlus

    Cannabis intoxication; Intoxication - marijuana (cannabis); Pot; Mary Jane; Weed; Grass; Cannabis ... The intoxicating effects of marijuana include relaxation, ... to fast and predictable signs and symptoms. Eating marijuana ...

  11. [A case of favourable outcome of severe acute intoxication with an animal poison after a bite by the monocled cobra].

    PubMed

    Livanov, G A; Batotsyrenkov, B V; Lodiagin, A N; Andrianov, A Iu; Kuznetsov, O A; Loladze, A T; Baranov, D V

    2014-01-01

    This paper reports a case of severe acute intoxication with an animal poison after a bite by the monocled cobra. Combined treatment including artificial lung ventilation, infusion-detoxication and desensitizing (hormonal) therapy, hemosorption, correction of metabolic disorders with cytoflavin, antibacterial therapy had positive effect on the patient's condition and ensured the favourable outcome ofpotentially lethal poisoning without the use ofa specific anti-snake venom serum. PMID:25790716

  12. Magnetic resonance analysis of the effects of acute ammonia intoxication on rat brain. Role of NMDA receptors.

    PubMed

    Cauli, Omar; López-Larrubia, Pilar; Rodrigues, Tiago B; Cerdán, Sebastián; Felipo, Vicente

    2007-11-01

    Acute ammonia intoxication leads to rapid death, which is prevented by blocking N-methyl-d-aspartate (NMDA) receptors. The subsequent mechanisms leading to death remain unclear. Brain edema seems an important step. The aim of this work was to study the effects of acute ammonia intoxication on different cerebral parameters in vivo using magnetic resonance and to assess which effects are mediated by NMDA receptors activation. To assess edema induction, we injected rats with ammonium acetate and measured apparent diffusion coefficient (ADC) in 16 brain areas. We also analyzed the effects on T1, T2, and T2* maps and whether these effects are prevented by blocking NMDA receptors. The effects of acute ammonia intoxication are different in different brain areas. T1 relaxation time is reduced in eight areas. T2 relaxation time is reduced only in ventral thalamus and globus pallidus. ADC values increased in hippocampus, caudate-putamen, substantia nigra and cerebellar cortex, reflecting vasogenic edema. ADC decreased in hypothalamus, reflecting cytotoxic edema. Myo-inositol increased in cerebellum and substantia nigra, reflecting vasogenic edema. N-acetyl-aspartate decreased in cerebellum, reflecting neuronal damage. Changes in N-acetyl-aspartate, T1 and T2 are prevented by blocking NMDA receptors with MK-801 while changes in ADC or myo-inositol (induction of edema) are not. PMID:17727627

  13. Structure-activity relationships among dithiocarbamate antidotes for acute cadmium chloride intoxication. [Mice

    SciTech Connect

    Jones, S.G.; Jones, M.M.

    1984-03-01

    Eight sodium dithiocarbamates (NaS/sub 2/CNR/sub 1/R/sub 2/) have been examined as antidotes for acute cadmium intoxication. While all of them possess an ability to increase survival when given to mice 2 hr after a lethal (>99%) intraperitoneal injection of 10 mg/kg of CdCl/sub 2/. 2.5H/sub 2/O, their effects on the organ distribution of cadmium vary considerably. It has been possible to show that the accumulation of cadmium in the brain and kidney as well as the survival rates can be correlated with a numerical measure of the polarity of the groups R/sub 1/ and R/sub 2/. Each factor has a different dependence on the polarity, but it is possible to construct a composite factor for antidotal efficacy which incorporates survival rate, brain cadmium levels and kidney cadmium levels. The factor constructed here exhibits an optimal value approximately in the middle of the polarity range studied. Compounds which have R/sub 1/ = -CH/sub 2/CH/sub 1/OH and R/sub 2/ = -CH/sub 2/CH/sub 2/OH, OR -CH/sub 3/ or -C/sub 2/H/sub 5/ appear to be the most effective antidotes of the compounds examined. 22 references, 4 figures 3 tables.

  14. Electrophysiological study of infant and adult rats under acute intoxication with fluoroacetamide.

    PubMed

    Kuznetsov, Sergey V; Jenkins, Richard O; Goncharov, Nikolay V

    2007-01-01

    A study was conducted of acute intoxication of infant and adult Wistar rats with fluoroacetamide (FAA), an inhibitor of oxidative metabolism. FAA was administered orally to adult rats at 1/2 LD(50) and subcutaneously to infant rats at LD(100) or 1/10 LD(50). Electrocardiogram (ECG), respiration and motor activity were registered for 7 days. Clinical analysis of ECG and the heart rate variability (HRV) was carried out to assess the state of the vegetative nervous system. In adult rats, FAA caused marked disturbances in the activity of cardiovascular and respiratory systems, including the development of a potentially lethal acute cor pulmonale. Conversely, there were no significant changes of cardiac function and respiration in infant rats; they died because of extreme emaciation accompanied by retardation of development. In adult rats, bursts of associated cardiac and respiratory tachyarrhythmia, as well as regular high amplitude spasmodic sighs having a deca-second rhythm were observed. In both infant and adult rats, FAA caused short-term enhancement of humoral (metabolic) and sympathetic activities, followed by a gradual and stable predominance of parasympathetic influence on HRV. Under conditions of FAA inhibition of the tricarboxylic acid cycle, the observed physiological reactions may be explained by activation of alternative metabolic pathways. This is also supported by a lack of ontogenetically caused inhibition of spontaneous motor activity in infant rats poisoned with FAA, which highlights the significance of the alternative metabolic pathways for implementation of deca-second and minute rhythms and a lack of a rigid dependence of these rhythms upon activity of neuronal networks. PMID:17351914

  15. Predictors of Acute Respiratory Distress Syndrome in Patients with Paraquat Intoxication

    PubMed Central

    Weng, Cheng-Hao; Hu, Ching-Chih; Lin, Ja-Liang; Lin-Tan, Dan-Tzu; Hsu, Ching-Wei; Yen, Tzung-Hai

    2013-01-01

    Introduction Paraquat poisoning is characterized by acute lung injury, pulmonary fibrosis, respiratory failure, and multi-organ failure, resulting in a high rate of mortality and morbidity. The objectives of this study were to identify predictors of acute respiratory distress syndrome (ARDS) in cases of paraquat poisoning and determine the association between these parameters. Materials and Methods In total, 187 patients were referred for management of intentional paraquat ingestion between 2000 and 2010. Demographic, clinical, and laboratory data were recorded. Sequential organ failure assessment (SOFA) and Acute Kidney Injury Network (AKIN) scores were collected, and predictors of ARDS were analyzed. Results The overall mortality rate for the entire population was 54% (101/187). Furthermore, the mortality rate was higher in the ARDS patients than in the non-ARDS patients (80% vs. 43.80%, P<0.001). Additionally, the ARDS patients not only had higher AKIN48-h scores (P<0.009), SOFA48-h scores (P<0.001), and time to ARDS/nadir PaO2 (P=0.008) but also suffered from lower nadir PaO2 (P<0.001), nadir AaDO2 (P<0.001), and nadir eGFR (P=0.001) compared to those in the non-ARDS patients. Moreover, pneumomediastinum episodes were more frequent in the ARDS patients than in the non-ARDS patients (P<0.001). A multivariate Cox regression model revealed that blood paraquat concentrations (P<0.001), SOFA48-h scores (P=0.001), and steroid and cyclophosphamide pulse therapies (P=0.024) were significant predictors of ARDS. The cumulative survival rates differed significantly (P<0.001) between patients with SOFA48-h scores <3 and SOFA48-h scores ≥3, with a sensitivity of 95.8%, specificity of 58.4%, and overall correctness of 67.6%. Finally, the area under the receiver operating characteristic (AUROC) analysis showed that SOFA48-h scores (P<0.001) had a better discriminatory power than blood paraquat concentrations (P=0.01) for predicting ARDS. Conclusions The analytical results

  16. Acute Alcohol Intoxication Prolongs Neuroinflammation without Exacerbating Neurobehavioral Dysfunction following Mild Traumatic Brain Injury

    PubMed Central

    Teng, Sophie X.

    2014-01-01

    Abstract Traumatic brain injury (TBI) represents a leading cause of death and disability among young persons with ∼1.7 million reported cases in the United States annually. Although acute alcohol intoxication (AAI) is frequently present at the time of TBI, conflicting animal and clinical reports have failed to establish whether AAI significantly impacts short-term outcomes after TBI. The objective of this study was to determine whether AAI at the time of TBI aggravates neurobehavioral outcomes and neuroinflammatory sequelae post-TBI. Adult male Sprague-Dawley rats were surgically instrumented with gastric and vascular catheters before a left lateral craniotomy. After recovery, rats received either a primed constant intragastric alcohol infusion (2.5 g/kg+0.3 g/kg/h for 15 h) or isocaloric/isovolumic dextrose infusion followed by a lateral fluid percussion TBI (∼1.4 J, ∼30 ms). TBI induced apnea and a delay in righting reflex. AAI at the time of injury increased the TBI induced delay in righting reflex without altering apnea duration. Neurological and behavioral dysfunction was observed at 6 h and 24 h post-TBI, and this was not exacerbated by AAI. TBI induced a transient upregulation of cortical interleukin (IL)-6 and monocyte chemotactic protein (MCP)-1 mRNA expression at 6 h, which was resolved at 24 h. AAI did not modulate the inflammatory response at 6 h but prevented resolution of inflammation (IL-1, IL-6, tumor necrosis factor-α, and MCP-1 expression) at 24 h post-TBI. AAI at the time of TBI did not delay the recovery of neurological and neurobehavioral function but prevented the resolution of neuroinflammation post-TBI. PMID:24050411

  17. Dormant Masculinity: Moderating Effects of Acute Alcohol Intoxication on the Relation Between Male Role Norms and Antigay Aggression

    PubMed Central

    Leone, Ruschelle M.; Parrott, Dominic J.

    2014-01-01

    Acute alcohol intoxication was examined as a moderator of the association between men’s adherence to traditional gender norms and aggression towards a gay male. Participants were 164 heterosexual drinking men between the ages of 21–30. Participants completed a battery of questionnaires that included a measure of adherence to male role norms (i.e., status, toughness, antifemininity), were randomly assigned to consume an alcohol or no-alcohol control beverage, and completed the Taylor Aggression Paradigm in which electric shocks were administered to, and received from, a fictitious gay or heterosexual male opponent. Results indicated a greater adherence to both the toughness (β = .50, p = .002) and antifeminine (β = .37, p = .023) norms predicted high levels of aggression towards a gay man only among participants who were intoxicated. This interaction effect was not detected for the status norm. Consistent with previous research, findings suggest that adherence to the toughness norm does not increase sober men’s risk of aggression toward gay men. However, this is the first study to demonstrate that alcohol intoxication may activate concepts of toughness, and thus influence men to act in line with this facet of the masculine concept. Importantly, these data support the view that men’s adherence to various dimensions of masculinity may be dormant in some contexts, only to be activated, and subsequently demonstrated, in other contexts. PMID:25750591

  18. Brain acetylcholinesterase activity recovery following acute methyl parathion intoxication in two feral rodent species: comparison to laboratory rodents

    SciTech Connect

    Roberts, D.K.; Silvey, N.J.; Bailey, E.M. Jr.

    1988-07-01

    Widespread use of organophosphorus insecticides (OPs) has produced both acute and chronic intoxication among nontarget organisms. Most such studies have included fish and birds as opposed to mammals. However, numerous OP toxicity studies have been conducted on laboratory rodents creating a temptation to apply this data to feral rodents. Chronic OP exposure has been reported to produce cholinergic adaptation which in turn lowers mortality rates following a subsequent acute anticholinesterase exposure. The relevance that these laboratory rodent studies have on feral rodents is subject to debate. Field studies involving OP exposure among nontarget feral mammals have produced contradictory results. Increased mortality as a result of repeated OP application has been reported. This observation may be of considerable importance to nontarget feral rodent populations due to the repetitive nature of OP application protocols. The ability of feral rodents to recover brain AChE activity (BAA) between OP application intervals undoubtedly promotes their survival. This study investigated and compared BAA recovery following acute oral methyl parathion intoxication among 2 feral rodent species and among 2 common laboratory rodent species.

  19. Digitalis must be banished from the table: a rare case of acute accidental Digitalis intoxication of a whole family.

    PubMed

    Maffè, Stefano; Cucchi, Lorenzo; Zenone, Franco; Bertoncelli, Cristina; Beldì, Federico; Colombo, Maria Laura; Bielli, Massimo; Paino, Anna Maria; Parravicini, Umberto; Paffoni, Paola; Dellavesa, Pierfranco; Perucca, Antonello; Pardo, Nicolò Franchetti; Signorotti, Fabiana; Didino, Claudio; Zanetta, Marco

    2009-09-01

    Advanced Digitalis intoxication is a rare event, mainly associated with overdose in patients with Digitalis therapy. We report an unusual case of acute 'familiar' digitalis poisoning in three patients who had eaten potato dumplings flavoured with leaves of Borago officinalis L. unconsciously mixed with leaves of Digitalis purpurea L. A complicated clinical course with marked bradyarrhythmias was presented, with good evolution thanks to the use of digoxin-specific antibody Fab fragments. The theme of the domestic use of plants with medicinal effects has been treated and discussed. PMID:19491701

  20. Brief motivational intervention for adolescents treated in emergency departments for acute alcohol intoxication – a randomized-controlled trial

    PubMed Central

    2014-01-01

    Background Alcohol misuse among youth is a major public health concern and numbers of adolescents admitted to the emergency department for acute alcoholic intoxication in Germany are recently growing. The emergency setting offers an opportunity to reach at-risk alcohol consuming adolescents and provide brief interventions in a potential “teachable moment”. However, studies on brief interventions targeting adolescents in emergency care are scarce and little is known about their effectiveness when delivered immediately following hospitalization for acute alcohol intoxication. In this protocol we present the HaLT-Hamburg trial evaluating a brief motivational intervention for adolescents treated in the emergency department after an episode of acute alcoholic intoxication. Methods The trial design is a parallel two-arm cluster randomized-controlled trial with follow-up assessment after 3 and 6 months. N = 312 participants aged 17 years and younger will be recruited Fridays to Sundays in 6 pediatric clinics over a period of 30 months. Intervention condition is a manual-based brief motivational intervention with a telephone booster after 6 weeks and a manual-guided intervention for caregivers which will be compared to treatment as usual. Primary outcomes are reduction in binge drinking episodes, quantity of alcohol use on a typical drinking day and alcohol-related problems. Secondary outcome is further treatment seeking. Linear mixed models adjusted for baseline differences will be conducted according to intention-to-treat (ITT) and completers (per-protocol) principles to examine intervention effects. We also examine quantitative and qualitative process data on feasibility, intervention delivery, implementation and receipt from intervention providers, receivers and regular emergency department staff. Discussion The study has a number of strengths. First, a rigorous evaluation of HaLT-Hamburg is timely because variations of the HaLT project are widely used in

  1. Rat liver mitochondrial damage under acute or chronic carbon tetrachloride-induced intoxication: Protection by melatonin and cranberry flavonoids

    SciTech Connect

    Cheshchevik, V.T.; Lapshina, E.A.; Dremza, I.K.; Zabrodskaya, S.V.; Reiter, R.J.; Prokopchik, N.I.; Zavodnik, I.B.

    2012-06-15

    In current societies, the risk of toxic liver damage has markedly increased. The aim of the present work was to carry out further research into the mechanism(s) of liver mitochondrial damage induced by acute (0.8 g/kg body weight, single injection) or chronic (1.6 g/ kg body weight, 30 days, biweekly injections) carbon tetrachloride – induced intoxication and to evaluate the hepatoprotective potential of the antioxidant, melatonin, as well as succinate and cranberry flavonoids in rats. Acute intoxication resulted in considerable impairment of mitochondrial respiratory parameters in the liver. The activity of mitochondrial succinate dehydrogenase (complex II) decreased (by 25%, p < 0.05). Short-term melatonin treatment (10 mg/kg, three times) of rats did not reduce the degree of toxic mitochondrial dysfunction but decreased the enhanced NO production. After 30-day chronic intoxication, no significant change in the respiratory activity of liver mitochondria was observed, despite marked changes in the redox-balance of mitochondria. The activities of the mitochondrial enzymes, succinate dehydrogenase and glutathione peroxidase, as well as that of cytoplasmic catalase in liver cells were inhibited significantly. Mitochondria isolated from the livers of the rats chronically treated with CCl{sub 4} displayed obvious irreversible impairments. Long-term melatonin administration (10 mg/kg, 30 days, daily) to chronically intoxicated rats diminished the toxic effects of CCl{sub 4}, reducing elevated plasma activities of alanine aminotransferase and aspartate aminotransferase and bilirubin concentration, prevented accumulation of membrane lipid peroxidation products in rat liver and resulted in apparent preservation of the mitochondrial ultrastructure. The treatment of the animals by the complex of melatonin (10 mg/kg) plus succinate (50 mg/kg) plus cranberry flavonoids (7 mg/kg) was even more effective in prevention of toxic liver injury and liver mitochondria damage

  2. Acute alcohol intoxication decreases glucose metabolism but increases acetate uptake in the human brain.

    PubMed

    Volkow, Nora D; Kim, Sung Won; Wang, Gene-Jack; Alexoff, David; Logan, Jean; Muench, Lisa; Shea, Colleen; Telang, Frank; Fowler, Joanna S; Wong, Christopher; Benveniste, Helene; Tomasi, Dardo

    2013-01-01

    Alcohol intoxication results in marked reductions in brain glucose metabolism, which we hypothesized reflect not just its GABAergic enhancing effects but also the metabolism of acetate as an alternative brain energy source. To test this hypothesis we separately assessed the effects of alcohol intoxication on brain glucose and acetate metabolism using Positron Emission Tomography (PET). We found that alcohol intoxication significantly decreased whole brain glucose metabolism (measured with FDG) with the largest decrements in cerebellum and occipital cortex and the smallest in the thalamus. In contrast, alcohol intoxication caused a significant increase in [1-(11)C]acetate brain uptake (measured as standard uptake value, SUV), with the largest increases occurring in the cerebellum and the smallest in the thalamus. In heavy alcohol drinkers [1-(11)C]acetate brain uptake during alcohol challenge tended to be higher than in occasional drinkers (p<0.06) and the increases in [1-(11)C]acetate uptake in cerebellum with alcohol were positively associated with the reported amount of alcohol consumed (r=0.66, p<0.01). Our findings corroborate a reduction of brain glucose metabolism during intoxication and document an increase in brain acetate uptake. The opposite changes observed between regional brain metabolic decrements and regional increases in [1-(11)C]acetate uptake support the hypothesis that during alcohol intoxication the brain may rely on acetate as an alternative brain energy source and provides preliminary evidence that heavy alcohol exposures may facilitate the use of acetate as an energy substrate. These findings raise the question of the potential therapeutic benefits that increasing plasma acetate concentration (i.e. ketogenic diets) may have in alcoholics undergoing alcohol detoxification. PMID:22947541

  3. PHYSIOLOGICAL RESPONSE OF RAINBOW TROUT ('SALMO GAIRDNERI') TO ACUTE FENVALERATE INTOXICATION

    EPA Science Inventory

    The physiological responses of rainbow trout (Salmo gairdneri) to fenvalerate intoxication during aqueous exposure were examined to provide information about the pyrethroid mode of action in fish. Trout (n = 4) were exposed to 412 + or - 50 micro/liter fenvalerate and died in 10....

  4. Determination of glyphosate and AMPA in blood and urine from humans: about 13 cases of acute intoxication.

    PubMed

    Zouaoui, K; Dulaurent, S; Gaulier, J M; Moesch, C; Lachâtre, G

    2013-03-10

    Acute intoxications after ingesting glyphosate are observed in suicidal or accidental cases. Despite low potential toxicity of this herbicide, a number of fatalities and severe outcomes are reported. Indeed, some authors have described the clinical features associated with blood and urine concentrations following intoxication. The purpose of this study is to describe the clinical feature and determinate the utility of the glyphosate concentration in blood and urine and the dose taken for predicting clinical outcomes. In 13 glyphosate poisoning cases treated in our laboratory within 7 years period from 2002 to 2009, we registered clinical observations and collected blood and urine samples to HPLC-MS-MS analysis. We classified our patients by the intoxication severity using simple clinical criteria. We obtained clinical observations from 10 patients and the others three patients were treated in forensic cases. Among the 10 patients, one was asymptomatic, 5 had mild to moderate poisoning and 2 had severe poisoning. There were 6 deaths whose 3 were forensic cases. The most common symptoms were oropharyngeal ulceration (5/10), nausea and vomiting (3/10). The main altered biological parameters were high lactate (3/10) and acidosis (7/10). We also noted respiratory distress (3/10), cardiac arrhythmia (4/10), hyperkaleamia, impaired renal function (2/10), hepatic toxicity (1/10) and altered consciousness (3/10). In fatalities, the common symptoms were cardiovascular shock, cardiorespiratory arrest, haemodynamic disturbance, intravascular disseminated coagulation and multiple organ failure. Blood glyphosate concentrations had a mean value of 61 mg/L (range 0.6-150 mg/L) and 4146 mg/L (range 690-7480 mg/L) respectively in mild-moderate intoxication and fatal cases. In the severe intoxication case for which blood has been sampled, the blood glyphosate concentration was found at 838 mg/L. Death was most of the time associated with larger taken dose (500 mL in one patient) and

  5. Acute alcohol intoxication increases atrogin-1 and MuRF1 mRNA without increasing proteolysis in skeletal muscle

    PubMed Central

    Vary, Thomas C.; Frost, Robert A.; Lang, Charles H.

    2008-01-01

    Acute alcohol intoxication decreases muscle protein synthesis, but there is a paucity of data on the ability of alcohol to regulate muscle protein degradation. Furthermore, various types of atrophic stimuli appear to regulate ubiquitin-proteasome-dependent proteolysis by increasing the muscle-specific E3 ligases atrogin-1 and MuRF1 (i.e., “atrogenes”). Therefore, the present study was designed to test the hypothesis that acute alcohol intoxication increases atrogene expression leading to an elevated rate of muscle protein breakdown. In male rats, the intraperitoneal injection of alcohol dose- and time-dependently increased atrogin-1 and MuRF1 mRNA in gastrocnemius, the latter of which was most pronounced. A comparable change was absent in the soleus and heart. The ability of in vivo-administered ethanol to increase atrogene expression was independent of the route of alcohol administration (intraperitoneal vs. oral), as well as of nutritional status (fed vs. fasted) and gender (male vs. female). The increase in atrogin-1 and MuRF1 was independent of alcohol metabolism, and the overproduction of endogenous glucocorticoids and could not be prevented by maintaining the circulating concentration of insulin-like growth factor-I. Despite marked changes in atrogene expression, acute alcohol in vivo did not alter the release of either 3-methylhistidine (MH) or tyrosine from the isolated perfused hindlimb, suggesting that the rate of muscle proteolysis remains unchanged. Moreover, alcohol did not increase the directly determined rate of protein degradation in isolated epitrochlearis muscles or cultured myocytes. Finally, no increase in atrogene expression or 3-MH release was detected in muscle from rats fed an alcohol-containing diet. Our results indicate that although acute alcohol intoxication increases atrogin-1 and MuRF1 mRNA preferentially in fast-twitch skeletal muscle, this change was not associated with increased rates of muscle proteolysis. Therefore, the loss

  6. Atropinic (Anticholinergic) Burden in Parkinson's Disease.

    PubMed

    De Germay, Sibylle; Montastruc, Jean-Louis; Rousseau, Vanessa; Chebane, Leila; Bondon-Guitton, Emmanuelle; Moulis, Florence; Durrieu, Genevieve; Bagheri, Haleh; Rascol, Olivier; Pariente, Antoine; Bégaud, Bernard; Montastruc, François

    2016-05-01

    Use of atropinic drugs remains controversial in Parkinson's disease (PD) because there is insufficient evidence about their efficacy and they can induce serious adverse drug reactions. Atropinic risk scales were developed to help to identify atropinic drugs in prescription forms and to evaluate their burden in clinical practice. In the present review, we discuss the few studies investigating atropinic burden in PD and present the results of our study indicating that atropinic drugs are still widely prescribed in PD (almost 3 of 5 prescriptions) with a clinically significant atropinic burden in around 1 of 6 PD patients. Drugs mainly responsible for high values of atropinic burden were those used for nonmotor symptoms. Clinically significant atropinic burdens were mainly induced by associations of several "low-risk" drugs. Physicians must be aware that in addition to classical atropinic antiparkinsonian drugs, many others (psychotropics) can contribute to increased atropinic burden in PD patients. © 2016 International Parkinson and Movement Disorder Society. PMID:27028036

  7. Association of the Superoxide Dismutase (V16A) and Catalase (C262T) Genetic Polymorphisms with the Clinical Outcome of Patients with Acute Paraquat Intoxication

    PubMed Central

    Hong, Joong-Rock; Seok, Su-Jin; Jeong, Du-Shin; Lee, Sang-Gon; Gil, Hyo-Wook; Yang, Jong-Oh; Lee, Eun-Young

    2010-01-01

    Background/Aims Many patients with acute paraquat (PQ) intoxication die even at low PQ concentrations, whereas others with similar concentrations recover. Therefore, it is possible that individual differences in antioxidant capacity are responsible for the variable clinical outcome in patients with acute PQ intoxication. Methods We investigated whether there was a relationship between the genetic polymorphisms of SOD (V16A), catalase (C262T), and GPX1 (C593T) in 62 patients with acute PQ intoxication and the clinical outcomes of these patients. Results The frequency of the Mn-SOD V/V, V/A, and A/A genotypes were 56.3, 43.5, and 0% in survivors and 86.9, 13.1, and 0% in non-survivors (p > 0.05). The GPX1 C/C, C/T, and T/T genotypes were present in 100, 0, and 0% of all subjects. The catalase C/C, C/T, and T/T genotypes were present in 100, 0, and 0% of survivors, and in 82.6, 17.4, and 0% of non-survivors. Neither erythrocyte SOD activity nor catalase activity were significantly different between survivors and non-survivors. Conclusions No association was found between clinical outcome of acute PQ intoxication and the genetic polymorphism of GPX1 (C593T) or the genetic polymorphisms or enzyme activity of superoxide dismutase (V16A) or catalase (C262T). PMID:21179281

  8. Acute Effects of Intoxication and Arousal on Approach/Avoidance Biases Toward Sexual Risk Stimuli in Heterosexual Men.

    PubMed

    Simons, Jeffrey S; Maisto, Stephen A; Wray, Tyler B; Emery, Noah N

    2016-01-01

    This study tested the effects of alcohol intoxication and physiological arousal on cognitive biases toward erotic stimuli and condoms. Ninety-seven heterosexual men were randomized to 1 of 6 independent conditions in a 2 (high arousal or control) × 3 (alcohol target BAC = 0.08, placebo, or juice control) design and then completed a variant of the Approach-Avoidance Task (AAT). The AAT assessed reaction times toward approaching and avoiding erotic stimuli and condoms with a joystick. Consistent with hypotheses, the alcohol condition exhibited an approach bias toward erotic stimuli, whereas the control and placebo groups exhibited an approach bias toward condom stimuli. Similarly, the participants in the high arousal condition exhibited an approach bias toward erotic stimuli and the low arousal control condition exhibited an approach bias toward condoms. The results suggest that acute changes in intoxication and physiological arousal independently foster biased responding toward sexual stimuli and these biases are associated with sexual risk intentions. PMID:25808719

  9. Acute Vitamin D Intoxication Possibly Due to Faulty Production of a Multivitamin Preparation

    PubMed Central

    Anık, Ahmet; Çatlı, Gönül; Abacı, Ayhan; Dizdarer, Ceyhun; Böber, Ece

    2013-01-01

    Vitamin D intoxication usually occurs as a result of inappropriate use of vitamin D preparations and can lead to life-threatening hypercalcemia. It is also known that there are a number of physicians who prescribe vitamin D supplements for various clinical conditions, such as poor appetite and failure to thrive. While inappropriate use of vitamin D supplements may lead to vitamin D intoxication, there are no reports of cases of vitamin D toxicity due to manufacturing errors of vitamin D preparations. Here, we present cases of hypervitaminosis D which developed following the use of a standard dose of a multivitamin preparation. All three cases presented with hypercalcemia symptoms and had characteristic laboratory findings such as hypercalcemia, hypercalciuria, low levels of parathyroid hormone. The very high serum 25(OH) vitamin D levels in these patients indicated vitamin D excess. The vitamin D level of the prescribed multivitamin preparation in the market was studied and was found to contain a very low level of vitamin D (10 IU/5 mL). Although the stated vitamin D content of the preparations ingested by these patients was not high, unproven but possible manufacturing errors were considered to be a possible cause of the hypervitaminosis D diagnosed in these three patients. Conflict of interest:None declared. PMID:23748070

  10. Acute Alcohol Intoxication and Suicide Among U.S. Ethnic/Racial Groups: Findings from the National Violent Death Reporting System

    PubMed Central

    Caetano, Raul; Kaplan, Mark S.; Huguet, Nathalie; McFarland, Bentson H.; Conner, Kenneth; Giesbrecht, Norman; Nolte, Kurt B.

    2012-01-01

    Background To assess the prevalence and sociodemographic correlates of suicide involving acute alcohol intoxication among U.S. ethnic minorities. Methods Data were derived from the restricted 2003–2009 National Violent Death Reporting System (NVDRS). The study focused on the sociodemographic and toxicological information of 59,384 male and female suicide decedents for 16 states of the U.S. Acute alcohol intoxication was defined as having a blood alcohol content (BAC) ≥ 0.08 g/dl. Overall, 76% of decedents were tested for the presence of alcohol. Results The proportion of suicide decedents with a positive BAC ranged from 47% among American Indians/Alaska Natives (AIs/ANs) to 23% among Asians/Pacific Islanders (PIs). Average BAC was highest among AIs/ANs. Among those who were tested for BAC, the proportion of decedents legally intoxicated prior to suicide was: Blacks, 15%; AIs/ANs, 36%; Asians/PIs, 13%; Hispanics, 28%. Bivariate associations showed that most suicide decedents who were legally intoxicated were male, younger than 30 years of age, with a high school education, not married, non-veterans, lived in metropolitan areas, and used a firearm to complete suicide. However, with the exception of Whites, most of these associations became not statistically significant in multivariate analysis. Conclusions Alcohol use and legal intoxication prior to completing suicide are common among U.S. ethnic groups, especially among males and those who are younger than 30 years of age. The AI/AN group had the highest mean BAC, the highest rate of legal intoxication and decedents who were particularly young. Suicide prevention strategies should address alcohol use as a risk factor. Alcohol problems prevention strategies should focus on suicide as a consequence of alcohol use, especially among AI/AN youth and young adults. PMID:23384174

  11. Effects of high doses of dexamethasone on hemodynamic and immunohistochemical characteristics of acute paraquat intoxication in rat kidneys.

    PubMed

    Ekerbicer, N; Gurpinar, T; Tarakci, F; Turkoz Uluer, E; İnan, S

    2016-01-01

    Paraquat (1,1'-dimethyl-4,4'-bipyridinium) (PQ), is a nonselective contact herbicide that is highly toxic to humans. The kidney is affected during PQ intoxication. Dexamethasone (Dexa) has anti-inflammatory effects and is used to treat cases of PQ poisoning. We investigated in rat kidney hemodynamic effects and immunohistochemical characteristics of Dexa treatment in acute PQ poisoning. Adult male rats were divided into four groups: 1, untreated control; 2, treated with 100 mg/kg Dexa; 3, treated with 25 mg/kg PQ; 4, treated with PQ + Dexa. Mean arterial pressure (MAP) and heart rate (HR) were recorded during the experimental period (2 h). Tissues were removed after 2 h and immunohistochemistry was performed after 24 h. Paraffin sections of kidney were prepared and anti-cyclo-oxygenase-1 (COX-1), anti-cyclo-oxygenase-2 (COX-2), anti-angiotensin converting enzyme (ACE), anti-aquaporin-1 (AQU-1), anti-vascular cell adhesion molecule (VCAM) primary antibodies were used for immunohistochemical examination. Immunoreactivities were scored as: (1) minimal, (2) weak, (3) mild, (4) moderate, (5) strong and (6) very strong. MAP and HR were measured at 10 min, 20 min, 1 h and 2 h. MAP at 10 and 20 min and 1 h was increased in the Dexa group. HR also was increased in all groups compared to controls at 2 h. Compared to groups 2 and 4, MAP values decreased significantly in group 3 at 1 h. The intensity of all of immunoreactivities was decreased in group 2. In group 3, immunoreactivities of COX-1, COX-2 and ACE were decreased compared to the control and the other groups, whereas AQU-1 and VCAM immunoreactivities were the same as the control group. ACE and VCAM immunoreactivities were decreased in group 4 compared to the control group, while COX-1, COX-2 and AQU-1 immunoreactivities were close to those of the control group. Dexa appears to be useful for treating PQ intoxication. PMID:26796020

  12. Inhibition of TGFβ type I receptor activity facilitates liver regeneration upon acute CCl4 intoxication in mice.

    PubMed

    Karkampouna, Sofia; Goumans, Marie-José; Ten Dijke, Peter; Dooley, Steven; Kruithof-de Julio, Marianna

    2016-02-01

    Liver exhibits a remarkable maintenance of functional homeostasis in the presence of a variety of damaging toxic factors. Tissue regeneration involves cell replenishment and extracellular matrix remodeling. Key regulator of homeostasis is the transforming growth factor-β (TGFβ) cytokine. To understand the role of TGFβ during liver regeneration, we used the single-dose carbon tetrachloride (CCl4) treatment in mice as a model of acute liver damage. We combined this with in vivo inhibition of the TGFβ pathway by a small molecule inhibitor, LY364947, which targets the TGFβ type I receptor kinase [activin receptor-like kinase 5 (ALK5)] in hepatocytes but not in activated stellate cells. Co-administration of LY364947 inhibitor and CCl4 toxic agent resulted in enhanced liver regeneration; cell proliferation (measured by PCNA, phosphorylated histone 3, p21) levels were increased in CCl4 + LY364947 versus CCl4-treated mice. Recovery of CCl4-metabolizing enzyme CYP2E1 expression in hepatocytes is enhanced 7 days after CCl4 intoxication in the mice that received also the TGFβ inhibitor. In summary, a small molecule inhibitor that blocks ALK5 downstream signaling and halts the cytostatic role of TGFβ pathway results in increased cell regeneration and improved liver function during acute liver damage. Thus, in vivo ALK5 modulation offers insight into the role of TGFβ, not only in matrix remodeling and fibrosis, but also in cell regeneration. PMID:25566828

  13. The Time between Paraquat Ingestion and a Negative Dithionite Urine Test in an Independent Risk Factor for Death and Organ Failure in Acute Paraquat Intoxication

    PubMed Central

    Seok, Sujin; Kim, Young-hee; Gil, Hyo-wook; Song, Ho-yeon

    2012-01-01

    To identify a prognostic marker that is less sensitive to variations in the elapsed time since paraquat ingestion, we assessed the time between paraquat ingestion and a negative dithionite urine test as a prognostic parameter in patients with acute paraquat intoxication. Forty-one patients with acute paraquat intoxication were enrolled in this study and analyzed to verify significant determinants of mortality and organ dysfunction. The amount of paraquat ingested, paraquat plasma levels, and the time to a negative urine dithionite test were significant independent risk factors predicting mortality. The amount of paraquat ingestion, and the time to a negative urine dithionite test were independent risk factors predicting organ dysfunction. With a cut-off value of 34.5 hr for the time to negative conversion of the urine dithionite test, the sensitivity and specificity for mortality were 71.4% and 75.0%, respectively. The incidence of acute kidney injury and respiratory failure above 34.5 hr were 100% and 85.0%, respectively. In conclusion, the time to a negative urine dithionite test is the reliable marker for predicting mortality and/or essential organ failure in patients with acute paraquat intoxication, who survive 72 hr. PMID:22969243

  14. Clinical, laboratory and pathological findings in sub-acute monensin intoxication in goats

    PubMed Central

    Deljou, Mahdi; Aslani, Mohammad Reza; Mohri, Mehrdad; Movassaghi, Ahmad Reza; Heidarpour, Mohammad

    2014-01-01

    Toxic effects of monensin, a polyether antibiotic mainly used as a coccidiostat, have been described in a wide range of animals. The present study was performed to investigate the toxic effects of monensin in goats. Seven adult goats were administered sodium monensin, 13.5 mg kg-1, daily for five consecutive days via gastric gavage. Monensin toxicity was evaluated by clinical signs, serum biochemistry and pathology. Monensin exposure caused diarrhea, tachycardia and reduction in ruminal movements and body temperature. Significant increase of creatine kinase, lactate dehydrogenase, aspartate aminotransferase, total bilirubin, blood urea nitrogen, creatinine and erythrocyte superoxide dismutase were observed in monensin exposed goats. Reduction of erythrocyte glutathione peroxidase and elevation of serum malondialdehyde and troponin I were inconsistent. In necropsy, there were effusions in body cavities, vacuolar degeneration and coagulative necrosis in cardiac and skeletal muscles and renal tubular necrosis. These findings suggested that monensin intoxication in goats leads to cardiac, skeletal and renal damage and a wide range of biochemical abnormalities. Oxidative stress may be involved in the pathogenesis of monensin poisoning. PMID:25568713

  15. Central anticholinergic syndrome vs. idiosyncratic reaction triggered by a small IV dose of atropine.

    PubMed

    Cao, X; Cui, Y; White, P F; Tang, J; Ma, H

    2016-02-01

    A 58-year-old male was scheduled to undergo radical gastrectomy for cancer under general anesthesia. The patient developed agitation and irregular breathing after receiving a single dose of atropine (0.5 mg) to treat bradycardia immediately prior to induction of anesthesia. Within 5 min after the atropine injection, the patient became unresponsive with facial flushing and diaphoresis. When a drop in oxygen saturation was observed, a laryngeal mask airway was inserted after administering a small bolus dose of propofol (80 mg) and the patient was ventilated with 100% oxygen. Physostigmine was not administered because of the relatively low dose of atropine and the fact that his symptoms were not totally consistent with central anticholinergic syndrome (CAS). The differential diagnosis at the time also included an acute cardiovascular event and an idiosyncratic reaction to atropine. The patient fully recovered within 80 min from this highly unusual reaction to a single 0.5 mg IV dose of atropine. PMID:26471203

  16. [Acute intoxication with nutmeg used as a recreational purpose--a case report].

    PubMed

    Sein Anand, Jacek; Barwina, Małgorzata; Waldman, Wojciech

    2013-01-01

    We present a case of acute nutmeg poisoning used for recreational purposes. Poisoning had a stormy clinical course with symptoms of gastrointestinal, cardiovascular and nervous system. The widespread availability of nutmeg suggests that real number of these poisonings may be underestimated in our country. PMID:24466724

  17. Quantifying alcohol-related emergency admissions in a UK tertiary referral hospital: a cross-sectional study of chronic alcohol dependency and acute alcohol intoxication

    PubMed Central

    Vardy, J; Keliher, T; Fisher, J; Ritchie, F; Bell, C; Chekroud, M; Clarey, F; Blackwood, L; Barry, L; Paton, E; Clark, A; Connelly, R

    2016-01-01

    Objectives Alcohol is responsible for a proportion of emergency admissions to hospital, with acute alcohol intoxication and chronic alcohol dependency (CAD) implicated. This study aims to quantify the proportion of hospital admissions through our emergency department (ED) which were thought by the admitting doctor to be (largely or partially) a result of alcohol consumption. Setting ED of a UK tertiary referral hospital. Participants All ED admissions occurring over 14 weeks from 1 September to 8 December 2012. Data obtained for 5497 of 5746 admissions (95.67%). Primary outcome measures Proportion of emergency admissions related to alcohol as defined by the admitting ED clinician. Secondary outcome measures Proportion of emergency admissions due to alcohol diagnosed with acute alcohol intoxication or CAD according to ICD-10 criteria. Results 1152 (21.0%, 95% CI 19.9% to 22.0%) of emergency admissions were thought to be due to alcohol. 74.6% of patients admitted due to alcohol had CAD, and significantly greater than the 26.4% with ‘Severe’ or ‘Very Severe’ acute alcohol intoxication (p<0.001). Admissions due to alcohol differed to admissions not due to alcohol being on average younger (45 vs 56 years, p<0.001) more often male (73.4% vs 45.1% males, p<0.001) and more likely to have a diagnosis synonymous with alcohol or related to recreational drug use, pancreatitis, deliberate self-harm, head injury, gastritis, suicidal ideation, upper gastrointestinal bleeds or seizures (p<0.001). An increase in admissions due to alcohol on Saturdays reflects a surge in admissions with acute alcohol intoxication above the weekly average (p=0.003). Conclusions Alcohol was thought to be implicated in 21% of emergency admissions in this cohort. CAD is responsible for a significantly greater proportion of admissions due to alcohol than acute intoxication. Interventions designed to reduce alcohol-related admissions must incorporate measures to tackle CAD. PMID:27324707

  18. Phenotypic differences in survival to an experimental acute carbon monoxide intoxication

    SciTech Connect

    Stupfel, M.; Pesce, V.H.D.; Perrot, A.

    1980-02-01

    Male and female 45-day-old mice of two inbred (CBA and C57B1) and of one outbred (OF/sub 1/), SPF (specific pathogen free), strains, LD/sub 12/ /sub 12/ (L = 150 lx) synchronized, were submitted to an acute carbon monoxide challenge giving an overall survival close to 50%. Under these conditions significantly (P < 0.001) less CBA survived than the two other strains. A sex-related significant (P < 0.001) difference was observed in OF/sub 1/. Strain survival differences are independent of body weights and of respiratory and displacement activity, but appear to be related to behavior reactions towards environmental stresses. These phenotypic differences are similar to previous findings obtained with these three strains of mice submitted to a 50% survival acute hypoxic hypoxia (M. Stupfel, A. Perramon, P. Merat, J.M. Faure, and H. Masse, 1979, Comp. Biochem. Physiol., 64A, 317 to 323).

  19. Drinking to near death--acute water intoxication leading to neurogenic stunned myocardium.

    PubMed

    Losonczy, Lia I; Lovallo, Emily; Schnorr, C Daniel; Mantuani, Daniel

    2016-01-01

    Neurogenic stunned myocardium is a rare disease entity that has been typically described as a consequence of subarachnoid hemorrhage and, less commonly, seizures. Here we describe a case of a healthy young woman who drank excessive free water causing acute hyponatremia complicated by cerebral edema and seizure, leading to cardiogenic shock from neurogenic stunned myocardium. Two days later, she had complete return of her normal cardiac function. PMID:26238098

  20. Hepatoprotective effects of polymethoxyflavones against acute and chronic carbon tetrachloride intoxication.

    PubMed

    Kim, Tae-Won; Lee, Dong-Ryung; Choi, Bong-Keun; Kang, Hwan-Kyu; Jung, Ju-Young; Lim, Seol-Wa; Yang, Seung Hwan; Suh, Joo-Won

    2016-05-01

    In the present study, we explore the protective effects of Citrus aurantium L. extract (CAE) against acute and chronic CCl4-induced hepatotoxicity. The quantitative analysis of CAE was performed using HPLC-UV to determine the nobiletin content was approximately 27%. For the acute model, the male ICR mice were orally treated with water, silymarin (positive control, 200 mg/kg) and CAE (50 and 200 mg/kg) for 3 days prior to CCl4 (1 mL/kg, 50% v/v in olive oil) IP injection. For the chronic model (n = 6/group), the mice were treated with each treatment for 28 consecutive days and CCl4 (1 mL/kg, 20%) was injected twice a week. In both the acute and chronic models, the CCl4 alone treated group showed histopathologic alterations with a significantly increase in serum hepatic enzyme levels together with a disrupted anti-oxidative status. In contrast, the CAE treatments restored pathologic alterations and recovered the oxidative status by enhancing antioxidant enzymes and reducing lipid peroxidation levels. Furthermore, CAE enhanced nuclear factor E2-related factor 2 (Nrf2) and its related cytoprotective signals, including NAD(P)H quinone oxidoreductase 1, UDP-glucuronosyltransferase, and γ-glutamylcysteine synthetase. Taken together, the present study demonstrates that CAE exerts a protective effect against CCl4-induced hepatotoxicity with its anti-oxidant, anti-inflammatory, and anti-apoptotic activity. PMID:26980244

  1. Cholinergic aspects of cyanide intoxication

    SciTech Connect

    Von Bredow, J.D.; Vick, J.A.

    1993-05-13

    The acute exposure of pentobarbital anesthetized dogs to cyanide leads to a rapid increase and sudden halt in respiration accompanied by cardiovascular irregularities and extreme bradycardia which ultimately lead to cardiac arrest and death. Cardiac irregularities and cardiac arrest in the presence of cyanide induced respiratory arrest are assumed to be due to anoxia and therefore unresponsive to cardiotonic agents. Pretreatment or treatment with atropine sulfate or methyl atropine nitrate provides a marked reduction in the cardiovascular irregularities, bradycardia and hypotension. The cyanide induced cardiovascular effect can also be prevented by bilateral vagotomy. An intramuscularly injected combination of 20 mg/kg sodium nitrite and 1 mg/kg of atropine sulfate ensured recovery of pentobarbital anesthetized dogs exposed to lethal concentrations (2.5 mg/kg i.v.) of sodium cyanide.

  2. Bioconcentration and Acute Intoxication of Brazilian Freshwater Fishes by the Methyl Parathion Organophosphate Pesticide

    PubMed Central

    Bosco de Salles, João; Matos Lopes, Renato; de Salles, Cristiane M. C.; Cassano, Vicente P. F.; de Oliveira, Manildo Marcião; Cunha Bastos, Vera L. F.; Bastos, Jayme Cunha

    2015-01-01

    Three species of freshwater Brazilian fishes (pacu, Piaractus mesopotamicus; piavussu, Leporinus macrocephalus, and curimbatá, Prochilodus lineatus) were exposed to an acute dose of 5 ppm methyl parathion organophosphate pesticide. Three to five individuals per species were exposed, one at a time, to 40 liters tap water spiked with Folidol 600. Pesticide concentrations and cholinesterase (ChE) activities were evaluated in serum, liver, brain, heart, and muscle. The bioconcentration of methyl parathion was similar for all studied fishes. Brain tissue showed the highest pesticide concentration, reaching 80 ppm after exposure for 30 min to methyl parathion. Three to 5 hours of 5 ppm methyl parathion exposure provoked the death of all P. lineatus at 92% brain AChE inhibition, whereas fish from the other two species survived for up to 78 hours with less than 80% brain AChE inhibition. Our results indicate that acute toxic effects of methyl parathion to fish are correlated with brain AChE sensitivity to methyl paraoxon. PMID:26339593

  3. Bioconcentration and Acute Intoxication of Brazilian Freshwater Fishes by the Methyl Parathion Organophosphate Pesticide.

    PubMed

    de Salles, João Bosco; Lopes, Renato Matos; de Salles, Cristiane M C; Cassano, Vicente P F; de Oliveira, Manildo Marcião; Bastos, Vera L F Cunha; Bastos, Jayme Cunha

    2015-01-01

    Three species of freshwater Brazilian fishes (pacu, Piaractus mesopotamicus; piavussu, Leporinus macrocephalus, and curimbatá, Prochilodus lineatus) were exposed to an acute dose of 5 ppm methyl parathion organophosphate pesticide. Three to five individuals per species were exposed, one at a time, to 40 liters tap water spiked with Folidol 600. Pesticide concentrations and cholinesterase (ChE) activities were evaluated in serum, liver, brain, heart, and muscle. The bioconcentration of methyl parathion was similar for all studied fishes. Brain tissue showed the highest pesticide concentration, reaching 80 ppm after exposure for 30 min to methyl parathion. Three to 5 hours of 5 ppm methyl parathion exposure provoked the death of all P. lineatus at 92% brain AChE inhibition, whereas fish from the other two species survived for up to 78 hours with less than 80% brain AChE inhibition. Our results indicate that acute toxic effects of methyl parathion to fish are correlated with brain AChE sensitivity to methyl paraoxon. PMID:26339593

  4. Characterization of the Psychological, Physiological and EEG Profile of Acute Betel Quid Intoxication in Naïve Subjects

    PubMed Central

    Osborne, Peter G.; Chou, Tung-Shan; Shen, Tsu-Wang

    2011-01-01

    Betel quid use and abuse is wide spread in Asia but the physiological basis of intoxication and addiction are unknown. In subjects naïve to the habit of betel quid intoxication, the psychological and physiological profile of intoxication has never been reported. We compared the effect of chewing gum or chewing betel quid, and subsequent betel quid intoxication, on psychological assessment, prospective time interval estimation, numerical and character digit span, computerized 2 choice tests and mental tasks such as reading and mathematics with concurrent monitoring of ECG, EEG and face temperature in healthy, non-sleep deprived, male subjects naïve to the habit of chewing betel quid. Betel quid intoxication, dose dependently induced tachycardia (max 30 bpm) and elevated face temperature (0.7°C) (P<0.001) above the effects observed in response to chewing gum (max 12 bpm and 0.3°C) in 12 subjects. Gross behavioral indices of working memory such as numerical or character digit span in 8 subjects, or simple visual-motor performance such as reaction speed or accuracy in a two choice scenario in 8 subjects were not affected by betel quid intoxication. Betel quid intoxication strongly influenced the psychological aspects of perception such as slowing of the prospective perception of passage of a 1 minute time interval in 8 subjects (P<0.05) and perceived increased arousal (P<0.01) and perceived decreased ability to think (P<0.05) in 31 subjects. The EEG spectral profile recorded from mental states associated with open and closed eyes, and mental tasks such as reading and eyes closed mental arithmetic were significantly modified (P<0.05) relative to chewing gum by betel quid intoxication in 10 subjects. The prevalence of betel quid consumption across a range of social and work settings warrants greater investigation of this widespread but largely under researched drug. PMID:21909371

  5. How CAGE, RAPS4-QF, and AUDIT Can Help Practitioners for Patients Admitted with Acute Alcohol Intoxication in Emergency Departments?

    PubMed Central

    Brousse, Georges; Arnaud, Benjamin; Geneste, Julie; Pereira, Bruno; De Chazeron, Ingrid; Teissedre, Frederique; Perrier, Christophe; Schwan, Raymund; Malet, Laurent; Schmidt, Jeannot; Llorca, Pierre Michel; Cherpitel, Cheryl J.

    2014-01-01

    Aims: To help clinicians to identify the severity of alcohol use disorders (AUDs) from optimal thresholds found for recommended scales. Especially, taking account of the high prevalence of alcohol dependence among patients admitted to the emergency department (ED) for acute alcohol intoxication (AAI), we propose to define thresholds of severity of dependence based on the AUDIT score. Methods: All patients admitted to the ED with AAI (blood alcohol level >0.8 g/L), in a 2-month period, were assessed using the CAGE, RAPS-QF, and AUDIT, with the alcohol dependence/abuse section of the mini international neuropsychiatric interview (MINI) used as the gold standard. To explore the relation between the AUDIT and the MINI the sum of the positive items on the MINI (dependence) as a quantitative variable and as an ordinal parameter were analyzed. From the threshold score found for each scale we proposed intervals of severity of AUDs. Results: The mean age of the sample (122 males, 42 females) was 46 years. Approximately 12% of the patients were identified with alcohol abuse and 78% with dependence (DSM-IV). Cut points were determined for the AUDIT in order to distinguish mild and moderate dependence from severe dependence. A strategy of intervention based on levels of severity of AUD was proposed. Conclusion: Different thresholds proposed for the CAGE, RAPS4-QF, and AUDIT could be used to guide the choice of intervention for a patient: brief intervention, brief negotiation interviewing, or longer more intensive motivational intervention. PMID:25009509

  6. Mechanisms of Acute Alcohol Intoxication-Induced Modulation of Cyclic Mobilization of [Ca2+] in Rat Mesenteric Lymphatic Vessels

    PubMed Central

    Kerut, Edmund K.; Breslin, Jerome W.; Molina, Patricia E.

    2015-01-01

    Abstract Background: We have demonstrated that acute alcohol intoxication (AAI) increases the magnitude of Ca2+ transients in pumping lymphatic vessels. We tested the contribution of extracellular Ca2+ via L-type Ca2+ channels and intracellular Ca2+ release from the sarcoplasmic reticulum (SR) to the AAI-induced increase in Ca2+ transients. Methods and Results: AAI was produced by intragastric administration of 30% alcohol to conscious, unrestrained rats; isovolumic administration of water served as the control. Mesenteric lymphatic vessels were isolated, cannulated, and loaded with Fura-2 AM to measure changes in intracellular Ca2+. Measurements were made at intraluminal pressures of 2, 6, and 10 cm H2O. L-type Ca2+ channels were blocked with nifedipine; IP-3 receptors were inhibited with xestospongin C; and SR Ca2+ release and Ca2+ pool (Ca2+ free APSS) were achieved using caffeine. Nifedipine reduced lymphatic Ca2+ transient magnitude in both AAI and control groups at all pressures tested, but reduced lymphatic contraction frequency only in the control group. Xestospongin C did not significantly change any of the Ca2+ parameters in either group; however, fractional shortening increased in the controls at low transmural pressure. RyR (ryanodine receptor) activation with caffeine resulted in a single contraction with a greater Ca2+ transient in lymphatics from AAI than those from controls. SR Ca2+ pool was also greater in lymphatics isolated from AAI- than from control animals. Conclusions: These data suggest that 1) L-type Ca2+ channels contribute to the AAI-induced increase in lymphatic Ca2+ transient, 2) blockage of IP-3 receptors could increase calcium sensitivity, and 3) AAI increases Ca2+ storage in the SR in lymphatic vessels. PMID:26056854

  7. Opioid intoxication

    MedlinePlus

    Intoxication - opioids ... In the United States, the most commonly abused opioids are heroin and methadone. People who become addicted ... of these drugs. Also, the use of prescription opioids for nonmedical reasons is an extensive and growing ...

  8. Regression of long standing anorexia nervosa following acute renal failure caused by gentamicin intoxication.

    PubMed

    Chodorowski, Zygmunt; Rutkowski, Bolesław; Sein Anand, Jacek; Rutkowski, Przemysław

    2005-01-01

    A female patient aged 22 with fully developed symptoms of anorexia nervosa presented the following metabolic disturbances: persistent hyperuricemia, hyponatruria, (sometimes with sodium lack in urine) as well as frequent hyponatremia and hyper-uricosuria. The patient's low arterial blood pressure (70/40 mm Hg on average) was not improved by pharmacological treatment, and only high oral doses of table salt (20-70 g/24 h) did prove effective in the therapy. The subject passed seven renal calculi composed of sodium urate and uric acid. Numerous urinalyses did not reveal any changes, and bacterial cultures of the urine were also negative. After 14 years of anorexia nervosa, the patient was treated for pneumonia with gentamicin at doses of 2 x 80 mg/24 h. Following third dose of the antibiotic, the patient developed acute renal failure and was treated by haemodialysis for six weeks. The renal function came gradually to the norm. Simultaneously, all the anorexia nervosa symptoms subsided along with sodium metabolism disturbances, while purine metabolism disorders got considerably alleviated. The patient started to have her menstrual cycles again, gained 12 kg in body weight, and one year afterwards bore a son. A further 10-year follow-up period was free of any pathological changes except for a slight hyperuricemia. To the best of our knowledge, the similar case has not been reported in the medical literature and electronic data bases. PMID:16225114

  9. Expression of heat shock protein (HSP 72 kD) during acute methamphetamine intoxication depends on brain hyperthermia: neurotoxicity or neuroprotection?

    PubMed Central

    Kiyatkin, Eugene A.; Sharma, Hari S.

    2011-01-01

    In the present study, light and electron microscopy were used to examine heat shock protein (HSP 72kD) expression during acute methamphetamine (METH) intoxication in rats and evaluate its relationships with brain temperature and alterations in a number of other histochemical and morphological parameters. Freely moving rats received METH at the same dose (9 mg/kg, sc) but at different ambient temperatures (23 and 29°C), showing a wide range of brain temperature elevations (37.6–42.5°C); brains were taken for histochemical and morphological evaluations at peak of brain temperature increase. We found that acute METH intoxication induces massive and wise-spread HSP expression in neural and glial cells examined in details in the cortex, hippocampus, thalamus, and hypothalamus. In each of these structures, the number of HSP-positive cells tightly correlated with brain temperature elevation. The changes in HSP immunoreactivity were also tightly related to alterations in permeability of the blood-brain barrier, acute glial activation and brain edema assessed by albumin and GFAP immunoreactivity and measuring tissue water content, respectively. While robust and generalized HSP production normally appears to be the part of an adaptive brain response associated with METH-induced metabolic activation, activation of this protective mechanism has its natural limits and could not counteract the damaging effects of oxidative stress, high temperature and edema – the leading factors of METH-induced neurotoxicity. PMID:20931246

  10. [Investigations of the distribution of aripiprazole in the internal organs and biological fluids of the laboratory animals in case of acute intoxication].

    PubMed

    Voronkov, A V; Remezova, I P; Lazaryan, D S; Avramenko, N S; Rybasova, A S

    2015-01-01

    Despite the present-day extensive application of aripiprazole, there are many cases of its overdose and of poisoning with this compound. The objective of the present study was to detect and quantify aripiprazole in the internal organs and biological fluids of the laboratory animals in case of acute intoxication. The experiments were carried out on white mice of both sexes weighing 20.5 and 25.7 g. Aripiprazole was isolated from the liver, kidneys, brain, and heart as described by A.A. Vasil'eva and from the plasma and urine by the newly developed original methods. Aripiprazole was identified and quantitatively determined in the extracts from the aforementioned organs and tissues with the use of HPLC. The data obtained on the completeness of extraction from the liver, kidneys , and brain of the laboratory animals indicate that aripiprazole accumulated in the highest concentrations in the brain and kidneys within 24 hours after acute poisoning. Ist content was significantly lower in the liver while no traces of aripiprazole were found in the heart of the mice. The methods for aripiprazole isolation from the urine and blood plasma are described. The maximum amounts of aripiprazole were detected in blood plasma within 24 hours after acute intoxication. It is concluded that the proposed methods for aripiprazole isolation from the biological fluids (blood plasma and urine) can be included in the scheme of the chemical toxicological analysis of this compound. PMID:26856058

  11. Assessing Women’s Sexual Arousal in the Context of Sexual Assault History and Acute Alcohol Intoxication

    PubMed Central

    Gilmore, Amanda K.; Schacht, Rebecca L.; George, William H.; Otto, Jacqueline M.; Davis, Kelly Cue; Heiman, Julia R.; Norris, Jeanette; Kajumulo, Kelly F.

    2011-01-01

    Introduction Few studies have examined differences in women’s sexual arousal based on sexual assault history (SAH) or in-the-moment alcohol intoxication. Only one has examined combined effects. Findings regarding the relationship between SAH and arousal are contradictory. Aim We aimed to determine the relationship between SAH, alcohol intoxication, and sexual arousal. Main Outcome Measures Genital response was measured by vaginal pulse amplitude (VPA) using vaginal photoplethysmography while watching erotic films. Self-reported sexual arousal was assessed after watching erotic films. Methods Women were randomly assigned to an alcohol (target blood alcohol level = .10%) or control condition and categorized as having a SAH or not. After beverage administration, all women watched erotic films while genital arousal (vaginal pulse amplitude; VPA) was measured. Afterwards self-reported sexual arousal was measured. Results Women with a SAH had smaller increases in genital arousal in response to the films than women without a SAH. Intoxicated women had smaller increases in genital arousal than sober women. However, no differences for SAH or intoxication were found in self-reported arousal. Conclusion SAH and alcohol intoxication are associated with smaller increases in genital arousal compared to women without a SAH and sober women, suggesting that these co-occurring factors impact sexual arousal. PMID:20367775

  12. [Acute alcohol intoxication among children and adolescents admitted to the Department of Pediatrics, Pediatric Endocrinology and Diabetes, Medical University of Silesia, Katowice during 2000-2010--preliminary study].

    PubMed

    Kamińska, Halla; Agnieszka, Zachurzok-Buczyńska; Gawlik, Aneta; Małecka-Tendera, Ewa

    2012-01-01

    The alcohol drinking at the young age is a risk factor of alcohol addiction later in life, and is connected with school problems, binge drinking, tobacco addiction, illegal drug use, violence, crime commitment, and risky sexual behaviors. Alcohol drinking in the last 12 months is declared by 78% Polish children. The aim of the study was to evaluate the frequency of admissions due to alcohol intoxication to the Department of Pediatrics, Pediatric Endocrinology and Diabetes, Pediatric Center of Silesia and the identification of the risk factors of the acute alcohol intoxication among Polish children and adolescents. Ten-year retrospective study includes investigation of patients medical records from the Department of Pediatrics. Among 8048 patients hospitalized in the Department of Pediatrics between the years 2000-2010, 220 (2.7%) cases of acute alcohol poisoning occurred The detailed data analysis from 139 patients [66 (47.5%) girls, 73 (52,5%) boys] was done. In the years 2006-2010 the number of girls admitted to the department increased in comparison to boys. The largest group of patients was at age between 14 and 16 years [61 (44%) children]. The blood alcohol concentration at the moment of admission to the hospital was 0.1 to 4.0 per thousand. In most cases (92.8%) the alcohol intoxication was intentional. Five percent of them were suicide attempts. In the youngest group of children alcohol abuse was unintentional. 23 (16.5%) of patients initially needed admission to the intensive care unit. In 30 (21.6%) patient the family was incomplete and five times more often father was absent. The alcohol addiction occurs in 18 (13.0%) fathers and 10 (7.2%) mothers of our patients. It is concluded that over the last decade the number of girls admitted due to alcohol abuse increased. Children at school grade between 7-9 are intoxicated most often. One six of intoxicated patents needed hospitalization at intensive care unit. PMID:23421032

  13. Post-exposure administration of diazepam combined with soluble epoxide hydrolase inhibition stops seizures and modulates neuroinflammation in a murine model of acute TETS intoxication

    SciTech Connect

    Vito, Stephen T.; Austin, Adam T.; Banks, Christopher N.; Inceoglu, Bora; Bruun, Donald A.; Zolkowska, Dorota; Tancredi, Daniel J.; Rogawski, Michael A.; Hammock, Bruce D.; Lein, Pamela J.

    2014-12-01

    Tetramethylenedisulfotetramine (TETS) is a potent convulsant poison for which there is currently no approved antidote. The convulsant action of TETS is thought to be mediated by inhibition of type A gamma-aminobutyric acid receptor (GABA{sub A}R) function. We, therefore, investigated the effects of post-exposure administration of diazepam, a GABA{sub A}R positive allosteric modulator, on seizure activity, death and neuroinflammation in adult male Swiss mice injected with a lethal dose of TETS (0.15 mg/kg, ip). Administration of a high dose of diazepam (5 mg/kg, ip) immediately following the second clonic seizure (approximately 20 min post-TETS injection) effectively prevented progression to tonic seizures and death. However, this treatment did not prevent persistent reactive astrogliosis and microglial activation, as determined by GFAP and Iba-1 immunoreactivity and microglial cell morphology. Inhibition of soluble epoxide hydrolase (sEH) has been shown to exert potent anti-inflammatory effects and to increase survival in mice intoxicated with other GABA{sub A}R antagonists. The sEH inhibitor TUPS (1 mg/kg, ip) administered immediately after the second clonic seizure did not protect TETS-intoxicated animals from tonic seizures or death. Combined administration of diazepam (5 mg/kg, ip) and TUPS (1 mg/kg, ip, starting 1 h after diazepam and repeated every 24 h) prevented TETS-induced lethality and influenced signs of neuroinflammation in some brain regions. Significantly decreased microglial activation and enhanced reactive astrogliosis were observed in the hippocampus, with no changes in the cortex. Combining an agent that targets specific anti-inflammatory mechanisms with a traditional antiseizure drug may enhance treatment outcome in TETS intoxication. - Highlights: • Acute TETS intoxication causes delayed and persistent neuroinflammation. • Diazepam given post-TETS prevents lethal tonic seizures but not neuroinflammation. • A soluble epoxide hydrolase

  14. Hypertonic saline resuscitation enhances blood pressure recovery and decreases organ injury following hemorrhage in acute alcohol intoxicated rodents

    PubMed Central

    Sulzer, Jesse K.; Whitaker, Annie M.; Molina, Patricia E.

    2012-01-01

    Background Acute alcohol intoxication (AAI) impairs the hemodynamic and arginine vasopressin (AVP) counter-regulation to hemorrhagic shock (HS) and lactated Ringer’s (LR) fluid resuscitation (FR). The mechanism of AAI-induced suppression of AVP release in response to HS involves accentuated nitric oxide (NO) inhibitory tone. In contrast, AAI does not prevent AVP response to increased osmolarity produced by hypertonic saline (HTS) infusion. We hypothesized that FR with HTS during AAI would enhance AVP release by decreasing PVN NO inhibitory tone subsequently improving mean arterial blood pressure (MABP) and organ perfusion. Methods Male Sprague Dawley rats received a 15h alcohol infusion (2.5g/kg + 0.3 g/kg/h) or dextrose (DEX) prior to HS (40mmHg × 60 min) and FR with HTS (7.5%; 4ml/kg) or LR (2.4 × blood volume removed). Organ blood flow was determined and brains collected for NO content at 2h post-FR. Results HTS improved MABP recovery in AAI (109 vs 80mmHg) and DEX (114 vs 83mmHg) animals compared to LR. This was associated with higher (>60%) circulating AVP levels at 2h post-FR than those detected in LR animals in both groups. Neither AAI alone nor HS in DEX animals resuscitated with LR altered organ blood flow. In AAI animals, HS and FR with LR reduced blood flow to liver (72%), small intestine (65%), and large intestine (67%) compared to shams. FR with HTS improved liver (3-fold) and small intestine (2-fold) blood flow compared to LR in AAI-HS animals. The enhanced MABP response to HTS was prevented by pretreatment with a systemic AVP V1a receptor antagonist. HTS decreased PVN NO content in both groups 2h post-FR. Conclusions These results suggest that FR with HTS in AAI results in removal of central NO inhibition of AVP, restoring AVP levels and improving MABP and organ perfusion in AAI-HS. PMID:23147176

  15. Synaptic membrane responses to acute and chronic alcohol intoxication in high alcohol sensitive (HAS) and low alcohol sensitive (LAS) selectively bred rats.

    PubMed

    Beaugé, F; Kerfriden, G; Ménez, J F; Aufrère, G; Le Bourhis, B

    1994-11-01

    HAS (high alcohol sensitive) and LAS (low alcohol sensitive) lines of rats have been selectively bred based on their differences in ethanol-induced sleep time. In the present study, the two lines were compared to examine another central effect of acute alcohol intoxication: namely, hypothermia. As the disturbances in membrane microorganization have been associated with the nervous system's sensitivity and tolerance to ethanol, the synaptic plasma membrane fluidity and acute sensitivity to ethanol were also evaluated by fluorescence polarization of DPH probes in the HAS and LAS rats. The two lines did not differ in the magnitude of their hypothermic response after acute injection of ethanol (3 g/kg body wt, i.p.). Although membranes in the HAS line were slightly more rigid than in the LAS line, the level of membrane disordering after acute ethanol addition was identical for the two lines in the region examined with the DPH probe. Following the chronic intoxication of the rats, the two lines developed tolerance to the hypnotic and hypothermic effects of ethanol. In the same way, a membrane resistance (i.e. tolerance) to the disordering effect of acute ethanol addition developed in the region probed with DPH. In general, the LAS line showed a more pronounced level of tolerance than the HAS line at both the functional and membrane level. These results suggest that different measures used to assess the depressant action of ethanol, such as sleep time, hypothermia or membrane disordering, may not be related and could indicate different genetic origins.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7695793

  16. Acute cholinergic syndrome following ingestion of contaminated herbal extract.

    PubMed

    Hsieh, M-J; Yen, Z-S; Chen, S-C; Fang, C-C

    2008-11-01

    Herbal preparations are becoming more and more popular and increasingly used in the USA. Herbs are from natural plants and therefore often considered to be harmless compared with western medicines. Nevertheless, as the use of herbal remedies has risen, so has the incidence of acute and chronic herbal intoxication. The case history is presented of a 68-year-old man who presented with an acute cholinergic syndrome soon after ingesting a herbal preparation containing Flemingia macrophylla and ginseng. His red blood cell acetylcholinesterase activity dropped to 50% of the normal reference range. He was treated successfully with atropine and supportive care. It was thought that contamination with pesticides, such as organophosphate residue, was the probable cause. This case highlights the need to be more aware of the possibility of acute pesticide intoxication in herbal users, even when only small amounts are consumed. PMID:18955628

  17. Anticonvulsants for nerve agent-induced seizures: The influence of the therapeutic dose of atropine.

    PubMed

    Shih, Tsung-Ming; Rowland, Tami C; McDonough, John H

    2007-01-01

    Two guinea pig models were used to study the anticonvulsant potency of diazepam, midazolam, and scopolamine against seizures induced by the nerve agents tabun, sarin, soman, cyclosarin, O-ethyl S-(2-(diisopropylamino)ethyl)methylphosphonothioate (VX), and O-isobutyl S-(2-diethylamino)ethyl)-methyl phosphonothioate (VR). Animals instrumented for electroencephalogram recording were pretreated with pyridostigmine bromide (0.026 mg/kg i.m.) 30 min before challenge with 2 x LD50 (s.c.) of a nerve agent. In model A, atropine sulfate (2.0 mg/kg i.m.) and pyridine-2-aldoxime methylchloride (2-PAM; 25.0 mg/kg i.m.) were given 1 min after nerve agent challenge, and the tested anticonvulsant was given (i.m.) 5 min after seizure onset. In model B, a lower dose of atropine sulfate (0.1 mg/kg i.m.) was given along with 2-PAM 1 min after nerve agent challenge, and the anticonvulsant was given at seizure onset. With the lower dose of atropine, seizure occurrence increased to virtually 100% for all agents; the time to seizure onset decreased for sarin, cyclosarin, and VX; the signs of nerve agent intoxication were more severe; and coma resulted frequently with cyclosarin. The anticonvulsant ED50 doses for scopolamine or diazepam were, in general, not different between the two models, whereas the anticonvulsant ED50 values of midazolam increased 3- to 17-fold with the lower atropine dose. Seizure termination times were not systematically effected by the different doses of atropine. The order of anticonvulsant effectiveness within each model was scopolamine > or = midazolam > diazepam. The findings indicate that the dose of atropine given as antidotal therapy can significantly influence measures of nerve agent toxicity and responsiveness to anticonvulsant therapy. PMID:17015638

  18. [Fatal intoxication with paramethoxyamphetamine].

    PubMed

    Chodorowski, Zygmunt; Wiergowski, Marek; Sein Anand, Jacek

    2002-01-01

    From August to December of the year 2000 we ascertained 7 rapid deaths because of acute intoxication with tablets colloquially called Ufo. There were five men and two women aged from 20 to 29 (average 24) years. Analytic tests showed that one tablet of Ufo contains 40 mg of paramethoxyamphetamine, 1.0 mg of amphetamine, 0.05 mg of methamphetamine, 0.03 mg of 3-4-methylenedioxymethamphetamine. The levels of paramethoxyamphe-tamine in the blood of the deceased, determined by gas chromatography, were from 0.68 to 10.0 (approx. 3.2) mg/L and in the urine from 16 to 64 (approx. 35) mg/L. The press and television campaign caused elimination of fatal intoxications with parametoxy-amphetamine during the last 13 months. PMID:12184013

  19. The effect of atropine on the activation of 5-hydroxytryptamine3 channels in rat nodose ganglion neurons.

    PubMed

    Fan, P; Weight, F F

    1994-10-01

    It has been suggested that changes in brain 5-hydroxytryptamine3 receptor function may contribute to some behavior disorders, such as anxiety, schizophrenia and drug abuse. We are using the whole-cell version of the patch-clamp technique to study the function of 5-hydroxytryptamine3 channels in neurons freshly dissociated from rat nodose ganglion. In these cells, 5-hydroxytryptamine elicits an inward current over the concentration range of 0.25-100 microM (EC50 = 2.62 microM) by activating 5-hydroxytryptamine3 receptors. The muscarinic cholinergic antagonist atropine reduced the amplitude of 5-hydroxytryptamine activated inward current in a concentration-dependent manner. Other muscarinic antagonists, scopolamine, dexetimide, the M1 muscarinic receptor antagonist pirenzepine, the M2 receptor antagonist methoctramine and the M3 receptor antagonist 4-DAMP methiodide also inhibited 5-hydroxytryptamine-induced inward current. Atropine did not appear to change the reversal potential of this current. In the presence of 5 microM atropine, the concentration-response curve for 5-hydroxytryptamine current was shifted to the right in a parallel fashion. The EC50 value for 5-hydroxytryptamine was increased from 2.62 to 8.76 microM. Schild plots of increasing atropine and 5-hydroxytryptamine concentrations revealed a pA2 value of 5.74 for atropine (apparent KD = 1.8 microM). These observations suggest that atropine competitively antagonizes the activation of a receptor for the neurotransmitter serotonin, a novel action of muscarinic antagonists in the nervous system. This effect of atropine may contribute to the clinical symptoms seen in severe atropine intoxication. PMID:7531305

  20. Effect of atropine sulfate on soman-induced blood-brain barrier (BBB) opening

    SciTech Connect

    Carpentier, P.; Lallement, G.; Tarricone, A.; Blanchet, G.

    1993-05-13

    Using Evans-Blue (EB) labeled serum albumin, it was recently shown that soman may produce seizure-related and reversible BBB opening in rats. Topographically, whereas hippocampus was never damaged, protein leakage was most frequent in the thalamus, and to a lesser degree, in certain basal formations (hypothalamus, amygdala, preoptic area, corpus mammillare) and lateral septum. In the present study, the distribution of soman-induced BBB opening was similar when intoxicated rats were pretreated by atropine methyl nitrate (AMN) a muscarinic blocker which does not penetrate the BBB. On the other hand, when AMN was substituted by atropine sulfate (AS), which is known to readily cross the BBB, thalamic nuclei became totally devoid of any vascular lesions whereas EB leakage still remained in the other normally damaged brain structures listed above. Therefore, the muscarinic cholinergic system appears to play a more prominent role on BBB control in the thalamus than in other cerebral regions.

  1. [A case of acute ethanol intoxication with remarkable hyperglycemia by "ume-shu", a Japanese apricot liquor made with a large amount of sugar].

    PubMed

    Sugano, Takayuki; Kojima, Naoki; Kaneko, Susumu; Ishida, Junro; Terada, Taizo; Inagawa, Hiroshi; Okada, Yasusei

    2002-07-01

    A 19-year-old woman ingested 2.2 L of "umeshu", a Japanese apricot liquor made with a large amount of sugar. She was unconscious and in shock. The estimated blood ethanol concentration was 607 mg/dl, and the blood glucose level was 576 mg/dl. Because her respiration and circulation was highly suppressed, blood purification was indicated. Continuous hemodiafiltration (CHDF) was performed instead of hemodialysis because her hemodynamics was unstable. After CHDF was instituted, her blood glucose level reduced to normal range, and her consciousness became alert. CHDF was effective in eliminating ethanol and stabilizing her hemodynamics within an early stage. Though acute ethanol intoxication is known to inhibit glucogenesis, leading to hypoglycemia, marked hyperglycemia was seen in this case. Ingestion of a large amount of glucose-rich liquor and being in shock seemed to be the causes of hyperglycemia. PMID:12415871

  2. Acute ethanol intoxication shows no effect on Ca sup 2+ -uptake of Ca sup 2+ -dependent ATPase activity in myocardial sarcoplasmic reticulum vesicles

    SciTech Connect

    McAllister, K.P.; Horton, J.W.; Kaufman, T.M.; White, D.J. )

    1989-02-09

    We have previously shown that acute ethanolism impairs left ventricular (LV) function. We hypothesized that cardiac dysfunction may be related to altered Ca{sup 2+} pump function by the sarcoplasmic reticulum (SR). In this study, LV function (in isolated perfused hearts) was compared to Ca{sup 2+} transport in SR vesicles isolated from nonperfused hearts in control (C) and acutely intoxicated (ETOH, 2.5 ml/kg IV) guinea pigs. Compared to control hearts, ETOH hearts had significantly lower LV systolic pressure maximal rate of LV pressure rise and fall. Ca{sup 2+}-ATPase activity was not significantly different in either group of animals. Although maximum Ca{sup 2+} uptake tended to be slightly lower in ETOH compared to control hearts coupling ratios (mol Ca{sup 2+} transported/mol ATP hydrolyzed) were not significantly different. We conclude that changes in SR Ca{sup 2+} pump function are not responsible for the depressed LV function seen in acute ethanolism.

  3. Barbiturate Intoxication

    PubMed Central

    Goodman, Jay M.; Bischel, Margaret D.; Wagers, Park W.; Barbour, Benjamin H.

    1976-01-01

    The complications encountered in caring for 185 patients intoxicated with barbiturates were reviewed. The population consisted of 142 patients with long-acting barbiturate concentrations of 8 mg per 100 ml or greater, 20 patients with short-acting barbiturate concentrations of 3 mg per 100 ml or greater and 23 consecutive patients with short-acting barbiturate intoxication referred for monitoring. Pneumonia was the major cause of morbidity and mortality and correlated best with the initial depth of coma and the use of an endotracheal tube in treatment. Cardiovascular instability manifested by pulmonary edema was the next leading cause of morbidity and mortality and correlated best with the initial depth of coma and the quantity of intravenous fluid administered. In retrospect, use of eliminative measures such as dialysis would probably not have altered the outcome in most of the patients who died and attempts at forced diuresis may have contributed to several deaths. Particular emphasis should be placed on the problems of sepsis and fluid therapy in the management of these patients. PMID:1258466

  4. Administration of Flumazenil in a Patient with Acute Abamectin Intoxication: Case Report and Review of the Literature.

    PubMed

    Sun, B; Jia, L; Nie, S

    2015-03-01

    Abamectin is used in several countries as a type of macrocyclic lactone insecticide to control nematodes and other pests in livestock and agriculture. This medicine, used for animals and crops, would be highly toxic to human if a person has intentional poisoning. We report a case of a 47-year old man who was admitted to the hospital after ingestion of a large dose of abamectin on purpose, and who rapidly recovered consciousness after administration of flumazenil. Although flumazenil is not the antidote of abamectin, we may hypothesize that it could reduce recovery time and shorten expenditures in hospital. This is the first report that focusses on a specific treatment which could possibly accelerate recovery of consciousness for patients with abamectin intoxication. PMID:26360693

  5. Administration of Flumazenil in a Patient with Acute Abamectin Intoxication: Case Report and Review of the Literature

    PubMed Central

    Sun, B; Jia, L; Nie, S

    2015-01-01

    ABSTRACT Abamectin is used in several countries as a type of macrocyclic lactone insecticide to control nematodes and other pests in livestock and agriculture. This medicine, used for animals and crops, would be highly toxic to humans if a person has intentional poisoning. We report a case of a 47-year old man who was admitted to the hospital after ingestion of a large dose of abamectin on purpose, and who rapidly recovered consciousness after administration of flumazenil. Although flumazenil is not the antidote of abamectin, we may hypothesize that it could reduce recovery time and shorten expenditures in hospital. This is the first report that focusses on a specific treatment which could possibly accelerate recovery of consciousness for patients with abamectin intoxication. PMID:26360693

  6. Patient with hepatocellular carcinoma related to prior acute arsenic intoxication and occult HBV: Epidemiological, clinical and therapeutic results after 14 years of follow-up

    PubMed Central

    Casanovas-Taltavull, Teresa; Ribes, Josepa; Berrozpe, Ana; Jordan, Sara; Casanova, Aurora; Sancho, Concha; Valls, Carles; Bosch, F Xavier

    2006-01-01

    Little is known about the long-term survivors of acute arsenic intoxication. We present here a clinical case report of a man with chronic hepatitis B virus (HBV) infection who developed hepatocellular carcinoma four years after acute arsenic poisoning. HBsAg was detected in serum in 1990 when he voluntarily donated blood. In 1991, the patient suffered from severe psychological depression that led him to attempt suicide by massive ingestion of an arsenic-containing rodenticide. He survived with polyneuropathy and paralysis of the lower limbs, and has been wheelchair-bound since then. During participation in a follow-up study conducted among HBV carriers, abdominal ultrasound detected a two-centimeter liver mass consistent with hepatocellular carcinoma. The tumor was confirmed by computed tomography (CT) and magnetic resonance image (MRI). Because of his significant comorbidity, the patient received palliative treatment with transarterial lipiodol chemoembolization (TACE) on three occasions (1996, 1997 and 1999). At his most recent visit in May 2005, the patient was asymptomatic, liver enzymes were normal and the tumor was in remission on ultrasound. PMID:16610011

  7. Acute toxicity of some synthetic cyanogens in rats: time-dependent cyanide generation and cytochrome oxidase inhibition in soft tissues after sub-lethal oral intoxication.

    PubMed

    Rao, Pooja; Singh, Poonam; Yadav, Shiv Kumar; Gujar, Niranjan L; Bhattacharya, Rahul

    2013-09-01

    Cyanogens include complex nitrile-containing compounds that can generate free cyanide of toxicological significance. Acute toxicity, time-dependent cyanide generation and cytochrome oxidase (CYTOX) inhibition in soft tissues, and urinary thiocyanate levels were measured after acute cyanogen intoxication in rats. Order of cyanogens in terms of LD₅₀ was: malononitrile (MCN)>propionitrile (PCN)≈sodium nitroprusside (SNP)>acrylonitrile (ACN)>succinonitrile (SCN)>acetonitrile (ATCN) for oral, and SNP>MCN>ACN>PCN>SCN>ATCN for intraperitoneal and subcutaneous routes. MCN was most toxic by oral (LD₅₀=66.4 mg/kg) and SNP by intraperitoneal (LD₅₀=16.7 mg/kg) and subcutaneous (LD₅₀=11.9 mg/kg) routes. Minimum survival time (25 min) was recorded after 4.0 LD₅₀ ATCN. Order of cyanogens (0.75 LD₅₀; oral) on the basis of maximum blood cyanide and time of peak cyanide generation were: ATCN>SNP>SCN>PCN>MCN>ACN, and MCN (30 min)

  8. Acute 3,4-methylenedioxy-N-ethylcathinone (ethylone) intoxication and related fatality: a case report with postmortem concentrations.

    PubMed

    McIntyre, Iain M; Hamm, Catherine E; Sherrard, James L; Gary, Ray D; Burton, Christopher G; Mena, Othon

    2015-04-01

    A 30-year-old man reportedly ingested pills and used illicit drugs with another person. They both fell asleep that night and the following afternoon the other person found him dead. There were used hypodermic needles and a metal spoon with dark tarry substance at the death scene, and two recent puncture sites were found on his body. It was uncertain if he had a history of illicit drug use. Postmortem blood initially screened borderline positive for methamphetamine by ELISA. An alkaline drug screen-detected ethylone which was subsequently confirmed and quantified by a specific GC-MS SIM analysis following solid-phase extraction. Concentrations were determined in the peripheral blood (0.39 mg/L), central blood (0.38 mg/L), liver (1.4 mg/kg), vitreous (0.58 mg/L), urine (20 mg/L) and gastric contents (12 mg). Other compounds detected in peripheral blood were morphine (0.05 mg/L), alprazolam (<0.05 mg/L), delta-9-THC (<1 ng/mL), delta-9-carboxy-THC (3.6 ng/mL) and naproxen (<5 mg/L). A urine screen (GC-MS) also confirmed 6-monoacetylmorphine, codeine and sildenafil. The cause of death was certified due to mixed ethylone, heroin and alprazolam intoxication. The manner of death was certified as accident. PMID:25540061

  9. Effects of atropine treatment on in vitro and in vivo binding of 4-[125I]-dexetimide to central and myocardial muscarinic receptors.

    PubMed

    Uno, Y; Matsumura, K; Scheffel, U; Wilson, A A; Dannals, R F; Wagner, H N

    1991-01-01

    Upregulation of muscarinic cholinergic receptors (mAChR) after chronic atropine treatment has been described previously. The present study was designed to evaluate 4-iodine-125 dexetimide as an agent to determine changes in the number of mAChR. Rats were injected subcutaneously with atropine (500 mg/kg) either once or chronically, once daily for 10 days, and sacrificed 24 h later. In vitro binding assays with 4-[125I]-dexetimide showed significant increases in the number of mAChR in cerebra (21%) and ventricles (45%) after chronic atropine treatment but not after acute treatment. The affinity of binding to cerebral and ventricular mAChR declined after acute and chronic atropine treatment. In vivo studies were carried out involving intravenous injection of 4-[125I]-dexetimide 24 h after atropine treatment. Binding was markedly reduced in the brain and heart. Upregulation of mAChR, as seen in in vitro studies, could not be observed because of the remaining atropine. Occupancy of mAChR by atropine persisted as long as 7 days after one dose. The results of these studies indicate that 4-[125I]-dexetimide binding reflects the effects of atropine on central and peripheral muscarinic cholinergic receptors in vitro and in vivo. PMID:1915471

  10. A prospective study of the influence of acute alcohol intoxication versus chronic alcohol consumption on outcome following traumatic brain injury.

    PubMed

    Lange, Rael T; Shewchuk, Jason R; Rauscher, Alexander; Jarrett, Michael; Heran, Manraj K S; Brubacher, Jeffrey R; Iverson, Grant L

    2014-08-01

    The purpose of the study was to disentangle the relative contributions of day-of-injury alcohol intoxication and pre-injury alcohol misuse on outcome from TBI. Participants were 142 patients enrolled from a Level 1 Trauma Center (in Vancouver, Canada) following a traumatic brain injury (TBI; 43 uncomplicated mild TBI and 63 complicated mild-severe TBI) or orthopedic injury [36 trauma controls (TC)]. At 6-8 weeks post-injury, diffusion tensor imaging (DTI) of the whole brain was undertaken using a Phillips 3T scanner. Participants also completed neuropsychological testing, an evaluation of lifetime alcohol consumption (LAC), and had blood alcohol levels (BALs) taken at the time of injury. Participants in the uncomplicated mild TBI and complicated mild-severe TBI groups had higher scores on measures of depression and postconcussion symptoms (d = 0.45-0.83), but not anxiety, compared with the TC group. The complicated mild-severe TBI group had more areas of abnormal white matter on DTI measures (all p < .05; d = 0.54-0.61) than the TC group. There were no difference between groups on all neurocognitive measures. Using hierarchical regression analyses and generalized linear modeling, LAC and BAL did provide a unique contribution toward the prediction of attention and executive functioning abilities; however, the variance accounted for was small. LAC and BAL did not provide a unique and meaningful contribution toward the prediction of self-reported symptoms, DTI measures, or the majority of neurocognitive measures. In this study, BAL and LAC were not predictive of mental health symptoms, postconcussion symptoms, cognition, or white-matter changes at 6-8 weeks following TBI. PMID:24964748

  11. Bilateral vagotomy or atropine pre-treatment reduces experimental diesel-soot induced lung inflammation

    SciTech Connect

    McQueen, D.S. . E-mail: D.S.McQueen@ed.ac.uk; Donaldson, K.; McNeilly, J.D.; Barton, N.J.; Duffin, R.

    2007-02-15

    To investigate the role of the vagus nerve in acute inflammatory and cardiorespiratory responses to diesel particulate (DP) in the rat airway, we measured changes in respiration, blood pressure and neutrophils in lungs of urethane anesthetized Wistar rats 6-h post-instillation of DP (500 {mu}g) and studied the effect of mid-cervical vagotomy or atropine (1 mg kg{sup -1}) pre-treatment. In conscious rats, we investigated DP, with and without atropine pre-treatment. DP increased neutrophil level in BAL (bronchoalveolar lavage) fluid from intact anesthetized rats to 2.5 {+-} 0.7 x 10{sup 6} cells (n = 8), compared with saline instillation (0.3 {+-} 0.1 x 10{sup 6}, n = 7; P < 0.05). Vagotomy reduced DP neutrophilia to 0.8 {+-} 0.2 x 10{sup 6} cells (n = 8; P < 0.05 vs. intact); atropine reduced DP-induced neutrophilia to 0.3 {+-} 0.2 x 10{sup 6} (n = 4; P < 0.05). In conscious rats, DP neutrophilia of 8.5 {+-} 1.8 x 10{sup 6}, n = 4, was reduced by pre-treatment with atropine to 2.2 {+-} 1.2 x 10{sup 6} cells, n = 3. Hyperventilation occurred 6 h after DP in anesthetized rats with intact vagi, but not in bilaterally vagotomized or atropine pre-treated animals and was abolished by vagotomy (P < 0.05, paired test). There were no significant differences in the other variables (mean blood pressure, heart rate and heart rate variability) measured before and 360 min after DP. In conclusion, DP activates a pro-inflammatory vago-vagal reflex which is reduced by atropine. Muscarinic ACh receptors in the rat lung are involved in DP-induced neutrophilia, and hence muscarinic antagonists may reduce airway and/or cardiovascular inflammation evoked by inhaled atmospheric DP in susceptible individuals.

  12. D-Galactosamine Intoxication in Experimental Animals: Is it Only an Experimental Model of Acute Liver Failure?

    PubMed Central

    Saracyn, Marek; Zdanowski, Robert; Brytan, Marek; Kade, Grzegorz; Nowak, Zbigniew; Patera, Janusz; Dyrla, Przemysław; Gil, Jerzy; Wańkowicz, Zofia

    2015-01-01

    Background Short-term administration of Galactosamine to experimental animals causes liver damage and acute liver failure (ALF), as well as acute renal failure in some cases. The aim of our study was to describe kidney disorders that developed in the course of galactosamine-induced liver failure. Material/Methods Sprague-Dawley rats were randomly divided into 2 groups: a study group administered galactosamine intraperitoneally and a control group administered saline. Results All the animals in the study group developed liver damage and failure within 48 h, with significant increase of alanine (p<0.001), aspartate aminotransferases (p<0.0001), bilirubin (p<0.004), and ammonia (p<0.005) and decrease of albumin (p<0.001) concentrations. Acute renal failure was observed in all test animals, with a significant increase in creatinine (p<0.001) and urea (p<0.001) concentrations and a decrease in creatinine clearance (p<0.0012). Moreover, osmotic clearance (p<0.001), daily natriuresis (p<0.003), and fractional sodium excretion (p<0.016) decreased significantly in this group of animals. The ratio of urine osmolality to serum osmolality did not change. Histopathology of the liver revealed massive necrosis of hepatocytes, whereas renal histopathology showed no changes. Conclusions Acute renal failure that developed in the course of galactosamine-induced ALF was of a functional nature, with the kidneys retaining the ability to concentrate urine and retain sodium, and there were no renal changes in the histopathological examination. It seems that the experimental model of ALF induced by galactosamine can be viewed as a model of hepatorenal syndrome that occurs in the course of acute damage and liver failure. PMID:26009004

  13. GHB Pharmacology and Toxicology: Acute Intoxication, Concentrations in Blood and Urine in Forensic Cases and Treatment of the Withdrawal Syndrome

    PubMed Central

    Busardò, Francesco P.; Jones, Alan W.

    2015-01-01

    The illicit recreational drug of abuse, γ-hydroxybutyrate (GHB) is a potent central nervous system depressant and is often encountered during forensic investigations of living and deceased persons. The sodium salt of GHB is registered as a therapeutic agent (Xyrem®), approved in some countries for the treatment of narcolepsy-associated cataplexy and (Alcover®) is an adjuvant medication for detoxification and withdrawal in alcoholics. Trace amounts of GHB are produced endogenously (0.5-1.0 mg/L) in various tissues, including the brain, where it functions as both a precursor and a metabolite of the major inhibitory neurotransmitter γ-aminobutyric acid (GABA). Available information indicates that GHB serves as a neurotransmitter or neuromodulator in the GABAergic system, especially via binding to the GABA-B receptor subtype. Although GHB is listed as a controlled substance in many countries abuse still continues, owing to the availability of precursor drugs, γ-butyrolactone (GBL) and 1,4-butanediol (BD), which are not regulated. After ingestion both GBL and BD are rapidly converted into GHB (t½ ~1 min). The Cmax occurs after 20-40 min and GHB is then eliminated from plasma with a half-life of 30-50 min. Only about 1-5% of the dose of GHB is recoverable in urine and the window of detection is relatively short (3-10 h). This calls for expeditious sampling when evidence of drug use and/or abuse is required in forensic casework. The recreational dose of GHB is not easy to estimate and a concentration in plasma of ~100 mg/L produces euphoria and disinhibition, whereas 500 mg/L might cause death from cardiorespiratory depression. Effective antidotes to reverse the sedative and intoxicating effects of GHB do not exist. The poisoned patients require supportive care, vital signs should be monitored and the airways kept clear in case of emesis. After prolonged regular use of GHB tolerance and dependence develop and abrupt cessation of drug use leads to unpleasant

  14. The effect of acute alcohol intoxication on gut wall integrity in healthy male volunteers; a randomized controlled trial.

    PubMed

    de Jong, W J; Cleveringa, A M; Greijdanus, B; Meyer, P; Heineman, E; Hulscher, J B

    2015-02-01

    The aim of the study is to determine the effect of acute alcohol consumption on enterocytes. Chronic alcohol consumption has been known to induce a decrease in gut wall integrity in actively drinking alcoholics and patients with alcohol-induced liver disease. Data on the extent of the damage induced by acute alcohol consumption in healthy human beings is scarce. Studies show that heavy incidental alcohol consumption is a growing problem in modern society. Data on this matter may provide insights into the consequences of this behavior for healthy individuals. In a randomized clinical trial in crossover design, 15 healthy volunteers consumed water one day and alcohol the other. One blood sample was collected pre-consumption, five every hour post-consumption, and one after 24 h. Intestinal fatty acid binding protein (I-FABP) was used as a marker for enterocyte damage. Liver fatty acid binding protein (L-FABP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) were used as markers for hepatocyte damage. Lipopolysaccharide binding protein (LBP) and soluble CD14 (sCD14) were used as a measure of translocation. Interleukin-6 (IL-6) was used to assess the acute inflammatory response to endotoxemia. Alcohol consumption caused a significant increase in serum I- and L-FABP levels, compared to water consumption. Levels increased directly post-consumption and decreased to normal levels within 4 h. LBP, sCD14, and IL-6 levels were not significantly higher in the alcohol group. Moderate acute alcohol consumption immediately damages the enterocyte but does not seem to cause endotoxemia. PMID:25559494

  15. Development of a combined solution formulation of atropine sulfate and obidoxime chloride for autoinjector and evaluation of its stability.

    PubMed

    Ettehadi, Hossein Ali; Ghalandari, Rouhollah; Shafaati, Alireza; Foroutan, Seyed Mohsen

    2013-01-01

    Atropine (AT) and oximes, alone or in combination, have been proven greatly valuable therapeutics in the treatment of organophosphates intoxications. An injectable mixture of AT and obidoxime (OB) was formulated for the administration by automatic self-injector. The aqueous single dose solution contained 275 mg obidoxime chloride and 2.5 mg atropine sulfate per 1 mL (220 mg and 2 mg per 0.8 effective dose, respectively). The final solution was sterilized by filtration through a 0.22 μm pore size filter. This more concentrated solution allowed to use a smaller size and lighter weight cartridge. Quality control tests, including assay of the two major compounds were performed separately, using reversed-phase HPLC methods. Besides, the stability test was carried out according to ICH guideline for the accelerated test. The obtained results showed that the proposed formulation is stable over a period of 2 years after preparation. PMID:24250669

  16. Development of a Combined Solution Formulation of Atropine Sulfate and Obidoxime Chloride for Autoinjector and Evaluation of Its Stability

    PubMed Central

    Ettehadi, Hossein Ali; Ghalandari, Rouhollah; Shafaati, Alireza; Foroutan, Seyed Mohsen

    2013-01-01

    Atropine (AT) and oximes, alone or in combination, have been proven greatly valuable therapeutics in the treatment of organophosphates intoxications. An injectable mixture of AT and obidoxime (OB) was formulated for the administration by automatic self-injector. The aqueous single dose solution contained 275 mg obidoxime chloride and 2.5 mg atropine sulfate per 1 mL (220 mg and 2 mg per 0.8 effective dose, respectively). The final solution was sterilized by filtration through a 0.22 μm pore size filter. This more concentrated solution allowed to use a smaller size and lighter weight cartridge. Quality control tests, including assay of the two major compounds were performed separately, using reversed-phase HPLC methods. Besides, the stability test was carried out according to ICH guideline for the accelerated test. The obtained results showed that the proposed formulation is stable over a period of 2 years after preparation. PMID:24250669

  17. [Research on whether atropine can be substituted by the powerful cycloplegic cyclopentolate].

    PubMed

    Xu, Jiang-tao

    2012-09-01

    For a long time, atropine eye ointment has been widely used as the cycloplegic for children's optometry in China, while internationally, cyclopentolate gutta is widely used as the first choice for cycloplegic. In recent years, 1% cyclopentolate hydrochloride ocular humor has been introduced to our country. This effective and powerful cycloplegic has already been paid close attention to by domestic pedo-ophthalmologists. According to a serious of studies both home and abroad on the therapeutic effects of the own control drugs, the cycloplegia effect of cyclopentolate is close to the atropine. Cyclopentolate can be widely used for the cycloplegia before optometry for the Chinese children. However, the effect of cyclopentolate is still not as good as atropine. So, for the children with farsightedness within 7 years old, all esotropia children, Am children, and children who suffer from decreased vision acuteness and needs to be excluded from accommodative myopia, atropine eye ointment should be routinely used for cycloplegia before optometry. In this article, we also discuss the medication dosage, medication method, possible drug adverse reactions of cyclopentolate humor ocular and the coping measures at the same time. PMID:23141569

  18. [Paraquat intoxication and hemocarboperfusion].

    PubMed

    Castro, Rui; Prata, Catarina; Oliveira, Luis; Carvalho, Maria João; Santos, Josefina; Carvalho, Félix; Morgado, Teresa

    2005-01-01

    In the northeast of Portugal, paraquat intoxication is common. We report 31 patients, admitted at our institution from April 1997 to June 2004, with suspected paraquat intoxication. Thirty cases had suicidal intention and all have ingested the toxic by mouth. Treatment consisted of skin and digestive decontamination with gastric washing and activated charcoal or Fuller's Earth. The first medical care was performed after 1 h 14 min at median [9 min-11 h 26 min]. By laboratory measurement (n=13) and/or clinical observation (n=11) it was possible to confirm the gastrointestinal absorption of paraquat for 24 patients (17 male-7 female; 49 +/- 17 years). The estimated ingested volume was higher for 15 non-survivors relatively to nine survivors (170 +/- 60 mL vs 25 +/- 10 mL; P<0,001). Initial serum paraquat of seven non-survivors was also higher than the serum level of six survivors (8.3 +/- 6.9 mg/L vs 0.4 +/- 0.3 mg/L; P < 0.01). Remarkably, all patients with serum paraquat higher than 1.7 ml/l did not survived. The paraquat urine level, simultaneous to the first serum determination, was higher for six survivors (38 +/- 37 mg/L) comparing with four non-survivors patients (465 +/- 536 mg/L; P<0.04). Hemoperfusion with activated charcoal was performed after December 1997 until June 2004 for 25 patients. Twenty of the 24 patients confirmed for paraquat intoxication were treated with this technique (12/15 of the non-survivors and 8/9 of the survivors; p=NS). Total number of sessions was identical (2.0 +/- 1.0 vs 1.5 +/- 1.2; P=NS), total time of hemoperfusion was higher (7 h 58 min vs 5 h 37 min; P=0.07) but the beginning of the first session was later (7 h 44 min vs 4 h 18 min; P=0.04) for the survivors. Clinical signs and laboratory analysis were collected at admission trying to detect markers of prognostic survival value. Hypernatremia, hypokaliemia, hyperglycemia and acute renal failure were more frequent for non-survivors (P<0.05) but the variable timing of the first

  19. Comparative studies of oral administration of marine collagen peptides from Chum Salmon (Oncorhynchus keta) pre- and post-acute ethanol intoxication in female Sprague-Dawley rats.

    PubMed

    Liang, Jiang; Li, Qiong; Lin, Bing; Yu, Yongchao; Ding, Ye; Dai, Xiaoqian; Li, Yong

    2014-09-01

    The present study aimed to evaluate the effect of an oral administration of marine collagen peptides (MCPs) pre- and post-acute ethanol intoxication in female Sprague-Dawley (SD) rats. MCPs were orally administered to rats at doses of 0 g per kg bw, 2.25 g per kg bw, 4.5 g per kg bw and 9.0 g per kg bw, prior to or after the oral administration of ethanol. Thirty minutes after ethanol treatment, the effect of MCPs on motor incoordination and hypnosis induced by ethanol were investigated using a screen test, fixed speed rotarod test (5 g per kg bw ethanol) and loss of righting reflex (7 g per kg bw ethanol). In addition, the blood ethanol concentrations at 30, 60, 90, and 120 minutes after ethanol administration (5 g per kg bw ethanol) were measured. The results of the screen test and fixed speed rotarod test suggested that treatment with MCPs at 4.5 g per kg bw and 9.0 g per kg bw prior to ethanol could attenuate ethanol-induced loss of motor coordination. Moreover, MCP administered both pre- and post-ethanol treatment had significant potency to alleviate the acute ethanol induced hypnotic states in the loss of righting reflex test. At 30, 60, 90 and 120 minutes after ethanol ingestion at 5 g per kg bw, the blood ethanol concentration (BEC) of control rats significantly increased compared with that in the 4.5 g per kg bw and 9.0 g per kg bw MCP pre-treated groups. However, post-treatment with MCPs did not exert a significant inhibitory effect on the BEC of the post-treated groups until 120 minutes after ethanol administration. Therefore, the anti-inebriation effect of MCPs was verified in SD rats with the possible mechanisms related to inhibiting ethanol absorption and facilitating ethanol metabolism. Moreover, the efficiency was better when MCPs were administered prior to ethanol. PMID:24992080

  20. Effect of L-ornithine L-aspartate on Liver Injury Due to Acute Ethyl Alcohol Intoxication in Rats

    PubMed Central

    Durgun, HM; Ozhasenekler, A; Dursun, R; Basarali, MK; Turkcu, G; Orak, M; Ustundag, M; Guloglu, C

    2015-01-01

    ABSTRACT Objective: Ethyl alcohol is a substance that is widely used worldwide and known to exert toxic effects on liver. In this study, we aimed to examine the effect of L-ornithine L-aspartate (LOLA) on the toxicity of a single dose of ethyl alcohol in rats. Subjects and Method: We used 32 randomly selected male Sprague-Dawley rats weighing 200–250 g. The rats were grouped into four groups with each group containing eight rats: Group 1: the control group, Group 2: the ethyl alcohol group, Group 3: the LOLA group and Group 4: the ethyl alcohol+LOLA group. Ethyl alcohol was administered orally through a nasogastric tube at a dose of 6 g/kg after diluting with distilled water. One hour after ethyl alcohol administration, LOLA was administered to pre-specified groups orally through a nasogastric tube at a dose of 200 mg/kg after diluting with distilled water. Liver tissue and blood samples were obtained from all rats 24 hours later to study total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) levels in liver samples, and aspartate aminotransferase (AST), alanine transferase (ALT), TAC, TOS and OSI levels in blood samples. Results: Serum TAC, TOS and OSI levels were higher in the groups that were administered ethyl alcohol. In addition, tissue TAC level was higher and TOS and OSI levels were lower in groups that were given ethyl alcohol. No significant changes were observed in serum and tissue TAC, TOS, OSI, ALT and AST levels in the LOLA administered groups. Conclusion: This study showed that LOLA was not biochemically effective and exerts no oxidative stress reducing activity in liver injury due to acute ethyl alcohol toxicity. PMID:26426168

  1. The influence of pilocarpine and atropine on pentobarbital-induced nystagmus in the New Zealand white rabbit.

    PubMed

    Kairys, D J; Smith, M B

    1979-12-01

    Nystagmus, induced by intravenous pentobarbital in rabbits, increased in frequency and amplitude as a result of intravenous pilocarpine administration. In seven of nine animals anesthetized with pentobarbital but not showing eye movements, pilocarpine injection elicited nystagmus. In all rabbits, nystagmus was terminated by subsequent intravenous administration of atropine, indicating that the parasympathetic nervous system contributes to nystagmus observed in barbiturate treated animals. The results reported here are of value in their implication for an understanding of the physiologic mechanisms which underlie eye movement disorders commonly observed in barbituarate intoxicated individuals. PMID:521585

  2. Plasma atropine concentrations via intravenous, endotracheal, and intraosseous administration.

    PubMed

    Prete, M R; Hannan, C J; Burkle, F M

    1987-03-01

    To date, there have been limited studies on the pharmacokinetics of intravenous atropine and no pharmacokinetic studies on the endotracheal or intraosseous administration of atropine. This study examines the time to peak plasma concentration of atropine following intravenous, endotracheal, and intraosseous administration in anesthetized monkeys using a triple crossover design. Plasma atropine was assayed by a radioreceptor method. The time to peak plasma concentration of atropine was shortest with intravenous administration; and longest with endotracheal administration. The mean plasma concentration of atropine was significantly higher in intravenous administrations than in endotracheal administrations at 0.75 and 2 minutes; compared to that noted in intraosseous administrations, the concentration was significantly higher only at 0.75 minutes. The mean plasma concentration of atropine administered intraosseously was significantly higher than that of endotracheal administrations at 5 minutes and was greater than that of intravenous and endotracheal administrations for the samples collected from 5 to 30 minutes. The endotracheal and intraosseous routes provide alternatives to the intravenous administration of atropine when intravenous access is limited or not available. PMID:3828010

  3. [Metabolic therapy of postperitoneal intoxication].

    PubMed

    Vlasov, A P; Anaskin, S G; Vlasova, T I; Chivisov, S M; Shibitov, V A; Potyanova, I V; Selentsov, P V

    2012-01-01

    This clinico-laboratory study showed that antihypoxant remaxol promoted normalization of lipid metabolism in acute peritonitis and significantly reduced membrane-destabilizing events. This resulted in rapid elimination of the inflammatory process in the abdominal cavity and lowering of the intensity of endogenous intoxication. This beneficial effect decreased the severity of myocardial lesions and resulted in the normalization of erythrocyte function. It is concluded that the regulatory action of remaxol on lipid metabolism is due to its ability to control free radicals in lipid peroxidation and reduce phospholipase A2 activity. PMID:23285765

  4. Fatal intoxication with methoxetamine.

    PubMed

    Adamowicz, Piotr; Zuba, Dariusz

    2015-01-01

    Methoxetamine (MXE) is a new synthetic drug of abuse structurally related to ketamine and phencyclidine. A case of a 29-year-old male with acute toxicity related to the analytically confirmed use of MXE is reported. The man was found dead at his residence. Biological material was analyzed using liquid chromatography-tandem mass spectrometry. The concentration of MXE in urine of the deceased was 85 μg/mL. Despite the vial containing the blood sample being destroyed during transportation and the blood leaking out into the cardboard packaging, the blood level of MXE was estimated. After determination of the cardboard grammage (approx. 400 g/m(3) ) and the mean mass of the blood obtained after drying (0.1785 ± 0.0173 g per 1 mL), the estimated blood concentration of MXE was found to be 5.8 μg/mL. The high concentration of MXE in blood and urine and the circumstances of the case indicate an unintentional, fatal intoxication with this substance. PMID:25413263

  5. Forensic electrochemistry: sensing the molecule of murder atropine.

    PubMed

    Ramdani, Ouissam; Metters, Jonathan P; Figueiredo-Filho, Luiz Carlos S; Fatibello-Filho, Orlando; Banks, Craig E

    2013-02-21

    We present the electroanalytical sensing of atropine using disposable and economic screen printed graphite sensors. The electroanalytical determination of atropine is found to be possible over the concentration range of 5 μM to 50 μM with a detection limit of 3.9 μM (based on 3-sigma) found to be possible. We demonstrate proof-of-concept that this approach provides a rapid and inexpensive sensing strategy for determining the molecule of murder atropine in diet Coca-Cola samples. PMID:23293786

  6. Chelating agents and cadmium intoxication

    SciTech Connect

    Shinobu, L.A.

    1985-01-01

    A wide range of conventional chelating agents have been screened for (a) antidotal activity in acute cadmium poisoning and (b) ability to reduce aged liver and kidney deposits of cadmium. Chelating agents belonging to the dithiocarbamate class have been synthesized and tested in both the acute and chronic modes of cadmium intoxication. Several dithiocarbamates, not only provide antidotal rescue, but also substantially decrease the intracellular deposits of cadmium associated with chronic cadmium intoxication. Fractionating the cytosol from the livers and kidneys of control and treated animals by Sephadex G-25 gel filtration clearly demonstrates that the dithiocarbamates are reducing the level of metallothionein-bound cadmium. However, the results of cell culture (Ehrlich ascites) studies designed to investigate the removal of cadmium from metallothionein and subsequent transport of the resultant cadmium complex across the cell membrane were inconclusive. In other in vitro investigations, the interaction between isolated native Cd, Zn-metallothionein and several chelating agents was explored. Ultracentrifugation, equilibrium dialysis, and Sephadex G-25 gel filtration studies have been carried out in an attempt to determine the rate of removal of cadmium from metallothionein by these small molecules. Chemical shifts for the relevant cadmium-dithiocarbamate complexes have been determined using natural abundance Cd-NMR.

  7. Barbiturate intoxication and overdose

    MedlinePlus

    Symptoms of barbiturate intoxication and overdose include: Altered level of consciousness Difficulty in thinking Drowsiness or coma Faulty judgment Lack of coordination Shallow breathing Slow, slurred speech Sluggishness Staggering Excessive and long-term use ...

  8. Development of status epilepticus, sustained calcium elevations and neuronal injury in a rat survival model of lethal paraoxon intoxication.

    PubMed

    Deshpande, Laxmikant S; Carter, Dawn S; Phillips, Kristin F; Blair, Robert E; DeLorenzo, Robert J

    2014-09-01

    Paraoxon (POX) is an active metabolite of organophosphate (OP) pesticide parathion that has been weaponized and used against civilian populations. Exposure to POX produces high mortality. OP poisoning is often associated with chronic neurological disorders. In this study, we optimize a rat survival model of lethal POX exposures in order to mimic both acute and long-term effects of POX intoxication. Male Sprague-Dawley rats injected with POX (4mg/kg, ice-cold PBS, s.c.) produced a rapid cholinergic crisis that evolved into status epilepticus (SE) and death within 6-8min. The EEG profile for POX induced SE was characterized and showed clinical and electrographic seizures with 7-10Hz spike activity. Treatment of 100% lethal POX intoxication with an optimized three drug regimen (atropine, 2mg/kg, i.p., 2-PAM, 25mg/kg, i.m. and diazepam, 5mg/kg, i.p.) promptly stopped SE and reduced acute mortality to 12% and chronic mortality to 18%. This model is ideally suited to test effective countermeasures against lethal POX exposure. Animals that survived the POX SE manifested prolonged elevations in hippocampal [Ca(2+)]i (Ca(2+) plateau) and significant multifocal neuronal injury. POX SE induced Ca(2+) plateau had its origin in Ca(2+) release from intracellular Ca(2+) stores since inhibition of ryanodine/IP3 receptor lowered elevated Ca(2+) levels post SE. POX SE induced neuronal injury and alterations in Ca(2+) dynamics may underlie some of the long term morbidity associated with OP toxicity. PMID:24785379

  9. Role of glutamatergic system in nerve agent intoxication

    SciTech Connect

    Blanchet, G.; Lallement, G.; Carpentier, P.; De Groot, D.; Bodjarian, N.

    1993-05-13

    Our recent studies concerning soman-induced seizures mechanisms and subsequent brain damage are reviewed. (1) Seizure activity was associated with transient increases of extracellular concentrations of acetylcholine (ACh) and with long-lasting releases of glutamate (Glu) in all limbic areas studied. (2) Preventive intraseptal application of atropine abolished the hippocampal increases of extracellular AChi and Glu indicating a key role of septum in triggering seizure activity. (3) Early increases of hippocampal AMPA receptor binding occurred before activation of NMDA receptors. (4) Pretreatment with NBQX, an antagonist of AMPA receptor, prevented convulsions and brain damage even without atropine. In the same conditions, no protection was afforded by TCP, a non-competitive antagonist of the NMDA receptor. (5) On the contrary, in the presence of pyridostigmine and atropine, TCP blocked the seizures induced by 2 x LD50 of soman. The anticonvulsant potency of TCP was particularly obvious when administered curatively. (6) Mossy fibers sprouting takes place in the supragranular-molecular layers of rat hippocampus long after brain injury associated with abnormal neuronal excitability. (7) Altogether, it appears that an AMPA component is involved in combination with cholinergic mechanisms in initiating seizures. A subsequent and long-lasting recruitment of NMDA receptors is then essential in sustaining the seizures. New anticonvulsant and neuroprotective approaches using Glu antagonists against nerve agents intoxication are discussed.

  10. Thallium intoxication. Case Report.

    PubMed

    Sojáková, Michaela; Žigrai, Miroslav; Karaman, Andrej; Plačková, Silvia; Klepancová, Petra; Hrušovský, Štefan

    2015-01-01

    We report a rare case of serious voluntary intoxication by laboratory thallium monobromate combined with alcohol intake by a 24-years old man. The diagnosis of thallium intoxication was based on history, nonspecific but typical clinical symptoms including gastrointestinal complaints, painful polyneuropathy, alopecia, and confirmed by the finding of increased thallium concentration in the urine. The treatment, performed at the due time, consisted of decontamination of the stomach by irrigation, administration of active charcoal and Prussian blue, correction of water and mineral dysbalance, symptomatic treatment, and led to complete recovery. PMID:26454485

  11. Effectiveness of a drinking-motive-tailored emergency-room intervention among adolescents admitted to hospital due to acute alcohol intoxication — A randomized controlled trial

    PubMed Central

    Wurdak, Mara; Wolstein, Jörg; Kuntsche, Emmanuel

    2015-01-01

    The aim of this study is to develop and test the effectiveness of a drinking-motive-tailored intervention for adolescents hospitalized due to alcohol intoxication in eight cities in Germany between December 2011 and May 2012 against a similar, non-motive-tailored intervention. In a randomized controlled trial, 254 adolescents received a psychosocial intervention plus motive-tailored (intervention group; IG) or general exercises (control group; CG). Adolescents in the IG received exercises in accordance with their drinking motives as indicated at baseline (e.g. alternative ways of spending leisure time or dealing with stress). Exercises for the CG contained alcohol-related information in general (e.g. legal issues). The data of 81 adolescents (age: M = 15.6, SD = 1.0; 42.0% female) who participated in both the baseline and the follow-up were compared using ANOVA with repeated measurements and effect sizes (available case analyses). Adolescents reported lower alcohol use at the four-week follow-up independently of the kind of intervention. Significant interaction effects between time and IG were found for girls in terms of drinking frequency (F = 7.770, p < 0.01) and binge drinking (F = 7.0005, p < 0.05) but not for boys. For the former, the proportional reductions and corresponding effect sizes of drinking frequency (d = − 1.18), binge drinking (d = − 1.61) and drunkenness (d = − 2.87) were much higher than the .8 threshold for large effects. Conducting psychosocial interventions in a motive-tailored way appears more effective for girls admitted to hospital due to alcohol intoxication than without motive-tailoring. Further research is required to address the specific needs of boys in such interventions. (German Clinical Trials Register, DRKS ID: DRKS00005588). PMID:26844193

  12. Effectiveness of a drinking-motive-tailored emergency-room intervention among adolescents admitted to hospital due to acute alcohol intoxication - A randomized controlled trial.

    PubMed

    Wurdak, Mara; Wolstein, Jörg; Kuntsche, Emmanuel

    2016-06-01

    The aim of this study is to develop and test the effectiveness of a drinking-motive-tailored intervention for adolescents hospitalized due to alcohol intoxication in eight cities in Germany between December 2011 and May 2012 against a similar, non-motive-tailored intervention. In a randomized controlled trial, 254 adolescents received a psychosocial intervention plus motive-tailored (intervention group; IG) or general exercises (control group; CG). Adolescents in the IG received exercises in accordance with their drinking motives as indicated at baseline (e.g. alternative ways of spending leisure time or dealing with stress). Exercises for the CG contained alcohol-related information in general (e.g. legal issues). The data of 81 adolescents (age: M = 15.6, SD = 1.0; 42.0% female) who participated in both the baseline and the follow-up were compared using ANOVA with repeated measurements and effect sizes (available case analyses). Adolescents reported lower alcohol use at the four-week follow-up independently of the kind of intervention. Significant interaction effects between time and IG were found for girls in terms of drinking frequency (F = 7.770, p < 0.01) and binge drinking (F = 7.0005, p < 0.05) but not for boys. For the former, the proportional reductions and corresponding effect sizes of drinking frequency (d = - 1.18), binge drinking (d = - 1.61) and drunkenness (d = - 2.87) were much higher than the .8 threshold for large effects. Conducting psychosocial interventions in a motive-tailored way appears more effective for girls admitted to hospital due to alcohol intoxication than without motive-tailoring. Further research is required to address the specific needs of boys in such interventions. (German Clinical Trials Register, DRKS ID: DRKS00005588). PMID:26844193

  13. Driving While Intoxicated.

    ERIC Educational Resources Information Center

    Brick, John

    Alcohol intoxication increases the risk of highway accidents, the relative risk of crash probability increasing as a function of blood alcohol content (BAC). Because alcohol use is more prevalent than use of other drugs, more is known about the relationship between alcohol use and driving. Most states presume a BAC of .10% to be evidence of drunk…

  14. 21 CFR 520.2520b - Trichlorfon and atropine.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 21 Food and Drugs 6 2014-04-01 2014-04-01 false Trichlorfon and atropine. 520.2520b Section 520.2520b Food and Drugs FOOD AND DRUG ADMINISTRATION, DEPARTMENT OF HEALTH AND HUMAN SERVICES (CONTINUED... cholinesterase activity, nor within 7 days before or after treatment with any other cholinesterase inhibitor....

  15. 21 CFR 520.2520b - Trichlorfon and atropine.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 21 Food and Drugs 6 2010-04-01 2010-04-01 false Trichlorfon and atropine. 520.2520b Section 520.2520b Food and Drugs FOOD AND DRUG ADMINISTRATION, DEPARTMENT OF HEALTH AND HUMAN SERVICES (CONTINUED... cholinesterase activity, nor within 7 days before or after treatment with any other cholinesterase inhibitor....

  16. 21 CFR 520.2520b - Trichlorfon and atropine.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 21 Food and Drugs 6 2012-04-01 2012-04-01 false Trichlorfon and atropine. 520.2520b Section 520.2520b Food and Drugs FOOD AND DRUG ADMINISTRATION, DEPARTMENT OF HEALTH AND HUMAN SERVICES (CONTINUED... cholinesterase activity, nor within 7 days before or after treatment with any other cholinesterase inhibitor....

  17. 21 CFR 520.2520b - Trichlorfon and atropine.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 21 Food and Drugs 6 2011-04-01 2011-04-01 false Trichlorfon and atropine. 520.2520b Section 520.2520b Food and Drugs FOOD AND DRUG ADMINISTRATION, DEPARTMENT OF HEALTH AND HUMAN SERVICES (CONTINUED... cholinesterase activity, nor within 7 days before or after treatment with any other cholinesterase inhibitor....

  18. 21 CFR 520.2520b - Trichlorfon and atropine.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 21 Food and Drugs 6 2013-04-01 2013-04-01 false Trichlorfon and atropine. 520.2520b Section 520.2520b Food and Drugs FOOD AND DRUG ADMINISTRATION, DEPARTMENT OF HEALTH AND HUMAN SERVICES (CONTINUED... cholinesterase activity, nor within 7 days before or after treatment with any other cholinesterase inhibitor....

  19. Effectiveness study of atropine for progressive myopia in Europeans

    PubMed Central

    Polling, J R; Kok, R G W; Tideman, J W L; Meskat, B; Klaver, C C W

    2016-01-01

    Purpose Randomized controlled trials have shown the efficacy of atropine for progressive myopia, and this treatment has become the preferred pattern for this condition in Taiwan. This study explores the effectiveness of atropine 0.5% treatment for progressive high myopia and adherence to therapy in a non-Asian country. Methods An effectiveness study was performed in Rotterdam, the Netherlands. Overall 77 children (mean age 10.3 years±2.3), of European (n=53), Asian (n=18), and African (n=6) descent with progressive myopia were prescribed atropine 0.5% eye drops daily. Both parents and children filled in a questionnaire regarding adverse events and adherence to therapy. A standardized eye examination including cycloplegic refraction and axial length was performed at baseline and 1, 4, and 12 months after initiation of therapy. Results Mean spherical equivalent at baseline was −6.6D (±3.3). The majority (60/77, 78%) of children adhered to atropine treatment for 12 months; 11 of the 17 children who discontinued therapy did so within 1 month after the start of therapy. The most prominent reported adverse events were photophobia (72%), followed by reading problems (38%), and headaches (22%). The progression rate of spherical equivalent before treatment (−1.0D/year±0.7) diminished substantially during treatment (−0.1D/year±0.7) compared to those who ceased therapy (−0.5D/year±0.6; P=0.03). Conclusions Despite the relatively high occurrence of adverse events, our study shows that atropine can be an effective and sustainable treatment for progressive high myopia in Europeans. PMID:27101751

  20. Effectiveness study of atropine for progressive myopia in Europeans.

    PubMed

    Polling, J R; Kok, R G W; Tideman, J W L; Meskat, B; Klaver, C C W

    2016-07-01

    PurposeRandomized controlled trials have shown the efficacy of atropine for progressive myopia, and this treatment has become the preferred pattern for this condition in Taiwan. This study explores the effectiveness of atropine 0.5% treatment for progressive high myopia and adherence to therapy in a non-Asian country.MethodsAn effectiveness study was performed in Rotterdam, the Netherlands. Overall 77 children (mean age 10.3 years±2.3), of European (n=53), Asian (n=18), and African (n=6) descent with progressive myopia were prescribed atropine 0.5% eye drops daily. Both parents and children filled in a questionnaire regarding adverse events and adherence to therapy. A standardized eye examination including cycloplegic refraction and axial length was performed at baseline and 1, 4, and 12 months after initiation of therapy.ResultsMean spherical equivalent at baseline was -6.6D (±3.3). The majority (60/77, 78%) of children adhered to atropine treatment for 12 months; 11 of the 17 children who discontinued therapy did so within 1 month after the start of therapy. The most prominent reported adverse events were photophobia (72%), followed by reading problems (38%), and headaches (22%). The progression rate of spherical equivalent before treatment (-1.0D/year±0.7) diminished substantially during treatment (-0.1D/year±0.7) compared to those who ceased therapy (-0.5D/year±0.6; P=0.03).ConclusionsDespite the relatively high occurrence of adverse events, our study shows that atropine can be an effective and sustainable treatment for progressive high myopia in Europeans. PMID:27101751

  1. Resource utilization and outcomes of intoxicated drivers

    PubMed Central

    2010-01-01

    hospital LOS, ICU LOS, and ventilator days. We also observed that intoxicated drivers were more likely to be self-pay, less likely to have charges > $50K, and less likely to pay ≥ 90% of the charges. Further research using multivariable analysis is needed to determine if these apparent outcomes differences are driven by acute intoxication, and the tendency for endotracheal intubation and ICU admission, rather than injury severity. PMID:20687912

  2. [Intoxication of botulinum toxin].

    PubMed

    Chudzicka, Aleksandra

    2015-09-01

    Botulinum toxin is an egzotoxin produced by Gram positive bacteria Clostridium botulinum. It is among the most potent toxins known. The 3 main clinical presentations of botulism are as follows: foodborne botulism, infant botulism and wound botulism. The main symptom of intoxication is flat muscles paralysis. The treatment is supportive care and administration of antitoxin. In prevention the correct preparing of canned food is most important. Botulinum toxin is accepted as a biological weapon. PMID:26449577

  3. Actions and interactions of cholinolytics and cholinesterase reactivators in the treatment of acute organophosphorus toxicity.

    PubMed

    Das Gupta, S; Ghosh, A K; Chowdhri, B L; Asthana, S N; Batra, B S

    1991-01-01

    Different drug combinations consisting of cholinolytic and a cholinesterase (ChE) reactivator provide greater therapeutic efficacy in acute organophosphorus (OP) poisoning in mice than when used alone. Maximum protection, as determined by a shift of the LD50 for the two OP agents, was observed with the cholinolytic benactyzine. A protection index (P.I.) of 42 was obtained when benactyzine was given along with obidoxime in diisopropylphosphorofluoridate (DFP) intoxication. With the more toxic OP agent soman (o-pinacolylmethylphosphonofluoridate), the same cholinolytic only offered a maximum P.I. of 3.2 when administered with HS-6, another bispyridinium ChE reactivator. This beneficial effect of benactyzine is possibly due to its greater antimuscarinic effect in the central nervous system than atropine or dexetimide. PMID:1935707

  4. Atropine sulfate and 2-pyridine aldoxime methylchloride elicit stress-induced convulsions and lethality in mice and guinea pigs.

    PubMed

    Donzanti, B A; Green, M D; Shores, E I

    1985-01-01

    The present study demonstrates that dose combinations of atropine sulfate and 2-pyridine aldoxime methylchloride (2-PAM), which do not produce any overt toxic effects on the behavior of mice or guinea pigs in a stable environment, elicit clonic-tonic convulsions and death when the animals are physically stressed by cold water swimming. Phenoxybenzamine (1-6 mg/kg), diazepam (0.625 and 1.25 mg/kg) and pilocarpine (2.5 and 5 mg/kg) significantly decreased (or abolished) the occurrence of atropine and 2-PAM stressed-induced convulsions and/or lethality. In contrast, propranolol (20 mg/kg), was ineffective in preventing either convulsions or lethality. Changes in plasma glucose levels and internal body temperature did not appear to explain the precipitation of convulsions or ensuing death. These results suggest that during acute physical stress, relatively low doses of atropine and 2-PAM produce toxic and lethal effects due to the activation of alpha-adrenergic mechanisms along with a concomitant inactivation of cholinergic mechanisms. PMID:4092617

  5. Multiple animal studies for medical chemical defense program in soldier/patient decontamination and drug development on task 85-18: Conduct of pralidoxime chloride, atropine in citrate buffer and pyridostigmine bromide pharmacokinetic studies, and comparative evaluation of the efficacy of pyridostigmine plus atropine. Final report, June 1985-August 1988

    SciTech Connect

    Joiner, R.L.; Kluwe, M.

    1988-08-01

    This study was conducted to evaluate the efficacy of the reversible acetylcholinesterase inhibitor, pyridostigmine bromide, as an addition to standard therapy with atropine pralidoxime bromide, as an addition to standard therapy with atropine and pralidoxime chloride (2-PM), against the acute lethal effects of Soman, GD, using a primate model (male, Rhesus monkey). In addition, the pharmacokinetics of pyridostigmine bromide (intragastric), atropine (intramuscular), and 2-PAM (intramuscular) were individually examined in the primate model using three different dose levels for each compound. In the efficacy study, the combined prophylactic/post/challenge therapy regimen resulted in survival following an intramuscular challenge dose as high as 617 micrograms/kg in contrast to an estimated, unprotected, median lethal GD dose (LD50) of 15.3 micrograms/kg for the same animals.

  6. Physostigmine (alone and together with adjunct) pretreatment against soman, sarin, tabun and vx intoxication. (Reannouncement with new availability information)

    SciTech Connect

    Harris, L.W.; Talbot, B.G.; Lennox, W.J.; Anderson, D.R.; Solana, R.P.

    1991-12-31

    A pretreatment for organophosphorus (OP) anticholinesterase (e. g. , soman) intoxication should prevent lethality and convulsions (CNV) at 2 LD50s and be behavioral-decrement-free when given alone. Behavioral-deficit-free pretreatment regimens (PRGs) for guinea pigs consisted of Physostigmine (0.15 mg/kg, im) and adjunct. Adjuncts MG/KG, IM tested were akineton 0.25, aprophen 8, trihexyphenidyl 2, atropine 16, azaprophen 51, BENACTYZINE 1.25, cogentin 4, dextromethorphan 7.5, ethopropazine 12, kemadrin 11, MEMANTINE 5, promethazine 5, scopolamine 0.081 AND CONTROL 2. PRGs were given 30 min before soman (60 ug/kg, sc; 2 LD50S) or other OP agents. Animals were then observed and graded for signs of intoxication, including CNV at 7 time points and at 24 hr. Physostigmine alone reduced the incidence of CNV and lethality induced by 2 LD50s of soman by 42 and 60%, respectively. All of the PRGs tested abolished lethality and 12 shortened recovery time to 2 hr or less. Also, PRGs including azaprophen or atropine prevented CNV. When selected PRGs were tested against intoxication by sarin, tabun or VX, the efficacy was generally superior to that for soman. The data show that several PRGs are effective against soman intoxication in guinea pigs. Pretreatment, physostigmine, anticholinesterases, soman (GD).

  7. [Lethal intoxication with baclofen].

    PubMed

    Dukova, O A; Pokrovsky, A A; Melent'ev, A V; Krasnov, E A; Suvorova, E V; Efremov, A A

    2015-01-01

    The objective of the present study was to select and develop simpler methods for the quantitative determination of baclofen in blood with the use of HPLC and tandem MS (MS-MS) techniques and its qualitative determination in cadaveric organs by the GC/MS technique. These mathods were shown to be suitable for the purpose of forensic medical analysis, clinical, toxicological, and therapeutic monitoring. The special emphasis is laid on the methods used to investigate the biological materials obtained from the subjects who died from baclofen intoxication. PMID:25874317

  8. A case of lethal intoxication after ingestion of toquilone compositum.

    PubMed

    Fucci, N

    1996-09-01

    A case of acute intoxication of both methaqualone and diphenhydramine is reported. The analysis of these compounds was performed by liquid-liquid extraction (Toxi-Lab DPC procedure) followed by gas chromatography/mass spectrometry determination; both substances are contained in the pharmaceutical formulation called Toquilone Compositum (Medichemie, Switzerland). PMID:8870874

  9. Unpacking intoxication, racialising disability.

    PubMed

    Chen, Mel Y

    2015-06-01

    This article examines concepts whose strictly medical applications have only partly informed their widespread use and suggests that demonstrably shared logics motivate our thinking across domains in the interest of a politically just engagement. It considers exchanges between the culturally complex concepts of 'toxicity' and 'intoxication', assessing the racialised conditions of their animation in several geopolitically--and quite radically--distinct scenarios. First, the article sets the framework through considering the racial implications of impairment and disability language of 'non-toxic' finance capital in the contemporary US financial crisis. Shifting material foci from 'illiquid financial bodies' to opiates while insisting that neither is 'more' metaphorically toxic than the other, the article turns to address the role of opium and temporality in the interanimations of race and disability in two sites of 19th-century British empire: Langdon Down's clinic for idiocy, and China's retort on opium to Queen Victoria. The article concludes with a provocation that suggests yet another crossing of borders, that between researcher and researched: 'intoxicated method' is a hypothetical mode of approach that refuses idealised research positions by 'critically disabling' the idealised cognitive and conceptual lens of analysis. PMID:26052116

  10. Immediate and Long-Term Outcome of Acute H2S Intoxication Induced Coma in Unanesthetized Rats: Effects of Methylene Blue

    PubMed Central

    Sonobe, Takashi; Chenuel, Bruno; Cooper, Timothy K.; Haouzi, Philippe

    2015-01-01

    Background Acute hydrogen sulfide (H2S) poisoning produces a coma, the outcome of which ranges from full recovery to severe neurological deficits. The aim of our study was to 1- describe the immediate and long-term neurological effects following H2S-induced coma in un-anesthetized rats, and 2- determine the potential benefit of methylene blue (MB), a compound we previously found to counteract acute sulfide cardiac toxicity. Methods NaHS was administered IP in un-sedated rats to produce a coma (n = 34). One minute into coma, the rats received MB (4 mg/kg IV) or saline. The surviving rats were followed clinically and assigned to Morris water maze (MWM) and open field testing then sacrificed at day 7. Results Sixty percent of the non-treated comatose rats died by pulseless electrical activity. Nine percent recovered with neurological deficits requiring euthanasia, their brain examination revealed major neuronal necrosis of the superficial and middle layers of the cerebral cortex and the posterior thalamus, with variable necrosis of the caudate putamen, but no lesions of the hippocampus or the cerebellum, in contrast to the typical distribution of post-ischemic lesions. The remaining animals displayed, on average, a significantly less effective search strategy than the control rats (n = 21) during MWM testing. Meanwhile, 75% of rats that received MB survived and could perform the MWM test (P<0.05 vs non-treated animals). The treated animals displayed a significantly higher occurrence of spatial search than the non-treated animals. However, a similar proportion of cortical necrosis was observed in both groups, with a milder clinical presentation following MB. Conclusion In conclusion, in rats surviving H2S induced coma, spatial search patterns were used less frequently than in control animals. A small percentage of rats presented necrotic neuronal lesions, which distribution differed from post-ischemic lesions. MB dramatically improved the immediate survival and spatial

  11. Emergency approach to intoxications.

    PubMed

    Hackett, T

    2000-05-01

    Many compounds, when absorbed or ingested, can cause harm to animals and people. Veterinarians are commonly faced with companion animals that have been exposed to these harmful compounds. Most poisonings are the result of curious exploration by the pet and a quest to taste everything in their path. Some poisonings are the result of malice, and many simply result from owner ignorance when pets are given medications without regard to dose or compatibility. It is the responsibility of the emergency clinician encountering these cases to prevent further exposure to the poison, enhance its elimination, and provide supportive and antidotal care. Antidotes when available are of little value if the animal has lost any vital functions. It is the purpose of this article to focus on the emergency management of intoxications by reviewing the general principles of triage and emergency care, and to discuss available procedures to stop the exposure, prevent further absorption, and hasten elimination of poisons from the patients body. PMID:10998820

  12. Carbon monoxide intoxication

    SciTech Connect

    Kales, S.N. )

    1993-11-01

    Carbon monoxide poisoning usually results from inhalation of exhaust fumes from motor vehicles, smoke from fires or fumes from faulty heating systems. Carbon monoxide has a high affinity for hemoglobin, with which it forms carboxyhemoglobin. The resulting decrease in both oxygen-carrying capacity and oxygen release can lead to end-organ hypoxia. The clinical presentation is nonspecific. Headache, dizziness, fatigue and nausea are common in mild to moderate carbon monoxide poisoning. In more severe cases, tachycardia, tachypnea and central nervous system depression occur. When carbon monoxide intoxication is suspected, empiric treatment with 100 percent oxygen should be initiated immediately. The diagnosis is confirmed by documenting an elevated carboxyhemoglobin level. Hyperbaric oxygen therapy is recommended in patients with neurologic dysfunction, cardiac dysfunction or a history of unconsciousness. 26 refs.

  13. Chelation in Metal Intoxication

    PubMed Central

    Flora, Swaran J.S.; Pachauri, Vidhu

    2010-01-01

    Chelation therapy is the preferred medical treatment for reducing the toxic effects of metals. Chelating agents are capable of binding to toxic metal ions to form complex structures which are easily excreted from the body removing them from intracellular or extracellular spaces. 2,3-Dimercaprol has long been the mainstay of chelation therapy for lead or arsenic poisoning, however its serious side effects have led researchers to develop less toxic analogues. Hydrophilic chelators like meso-2,3-dimercaptosuccinic acid effectively promote renal metal excretion, but their ability to access intracellular metals is weak. Newer strategies to address these drawbacks like combination therapy (use of structurally different chelating agents) or co-administration of antioxidants have been reported recently. In this review we provide an update of the existing chelating agents and the various strategies available for the treatment of heavy metals and metalloid intoxications. PMID:20717537

  14. Effects of atropine on the repeated acquisition and performance of response sequences in humans.

    PubMed Central

    Higgins, S T; Woodward, B M; Henningfield, J E

    1989-01-01

    The present study assessed a 24-hr time course for the acute effects of intramuscular injections of atropine sulfate (0, 1.5, 3.0, and 6.0 mg/70 kg) in healthy adult humans responding under a two-component multiple schedule of repeated acquisition and performance of response sequences. Subjects resided in an inpatient research ward for the duration of the study. In each component of the multiple schedule, subjects completed a different sequence of 10 responses in a predetermined order using three keys of a numeric keypad. In the acquisition component, the subjects' task was to acquire a new sequence each session. Eight sessions were conducted daily: one immediately before administration of the drug and then 0.5, 1.5, 3.0, 5.0, 7.0, 9.0, and 24.0 hr after administration. In the performance component, the response sequence always remained the same. Overall percentage of errors increased and overall response rates decreased in the acquisition and performance components as an orderly function of drug dose. However, these effects were selective in that behavior in the acquisition component generally was affected at lower doses than in the performance component. When behavior was affected in both the acquisition and performance components, the time courses of effects were similar. Drug effects began at 0.5 or 1.5 hr, reached peak effects between 3.0 and 5.0 hr, and returned to placebo levels between 7.0 and 9.0 hr postdrug in both schedule components. None of the drug doses produced reliable effects the day after drug administration (24-hr postdrug) in either schedule component. The present study provides the first within-subject assessment of the magnitude and duration of the effects of an anticholinergic on repeated acquisition and performance baselines and extends to atropine the selective effects on these two baselines demonstrated previously with other compounds in humans and nonhumans. PMID:2921588

  15. Multiple organ dysfunction syndrome, an unusual complication of heroin intoxication: a case report and review of literature

    PubMed Central

    Feng, Gang; Luo, Qiancheng; Guo, Enwei; Yao, Yulan; Yang, Feng; Zhang, Bingyu; Li, Longxuan

    2015-01-01

    Multiple organ dysfunction syndrome (MODS) has rarely been described in patients with heroin intoxication. Here, we report a rare case of MODS involving six organs, due to heroin intoxication. The patient was a 32-year-old Chinese man with severe heroin intoxication complicated by acute pulmonary edema and respiratory insufficiency, shock, myocardial damage and cardiac insufficiency, rhabdomyolysis and acute renal insufficiency, acute liver injury and hepatic insufficiency, toxic leukoencephalopathy, and hypoglycemia. He managed to survive and was discharged after 10 weeks of intensive care. The possible pathogenesis and therapeutic measures of MODS induced by heroin intoxication and some suggestions for preventing and treating severe complications of heroin intoxication, based on clinical evidence and the pertinent literature, are discussed in this report. PMID:26617935

  16. Use of pralidoxime without atropine in rivastigmine (carbamate) toxicity.

    PubMed

    Hoffman, R S; Manini, A F; Russell-Haders, A L; Felberbaum, M; Mercurio-Zappala, M

    2009-09-01

    Some experimental models suggest that the use of pralidoxime in carbamate toxicity is deleterious. Although pretreatment with atropine minimizes the adverse effect of pralidoxime reported in these models, concerns over the risks of pralidoxime in humans with carbamate poisoning continue. We present a unique case of carbamate toxicity treated successfully with pralidoxime alone. An 80-year-old woman with Alzheimer's dementia presented to the emergency department with 3-4 days of lightheadedness, vomiting, diarrhea, and bilateral lower extremity muscle pain. Extensive review of systems was otherwise negative. Her vital signs were BP, 207/85 mmHg; pulse, 101 beats/min; rectal temperature, 36.6( degrees )C; respirations, 18/min; and SpO(2), 95% breathing room air. Her bedside glucose measurement was 6.7 mmol/L. Physical examination revealed a confused, diaphoretic, ill-appearing woman with miosis and fasciculations of the tongue, eyelids, gastrocnemius and quadriceps bilaterally. The heart, lung, abdominal and head, eyes, ears, nose and throat examinations were otherwise unremarkable. Nine 5-cm(2) rivastigmine patches (9.5 mg/24-hour) were found adherent to her torso and lower extremities. The patches were immediately removed and underlying skin cleansed with soap and water. Laboratory values including complete blood count, basic metabolic panel, calcium, magnesium, phosphorus, troponin, coagulation studies and urinalysis were unremarkable. Due to the absence of pulmonary muscarinic findings, no atropine was administered. However, 1 g of pralidoxime was administered intravenously over 30 min to treat fasciculations. Within 30 min of this treatment, there was significant improvement in symptoms and resolution of fasciculations. She was admitted to the hospital, required no further pralidoxime therapy and was discharged after 3 days. Rivastigmine is a reversible (carbamate) cholinesterase inhibitor used to treat dementia. In overdose, cholinergic crisis is expected and

  17. Alcohol intoxication and condom use self-efficacy effects on women's condom use intentions.

    PubMed

    Davis, Kelly Cue; Masters, N Tatiana; Eakins, Danielle; Danube, Cinnamon L; George, William H; Norris, Jeanette; Heiman, Julia R

    2014-01-01

    Although research has consistently demonstrated that condom use self-efficacy significantly predicts condom use, there has been little investigation of whether acute alcohol intoxication moderates this relationship. Because alcohol intoxication is often associated with increased sexual risk taking, further examination of such moderating effects is warranted. Using a community sample of young heterosexual women (n=436) with a history of heavy episodic drinking, this alcohol administration experiment examined the effects of intoxication and condom use self-efficacy on women's condom negotiation and future condom use intentions. After a questionnaire session, alcohol condition (control, .10% target peak BAL) was experimentally manipulated between subjects. Participants then read and responded to a hypothetical risky sexual decision-making scenario. SEM analyses revealed that alcohol intoxication directly decreased women's intentions to use condoms in the future. Women with greater condom use self-efficacy had stronger intentions to engage in condom negotiation; however, this effect was moderated by intoxication. Specifically, the association between condom use self-efficacy and condom negotiation intentions was stronger for intoxicated women than for sober women. These novel findings regarding the synergistic effects of alcohol intoxication and condom use self-efficacy support continued prevention efforts aimed at strengthening women's condom use self-efficacy, which may reduce even those sexual risk decisions made during states of intoxication. PMID:24129265

  18. Susceptibility-weighted imaging findings of subacute delayed carbon monoxide intoxication: a report of five cases.

    PubMed

    Bae, Jin-Won; Cha, Seong-Yi; Kang, Tae-Ho; Lee, Jae-Hyeok; Kim, Hak-Jin; Jung, Dae Soo; Kim, Eun-Joo

    2012-01-15

    Brain injury from carbon monoxide (CO) poisoning occurs due to tissue hypoxia and direct CO-mediated histotoxicity. Recently developed susceptibility-weighted imaging (SWI) is sensitive for the detection of accumulated hemosiderin and iron secondary to cerebral hemorrhage. Therefore, we hypothesized that SWI may be helpful for identifying petechial hemorrhagic transformation secondary to acute hypoxic damage during subacute CO intoxication. Our case series with subacute CO intoxication revealed that the SWIs of all patients showed low signal intensities in the globus pallidus, representing the accumulation of iron or calcium secondary to hypoxic damage from acute CO intoxication. These results suggest that SWI may be a useful MR technique for illustrating brain damage in subacute delayed CO intoxication. PMID:21914555

  19. Neurological manifestation of methyl bromide intoxication.

    PubMed

    Suwanlaong, Kanokrat; Phanthumchinda, Kammant

    2008-03-01

    Methyl bromide is a highly toxic gas with poor olfactory warning properties. It is widely used as insecticidal fumigant for dry foodstuffs and can be toxic to central and peripheral nervous systems. Most neurological manifestations of methyl bromide intoxication occur from inhalation. Acute toxicity characterized by headache, dizziness, abdominal pain, nausea, vomiting and visual disturbances. Tremor, convulsion, unconsciousness and permanent brain damage may occur in severe poisoning. Chronic exposure can cause neuropathy, pyramidal and cerebellar dysfunction, as well as neuropsychiatric disturbances. The first case of methyl bromide intoxication in Thailand has been described. The patient was a 24-year-old man who worked in a warehouse of imported vegetables fumigated with methyl bromide. He presented with unstable gait, vertigo and paresthesia of both feet, for two weeks. He had a history of chronic exposure to methyl bromide for three years. His fourteen co-workers also developed the same symptoms but less in severity. Neurological examination revealed ataxic gait, decreased pain and vibratory sense on both feet, impaired cerebellar signs and hyperactive reflex in all extremities. The serum concentration of methyl bromide was 8.18 mg/dl. Electrophysilogical study was normal. Magnetic resonance imaging of the brain (MRI) revealed bilateral symmetrical lesion of abnormal hypersignal intensity on T2 and fluid-attenuation inversion recovery (FLAIR) sequences at bilateral dentate nuclei of cerebellum and periventricular area of the fourth ventricle. This incident stresses the need for improvement of worker education and safety precautions during all stages of methyl bromide fumigation. PMID:18575299

  20. Lead intoxication in cattle: a case report.

    PubMed

    Baars, A J; van Beek, H; Visser, I J; Vos, G; van Delft, W; Fennema, G; Lieben, G W; Lautenbag, K; Nieuwenhuijs, J H; de Lezenne Coulander, P A

    1992-01-01

    During the autumn of 1989 a feed contamination induced a widespread lead intoxication of cattle in the northern provinces of The Netherlands (Groningen and Friesland). Over 300 farms were involved, affecting about 15,500 animals (mostly dairy cattle). For a period of one to four weeks these animals took up a thousand kg of lead. This resulted in lead levels in milk, livers, and kidneys above the regulatory safety limits. Due to the chelating therapy, which was rapidly applied by the local veterinarians, only about 30 animals died of an acute lead intoxication. A joint action of the governmental and private authorities prevented exposure of consumers to lead-contaminated animal products. Based on observations, measurements and literature data, predictions were made of the lead levels to be expected in animal products and the time needed for depletion of these levels. The appropriate animals were ear-tagged to ensure their identification, and the decline in time of the lead levels in milk and offals was conscientiously monitored. In the second week of 1990 the lead concentrations were decreased to levels well below the regulatory limits, and hence the tags were removed. The present paper reports our observations and conclusions, especially regarding treatment, predictions and outcome of this incident. PMID:1493885

  1. Vitamin D intoxication.

    PubMed

    Ozkan, Behzat; Hatun, Sükrü; Bereket, Abdullah

    2012-01-01

    Vitamin D intoxication (VDI) may result from supplementation rarely, but it has been reported more frequently in recent years. This may be attributable to an increase in vitamin D supplement intake due to an understanding of the role of vitamin D (25OHD) in the pathogenesis of several diseases. The symptoms and findings associated with VDI are closely related to serum calcium concentration and duration of hypercalcemia. In patients with VDI, hypercalcemia, normal or high serum phosphorus levels, normal or low levels of alkaline phosphatase (ALP), high levels of serum 25OHD, low serum parathyroid hormone (PTH), and high urine calcium/creatinine are usually present. Serum 25OHD levels above 150 ng/ml are considered as VDI. The main goal of treatment for VDI is correction of the hypercalcemia. When the calcium concentration exceeds 14 mg/dl, emergency intervention is necessary because of the adverse effects of hypercalcemia on cardiac, central nervous system, renal, and gastrointestinal functions. However, since vitamin D is stored in fat tissues, effects of toxicity may last for months despite the removal of the exogenous source of vitamin D. Treatment for VDI includes: discontinuation of intake, a diet with low calcium and phosphorus content, intravenous hydration with saline, loop diuretics, glucocorticoids, calcitonin, and bisphosphonates. In conclusion, the diagnosis of vitamin D deficiency rickets (VDDR) without checking serum 25OHD level may cause redundant treatment that leads to VDI. All patients who are clinically suspected of VDDR should be checked for serum vitamin D status and questioned for previous vitamin D administration before starting vitamin D therapy. On the other hand, parents of all infants should be asked whether they are using dietary or oral supplements, and serial questioning may be required during supplementation to avoid excessive intake. PMID:22734293

  2. [Residual cerebellar ataxia following acute phenytoin intoxication].

    PubMed

    Awada, A; Amene, P; al Jumah, M; al Beladi, K

    1999-04-01

    A 30-year-old man was given high doses of phenytoin together with 4 antituberculous drugs for a seizure associated with a probable brain tuberculoma. He developed hepatic toxicity and his serum phenytoin reached the high level of 298 mumol/l (therapeutic range 40-79 mumol/l). All drugs were stopped and the biological parameters returned progressively to normal over the next 15 days. However, he remained with a cerebellar axial syndrome and was still severely ataxic 2 months later. Brain CT and MRI showed mild cerebellar atrophy. This case and the few other published ones, together with some recent experimental data, show that high doses of phenytoin can be toxic to the cerebellar cortical cells. The rarity of similar cases, while millions of epileptics are under phenytoin treatment, would however suggest that individual susceptibility may play a role in this toxicity. PMID:10367328

  3. Successful Pancreas Transplantation From a Deceased Donor Intoxicated With Oral Antidiabetic Agent: A Case Report.

    PubMed

    Rodríguez-Villar, C; Conget, I; Ferrer-Fàbrega, J; Paredes, D; Ruíz, A; Roque, R; Rull, R; López-Boado, M; Ricart, M J; Garcia, R; Adalia, R

    2015-10-01

    Simultaneous kidney pancreas transplantation (SKP) is a common procedure for the patient with long-term type 1 diabetes mellitus (DM) with terminal renal failure. It is unusual to consider the pancreas from a deceased donor who died after an acute intoxication with oral antidiabetic agent (OAA), which would suggest an abnormal functionality of the organ and preclude the potential use of the graft. We present a case of a successful pancreatic transplantation from a donor who died of acute cerebral edema secondary to severe hypoglycemia induced by OAA acute intoxication. PMID:26518941

  4. Fatal flecainide intoxication.

    PubMed Central

    Brazil, E; Bodiwala, G G; Bouch, D C

    1998-01-01

    Flecainide acetate is a potent class 1C antiarrhythmic agent used mainly for the treatment of supraventricular arrhythmias. Acute overdose of this drug is rare but frequently fatal. The clinical course of a patient that ingested a large quantity of flecainide as a suicide attempt is described and current therapeutic strategies discussed. PMID:9825278

  5. Water intoxication in adult cattle.

    PubMed

    Kawahara, Naoya; Ofuji, Sosuke; Abe, Sakae; Tanaka, Ai; Uematsu, Masami; Ogata, Yoshimi

    2016-05-01

    Water intoxication is a common disorder in calves and is usually characterized by transient hemoglobinuria. In contrast, the condition is very rare in adult cattle, with few reports on naturally occurring cases. In the present report, four female Japanese Black cattle, aged 16-25 months, showed neurological signs when they drank water following a water outage. Hemoglobinuria was not grossly observed, while severe hyponatremia was revealed by laboratory tests. Autopsy indicated cerebral edema with accumulation of serous fluid in expanded Virchow-Robin spaces. These results indicate the possibility of water intoxication associated with cerebral edema due to severe dilutional hyponatremia in adult cattle. PMID:27506091

  6. Evaluation of atropine 1% ophthalmic solution administered sublingually for the management of terminal respiratory secretions.

    PubMed

    Protus, Bridget McCrate; Grauer, Phyllis A; Kimbrel, Jason M

    2013-06-01

    Terminal respiratory secretions (TRS) or "death rattle" is a common symptom in the dying patient. Current practice for the prevention and treatment of TRS involves the use of oral, sublingual, transdermal, or parenteral anticholinergic medications. A retrospective chart review of patients admitted to a hospice inpatient unit for terminal care and treated with sublingual atropine 1% ophthalmic drops for TRS was conducted. A total of 19 of 22 patients treated with atropine had documented reduction or resolution of TRS. This study suggests that atropine 1% ophthalmic drops administered sublingually are a reasonable option for the management of TRS. Problematic cardiac or central nervous system symptoms were not found in the present study. Results should aid hospice programs who are seeking guidance on the management of TRS with atropine 1% ophthalmic drops. PMID:22833553

  7. Arsenic: homicidal intoxication

    SciTech Connect

    Massey, E.W.; Wold, D.; Heyman, A.

    1984-07-01

    Arsenic-induced deaths have been known to occur from accidental poisoning, as a result of medical therapy, and from intentional poisonings in homicide and suicide. Twenty-eight arsenic deaths in North Carolina from 1972 to 1982 included 14 homicides and seven suicides. In addition, 56 hospitalized victims of arsenic poisoning were identified at Duke Medical Center from 1970 to 1980. Four case histories of arsenic poisoning in North Carolina are presented and clinical manifestations are discussed. In view of the continued widespread use of arsenic in industry and agriculture, and its ubiquity in the environment, arsenic poisoning will continue to occur. A need for knowledge of its toxicity and of the clinical manifestations of acute and chronic arsenic poisoning will also continue.

  8. Paralytic ileus as a complication of atropine therapy following severe organophosphate poisoning.

    PubMed

    Beards, S C; Kraus, P; Lipman, J

    1994-09-01

    A 32-year-old man presented with symptoms of severe organophosphate poisoning and required an atropine infusion for 5 weeks. We believe the development of a paralytic ileus occurred as a rare feature of atropine toxicity when other signs were masked by the underlying condition. The onset of a paralytic ileus coincided with a spontaneous increase in red cell cholinesterase levels and may be an early sign of recovery from organophosphate poisoning. PMID:7978137

  9. [Clozapine intoxication: theoretical aspects and forensic-medical examination ].

    PubMed

    Shigeev, S V; Ivanova, N A; Ivanov, S V

    2013-01-01

    This literature review is focused on diagnostics of acute clozapine intoxication with the fatal outcome. According to the Russian authors, clozapine intoxication ranks first in the structure of criminal poisoning and accounted for 99.7% of all the cases that occurred in Moscow during the period from 2003 to 2006. Toximetric investigations of clinical manifestations of clozapine intoxication revealed that the threshold clozapine concentration in blood is 0.12 ± 0.06 mg/I, the critical and lethal concentrations are 1.01 ± 0.2 mg/I and 3.5 ± 1.5 mg/I respectively. Autopsy on corpses of the victims of clozapine intoxication showed that most clozapine-induced pathological changes have a non-specific character (including largely circulatory disorders and dystrophic changes in parenchymatous organs). Clozapine poisoning is associated with the lengthening of QT-interval on ECG; at the values in excess of 500 ms, the risk of severe arrhythmia and sudden death significantly increases. Clozapine intake may lead to the development of potentially fatal myocarditis (the so-called clozapine-associated eosinophilic myocardium) in somatically healthy subjects. Foreign researchers report the possibility of a post-mortem increase of blood clozapine content compared with its antemortem level. They also showed that simultaneous use of substances stimulating activity of cytochrome P-450 enzymes (ethyl alcohol, finlepsin, fenitrin, nicotine) and clozapine accelerates metabolism and thereby reduces clozapine concentration in blood. It is concluded that comprehensive investigations of clozapine intoxication are needed taking into consideration pathomorphological changes induced by this agent, its potential interaction with other factors influencing human body, and the results of forensic chemical expertise of the fatal cases. PMID:25474921

  10. Atropine unmasks bed-rest effect - A spectral analysis of cardiac interbeat intervals

    NASA Technical Reports Server (NTRS)

    Goldberger, Ary L.; Goldwater, Danielle; Bhargava, Valmik

    1986-01-01

    Heart rate spectral data obtained for 10 male subjects between 35-49 years following orthostatic tolerance testing with lower body negative pressure prebed rest and after 7-10 days of bed rest, while on placebo and after intravenous atropine are analyzed. Comparison of the spectral atropine rms for subjects prebed rest and after bed rest reveal a decrease from 63 + or - 24 ms to 40 + or - 23 ms. It is observed that heart rate interval variability for subjects after bed rest and with atropine is reduced; the heart rate at bed rest with atropine is increased from 70.4 + or - 12.4 beats/min prebed rest to 83.7 + or - 18.9 beats/min; and the exercise tolerance time for subjects in the atropine prebed-rest phase (658 + or - 352 s) is higher than the bed-rest phase (505 + or - 252 s). It is noted that bed rest impairs the cardiovascular capacity to adaptively modulate physiological responses, atropine exposes bed-rest deconditioning effects, and spectral analysis is useful for studying the effects of bed-rest deconditioning on cardiac dynamics.

  11. Effect of physostigmine and atropine on acetylcholine turnover in mouse brain.

    PubMed

    Karlén, B; Lundgren, G; Lundin, J; Holmstedt, B

    1979-07-01

    The effect of physostigmine salicylate (0.5 mg/kg, i.p.) alone and in combination with atropine sulfate (25 mg/kg, i.p.) on levels of acetylcholine (ACh) and choline (Ch) and turnover of ACh has been studied in whole brain and striatum of mice. The animals were killed by focussed microwave irradiation and the turnover of ACh was studied after i.v. injection of deuterium labelled Ch by employing mass fragmentography. Physostigmine increased the levels of ACh in whole brain from 24.5--28.0 nmol/g(P less than 0.001) whereas there was no significant increase in striatum. The levels of Ch were also increased. The turnover rate of ACh was decreased in whole brain from 15.4 to 8.4 and in striatum from 52.9 to 24.4 nmol/g . min. Physostigmine given before or after atropine did not completely block the ACh lowering effect of atropine. When atropine was given before physostigmine the turnover rate of ACh in whole brain was increased to 24.2 nmoles/g . min. The results seem to indicate that there is no clear cut relation between the turnover rate and level of ACh in vivo. The increase of the turnover rate induced by atropine is masked unless a cholinesterase inhibitor is given to protect the newly synthesized labelled ACh released by atropine. PMID:492354

  12. Patching vs Atropine to Treat Amblyopia in Children Aged 7 to 12 Years: A Randomized Trial

    PubMed Central

    2008-01-01

    Objective To compare patching with atropine eye drops in the treatment of moderate amblyopia (20/40 -20/100) in children age 7 to 12 years. Methods In a randomized multi-center clinical trial, 193 children with amblyopia were randomized to weekend atropine or patching 2 hours per day of the sound eye. Main Outcome Measure Masked assessment of amblyopic eye visual acuity using the EETDRS testing protocol at 17 weeks. Results At 17 weeks, visual acuity had improved from baseline by an average of 7.6 letters in the atropine group and 8.6 letters in the patching group. The mean difference (patching minus atropine) between groups adjusted for baseline acuity was 1.2 letters (ends of complementary 1-sided 95% confidence intervals for noninferiority = -0.7 and +3.1 letters). Based on the confidence intervals this difference met the pre-specified definition for equivalence (ends of confidence intervals <5 letters). Amblyopic eye visual acuity was 20/25 or better in 15 subjects (17%) in the atropine group and 20 subjects (24%) in the patching group (difference = 7%, 95% confidence interval = -3% to 17%). Conclusions Treatment with atropine or patching leads to similar degrees of improvement in 7 to 12 year old children with moderate amblyopia. About 1 in 5 achieves 20/25 or better visual acuity in the amblyopic eye. Application to Clinical Practice Treatment of older children with unilateral amblyopia. PMID:19064841

  13. [Carbon monoxide intoxications in Portugal].

    PubMed

    Sá, Márcia Christel; Rodrigues, Rui Paulo; Moura, Daniel

    2011-01-01

    The prevalence of carbon monoxide intoxication in the World shows that this is a common situation. In Portugal, there are no concrete data available in literature and its incidence remains unknown. Currently, the use of hyperbaric oxygen is a valid therapeutic for carbon monoxide poisoning management. However, its effectiveness and its proper handling are still controversial. The first aim of this study was to estimate the incidence of carbon monoxide intoxication in Portugal and to analyze its demographic characteristics. The second objective of this work was to evaluate the possible change in the type of treatment applied in areas near de hyperbaric chamber of Unidade Local de Saúde de Matosinhos, since its opening in June 2006. To achieve these objectives, we conducted a survey on admissions data for carbon monoxide intoxication occured between January first, 2000 and December 31, 2007. These data was collected in seven hospitals and in the Administração Central do Sistema de Saúde, I.P. Nationally, 621 hospitalizations were recorded, which represents an incidence of 5,86/100000 in 8 years. In the seven hospitals, there were 93 hospitalizations due to carbon monoxide intoxication during the same period of time. There was a peak of incidence during winter, between November and March and there was a similar distribution in men (47,3%) and women (52,7%). Since June 2006, date of opening of the hyperbaric chamber, the Unidade Local de Saúde de Matosinhos, E.P.E. recorded a sharp increase in the number of hospitalization for carbon monoxide intoxication. The number of admissions in the 19 months after the chamber opening was double the number of all cases occurred in that institution in the 65 months prior. We concluded that, in Portugal, carbon monoxide intoxication is an uncommon situation but it´s still an important cause of hospitalization. The referral of cases to the Unidade Local de Saúde de Matosinhos, E.P.E. since the opening of hyperbaric chamber

  14. An interesting thinner intoxication case: intrathoracic injection.

    PubMed

    Solak, Ilhami; Cankayali, Ilkin; Aksu, Hasim; Moral, Ali Resat

    2006-01-01

    Thinners, including aromatic hydrocarbons such as toluene, xylene, and N-hexane, are widely used in industry for the production of plastics, varnish, paint, and glue. Use of these toxic agents frequently leads to chronic intoxication caused by abuse or misuse of solvents, which are usually taken in through inhalation. Thinners may have neurotoxic, myotoxic, hepatotoxic, nephrotoxic, and cardiotoxic systemic effects. The patient described in this report attempted to commit suicide by injecting 10 cc thinner into the left hemithorax. Acute chemical empyema developed at the left hemithorax. No bacterial growth was noted in empyema liquid and blood samples. Empyema was treated with tube thoracostomy, and full remission was observed after 33 d. No systemic toxic signs were noted, other than a low level of hepatotoxicity. Although pleural effusion, atelectasis, and pleural thickening were observed at the acute phase on computed tomography (CT) of the thorax, only pleural thickening persisted on CT of the thorax after 1 y. Investigators could not find a documented case of parenteral use of thinners in the medical literature. PMID:16912033

  15. The parasympatholytic effects of atropine sulfate and glycopyrrolate in rats and rabbits.

    PubMed Central

    Olson, M E; Vizzutti, D; Morck, D W; Cox, A K

    1994-01-01

    Nine groups of rats (n = 5 per group) received an intramuscular (IM) injection of one of the following drugs or drug combinations: saline, atropine (0.05 mg/kg), glycopyrrolate (0.5 mg/kg), ketamine:xylazine (85:15 mg/kg), ketamine:detomidine (60:10 mg/kg), atropine:ketamine:xylazine (0.05: 85:15 mg/kg), glycopyrrolate: ketamine:xylazine (0.5:85:15 mg/kg), atropine:ketamine:detomidine (0.05: 60:10 mg/kg) or glycopyrrolate: ketamine:detomidine (0.5:60:10). Similarly six groups of rabbits (n = 5) received an IM injection of either saline, atropine (0.2 mg/kg), atropine (2 mg/kg), glycopyrrolate (0.1 mg/kg), ketamine:xylazine (35:10 mg/kg) or glycopyrrolate:ketamine:xylazine (0.1:35:10 mg/kg). In rats, atropine sulfate (0.05 mg/kg) and glycopyrrolate (0.5 mg/kg) produced an increase in heart rate for 30 and 240 min, respectively. In rabbits atropine sulfate at either 0.2 or 2.0 mg/kg did not induce a significant increase in heart rate, but glycopyrrolate (0.1 mg/kg) elevated the heart rate above saline treated animals for over 50 min. Both atropine and glycopyrrolate provided protection against a decrease in heart rate in rats anesthetized with ketamine: xylazine (85:15 mg/kg) or ketamine: detomidine (60:10 mg/kg); however, glycopyrrolate was significantly more effective in maintaining the heart rate within the normal range. Glycopprrolate also prevented a decrease in heart rate in rabbits anesthetized with ketamine:xylazine (35:5 mg/kg). Neither glycopyrrolate nor atropine influenced respiration rate, core body temperature or systolic blood pressure when used alone or when combined with the injectable anesthetic. Glycopyrrolate is an effective anticholinergic agent in rabbits and rodents and more useful as a preanesthetic agent than atropine sulfate in these animals. PMID:7889456

  16. Proteinuria of industrial lead intoxication

    SciTech Connect

    Vacca, C.V.; Hines, J.D.; Hall, P.W. III

    1986-12-01

    Studies of protein excretion were undertaken in seven males, aged 35-42 years, who had more than 5 years exposure to industrial lead and had clinically established Pb intoxication. Heavy metal intoxication with Cd and Hg causes proximal tubular abnormalities, i.e., aminoaciduria, glycosuria, phosphaturia. Similar abnormalities occur in Pb intoxication except that the nature of the proteinuria remains controversial. Studies of urinary proteins included 24-hr urine protein excretion, dextran gel separations, sodium dodecyl sulfate-polyacryl-amide gel electrophoresis (SDS-PAGE), and ..beta../sub 2/ microglobulin (B/sub 2/M) measurements. Creatinine clearances, and serum B/sub 2/M concentrations were normal. Urine total protein distribution by SDS-PAGE and the B/sub 2/M excretion rate were also normal. These data imply that the nephrotoxicity of Cd and Hg are different than that of Pb. The authors speculate on what might account for this difference. This study suggests that when examining a population exposed to Pb, the finding of tubular proteinuria should alert investigators to search for the presence of other toxic agents.

  17. Carbon monoxide intoxication.

    PubMed

    Bleecker, Margit L

    2015-01-01

    Carbon monoxide (CO) is a colorless, odorless, nonirritant gas that accounts for numerous cases of CO poisoning every year from a variety of sources of incomplete combustion of hydrocarbons. These include poorly functioning heating systems, indoor propane-powered forklifts, indoor burning of charcoal burning briquettes, riding in the back of pick-up trucks, ice skating rinks using propane-powered resurfacing machines, and gasoline-powered generators that are not in correct locations. Once CO is inhaled it binds with hemoglobin to form carboxyhemoglobin (COHb) with an affinity 200 times greater than oxygen that leads to decreased oxygen-carrying capacity and decreased release of oxygen to tissues leading to tissue hypoxia. Ischemia occurs with CO poisoning when there is loss of consciousness that is accompanied by hypotension and ischemia in the arterial border zones of the brain. Besides binding to many heme-containing proteins, CO disrupts oxidative metabolism leading to the formation of free radicals. Once hypotension and unconsciousness occur with CO poisoning, lipid peroxidation and apoptosis follow. Because COHb has a short half-life, examination of other biomarkers of CO neurotoxicity that reflect inflammation or neuronal damage has not demonstrated consistent results. The initial symptoms with CO exposure when COHb is 15-30% are nonspecific, namely, headache, dizziness, nausea, fatigue, and impaired manual dexterity. However individuals with ischemic heart disease may experience chest pain and decreased exercise duration at COHb levels between 1% and 9%. COHb levels between 30% and 70% lead to loss of consciousness and eventually death. Following resolution of acute symptoms there may be a lucid interval of 2-40 days before the development of delayed neurologic sequelae (DNS), with diffuse demyelination in the brain accompanied by lethargy, behavior changes, forgetfulness, memory loss, and parkinsonian features. Seventy-five percent of patients with DNS

  18. Last call: ethanol metabolism and the implications for emergency department clinicians managing patients with extreme ethanol intoxication.

    PubMed

    Johnson, Jeremy M

    2009-01-01

    The legal consumption of alcohol at a drinking age of 21 years and the accepting, ubiquitous nature of our society has caused alcohol consumption to become highly prevalent in our society. To this avail, emergency departments will continue to see a greater number of intoxicated patients, and it is imperative that clinicians remain up to date about treatment strategies and general management of the acutely intoxicated individual. This article expounds on many of the subtle presentations that may be featured by the intoxicated patient and discusses the current treatment modalities and pitfalls utilized by today's emergency clinician. PMID:20118874

  19. Effect of acid secretion blockade on acute gastric mucosal lesions induced by Tityus serrulatus scorpion toxin in anaesthetized rats.

    PubMed

    Melo, Júnio Rios; de Araújo, Gnana Keith Marques; da Luz, Magda Maria Profeta; da Conceição, Sérgio Alexandre; Lisboa, Felipe Assis; Moraes-Santos, Tasso; Cunha-Melo, José Renan

    2006-10-01

    Scorpion venom (TX) promotes gastric acid and pepsin secretion leading to acute gastric mucosal lesions (AGML), when injected in animals. The goal of the present study was to observe the effects of acid gastric secretion blockers over the incidence of TX-induced AGML in vivo. To verify this model, we used male albino rats, fasted 18-20 h (n=122) and anaesthetized with urethane (1.4 g/kg, i.p.). Their trachea and left femoral vein were both cannulated; the first to avoid airway obstructions during scorpion intoxication and the second for administration of saline, TX and acid blockers. Following the surgical procedure, the animals were divided in 10 groups of at least 10 animals each. Control groups were injected with NaCl 0.9% 1 ml/kg (n=10) or TX 375 microg/kg (n=32). Test groups (n=10, each) received atropine 5 mg/kg, cimetidine 10mg/kg, ranitidine 2.5mg/kg, ranitidine 5mg/kg, omeprazol 1 mg/kg, omeprazol 4 mg/kg, octreotide 80 and octreotide 100 microg/kg 10 min before the TX was injected. After 1h of intoxication, the stomach was resected for macroscopic study and the gastric secretion was collected for volume, pH and acid output assessment. We observed that all blockers were able to completely or partially prevent the TX-induced acid secretion as well as the AGML (p<0.05). Our data suggest the TX-induced AGML can be prevented by different class of acid blockers injected before the intoxication. PMID:16926041

  20. Simple Diagnostic Tests to Detect Toxic Alcohol Intoxications

    PubMed Central

    Shin, Jai Moo; Sachs, George; Kraut, Jeffrey A.

    2008-01-01

    Methanol, ethylene glycol, and diethylene glycol intoxications can produce visual disturbances, neurological disturbances, acute renal failure, pulmonary dysfunction, cardiac dysfunction, metabolic acidosis, and death. Metabolic acidosis and an increased serum osmolality are important clues to their diagnosis. The former reflects the organic acids produced by metabolism of the parent alcohol, while the latter is due to accumulation of the offending alcohol. However, neither the clinical nor the laboratory findings are specific for toxic alcohol ingestions. The definitive diagnosis of the alcohol intoxications is commonly based on detection of the alcohol or its metabolites in blood. Early diagnosis is important, because initiation of appropriate treatment can markedly lessen their morbidity and mortality. At present detection of the parent alcohol in body fluids is inferred from its measurement in blood. This measurement is often performed by specialty laboratories using expensive equipment, and a long delay between obtaining the specimen and getting the results is not unusual. In this report, we describe liquid- based tests that detect methanol, ethylene glycol, diethylene glycol, and ethanol in saliva. The tests are sensitive and they have different specificity for each of the alcohols facilitating distinction among them. The relatively high sensitivity and specificity of the tests as a whole will facilitate the rapid diagnosis of each of these alcohol intoxications. PMID:18940722

  1. Brodifacoum intoxication with marijuana smoking.

    PubMed

    La Rosa, F G; Clarke, S H; Lefkowitz, J B

    1997-01-01

    We report the case of a 17-year-old boy with a significant history of drug and alcohol abuse, which included smoking marijuana mixed with brodifacoum. As a consequence, the patient developed a prolonged coagulopathy that persisted for more than 1 year. To our knowledge, this is the first case reported in the literature in which super-warfarin intoxication has been associated with marijuana smoking. This report should increase the awareness of pathologists and clinicians when examining a patient with a history of drug abuse who exhibits persistent vitamin K1-dependent coagulopathy. PMID:9111096

  2. Effects of Alcohol Intoxication on Anger Experience and Expression among Partner Assaultive Men

    ERIC Educational Resources Information Center

    Eckhardt, Christopher I.

    2007-01-01

    The author investigated the acute effects of alcohol intoxication on anger experience and expression among 46 maritally violent (MV) and 56 maritally nonviolent (NV) men randomly assigned to receive alcohol, placebo, or no alcohol. Participants completed an anger-arousing articulated thoughts in simulated situations (ATSS) paradigm and imagined…

  3. Xanthine oxidase status in ethanol-intoxicated rat liver.

    PubMed

    Abbondanza, A; Battelli, M G; Soffritti, M; Cessi, C

    1989-12-01

    The status of xanthine oxidase in ethanol-induced liver injury has been investigated in the rat, by acute and chronic ethanol treatments. A 38% increase of the enzyme O-form was observed after repeated ethanol administration. Chronic intoxication caused a significant decrease of total xanthine oxidase activity after both prolonged ethanol feeding and life span ethanol ingestion. The intermediate D/O-form of xanthine oxidase (that can act either as an oxidase or as a dehydrogenase, being able to react with O2 as well as with NAD+ as electron acceptor) increased 5.5-fold after prolonged ethanol feeding. PMID:2690670

  4. Perceived Intoxication: Implications for Alcohol Education.

    ERIC Educational Resources Information Center

    Nicholson, Mary E.; And Others

    1994-01-01

    This study examined the relationships among perceived levels of intoxication, blood alcohol levels, and impairment of selected psychomotor skills used in driving. Results reinforced previous findings which correlated perceptions of intoxication and other measures. These findings suggest that alcohol consumption tables, which calculate one's…

  5. 25 CFR 140.18 - Intoxicating liquors.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 25 Indians 1 2010-04-01 2010-04-01 false Intoxicating liquors. 140.18 Section 140.18 Indians BUREAU OF INDIAN AFFAIRS, DEPARTMENT OF THE INTERIOR FINANCIAL ACTIVITIES LICENSED INDIAN TRADERS § 140.18 Intoxicating liquors. No trader shall use or permit to be used his premises for any unlawful conduct or purpose whatsoever. No trader shall use...

  6. [Datura intoxication--report of three cases].

    PubMed

    Nowak, Agnieszka; Łata, Stanisław

    2010-01-01

    In recent months, more and more reports have appeared about datura seed poisoning. Datura is widespread and has hallucinogenic properties. It is part of the increase in drug use among the younger generation that is experimenting with intoxicants. The hallucinogenic and poisonous effects of datura involve the presence of tropine alkaloids: atropine and scopolamine. They both have similar effects, suppressing the parasympathetic peripheral nervous system. In large doses they lead to death as a result of respiratory paralysis. Treatment addresses the symptoms. In order to eliminate toxic effects of atropine, an antagonistic medication such as neostigmine is given. PMID:20684356

  7. Three fatal intoxications due to methylone.

    PubMed

    Pearson, Julia M; Hargraves, Tiffanie L; Hair, Laura S; Massucci, Charles J; Frazee, C Clinton; Garg, Uttam; Pietak, B Robert

    2012-07-01

    We present three fatal intoxications of methylone, a cathinone derivative. Blood was analyzed with a routine alkaline liquid-liquid extraction and analyzed by gas chromatography coupled with a mass spectrometer (GC-MS). Methylone was identified by a full scan mass spectral comparison to an analytical standard of methylone. For a definitive and conclusive confirmation and quantitation, methylone was also derivatized with heptafluorobutyric anhydride and analyzed by GC-MS. In all three fatalities, the deceased exhibited seizure-like activity and elevated body temperatures (103.9, 105.9 and 107°F) before death. Two of the three cases also exhibited metabolic acidosis. One of the three cases had prolonged treatment and hospitalization before death with symptoms similar to sympathomimetic toxicity, including metabolic acidosis, rhabdomyolysis, acute renal failure and disseminated intravascular coagulation. The laboratory results for this patient over the 24 h period of hospitalization were significant for increased lactate, liver transaminases, creatinine, myoglobin, creatine kinase and clotting times, and decreased pH, glucose and calcium. Peripheral blood methylone concentrations in the three fatal cases were 0.84, 3.3 and 0.56 mg/L. In conlusion, peripheral blood methylone concentrations in excess of 0.5 mg/L may result in death due to its toxic properties, which can include elevated body temperature and other sympathomimetic-like symptoms. PMID:22589523

  8. Fatal intoxication from 3,4-methylenedioxyamphetamine.

    PubMed

    Poklis, A; Mackell, M A; Drake, W K

    1979-01-01

    The symptoms of MDA intoxication exhibited by the decedent prior to death closely mimic those of acute amphetamine poisoning: profuse sweating, violent and irrational behavior, and stereotypically compulsive behavior. Therefore, if amphetamines are not detected in specimens from a person displaying classic symptoms of amphetamine poisoning, hallucinogenic amphetamine derivatives may be considered. In the case described, a divided dose of 850 mg of MDA ingested within 2 h and 15 min was sufficient to cause the death of a 24-year-old male, 4 h after the final dose. While the methaqualone may have contributed to the demise of the decedent, the authors think that the MDA itself was sufficient to cause death. Results of limited recovery studies of MDA extraction from blood and elution from TLC plates supported the observations of Cimbura [13]. Approximately 85% of MDA is extracted by the method described and its elution from TLC plates is quantitative. This case points out once again the dangers of false advertising in the illicit market. The decedent, himself a dealer in the illicit drug market, and all present at the party believed the ingested white powder to be a mixture of morphine, LSD, and amphetamine, hence MDA. They were totally unfamiliar with 3,4-methylenedioxyamphetamine, MDA. PMID:512617

  9. [METABOLIC INTOXICATION IN THERMIC TRAUMA].

    PubMed

    Kovalenko, O M

    2015-05-01

    In 76 injured persons with deep and superficial burns, having area from 3 to 65% of the total body surface and ageing 5-16 yrs old, there was investigated the impact of early surgical treatment on the metabolic intoxication severity in accordance to content of the oxidatively modified proteins carbonyl groups in the blood serum, and of a ceruloplasmin, what was considered as integral express-index of the organism antioxidant system state. Changes of these indices in ambustial disease of middle severity have witnessed a sufficiently compensated reaction of organism: of severe and extremely severe one--there were noted a deficiency of the organism antioxidant defense; and in stages of toxemia and septicotoxemia--attrition of the organism oxidant reserves and danger of the septic complications occurrence. Conduction of early surgical intervention have guaranteed maintenance of a ceruloplasmin content in stages of toxemia and septicotoxemia on the level of healthy persons, relief of the ambustial disease course, absence of critical metabolic intoxication and carbonyl stress, reduction of the septic complications rate in 1.5 times. PMID:26419044

  10. Accidental monensin sodium intoxication of feedlot cattle.

    PubMed

    Schweitzer, D; Kimberling, C; Spraker, T; Sterner, F E; McChesney, A E

    1984-05-15

    Of 1,994 yearling and 2-year-old cattle in a winter feeding program, 117 died within 42 days of being fed toxic amounts of monensin sodium in a liquid protein supplement. Death losses commenced on the third day after ingestion of a toxic amount in the feed. Clinical signs in cattle that died in less than 9 days included anorexia, pica, diarrhea, depression, mild hindlimb ataxia, and dyspnea. Gross necropsy findings in cattle dying in the acute phase of the illness included hydrothorax, ascites, and pulmonary edema, as well as petechial hemorrhages, edema, and yellow streaking in skeletal and cardiac muscle. Cattle dying after 9 days had gray streaks in heart and skeletal muscle, generalized ventral edema, enlarged, firm, bluish discolored liver, and enlarged heart. Microscopic changes in cattle dying in the acute phase (less than 9 days) consisted of pulmonary edema, congestion, and hemorrhage. Cardiac and skeletal muscle had localized areas of edema, hemorrhage, and coagulative necrosis. In cattle dying after 9 days of illness, the changes included lymphocytic infiltration, sarcolemmal nuclear proliferation, and fibrosis in skeletal and cardiac muscle. Lungs contained increased alveolar macrophages and a few neutrophils. Centrilobular necrosis and mild fibrosis were found in the liver. Changes varied somewhat according to the area of heart or skeletal muscle that was affected. Active muscles, eg, those in the heart ventricles and diaphragm, were altered most severely. Intoxication appeared to be a result of sedimentation of monensin in the molasses carrier to give remarkable concentrations of the substance at the bottom of the holding tank. PMID:6735846

  11. Effects of acepromazine, pethidine and atropine premedication on lower oesophageal sphincter pressure and barrier pressure in anaesthetised cats.

    PubMed

    Hashim, M A; Waterman, A E

    1993-08-14

    Combinations of acepromazine maleate, pethidine hydrochloride and atropine sulphate (0.05 mg/kg) or acepromazine maleate and pethidine hydrochloride and acepromazine maleate alone or atropine sulphate (0.1 mg/kg) alone were used to premedicate cats before they were anaesthetised with thiopentone, to investigate their effects on gastric pressure, lower oesophageal sphincter pressure and barrier pressure under anaesthesia. Manometric measurements were made by using a non-perfused manometric technique. The lower oesophageal sphincter pressure was lowest in the cats premedicated with atropine sulphate alone. The difference in barrier pressure between the atropine (0.1 mg/kg) and acepromazine treated cats was highly significant. The risk of gastro-oesophageal reflux appeared to be highest with atropine (0.1 mg/kg) if barrier pressure is used as an indicator of the likelihood of reflux. PMID:8236702

  12. Cycloplegic effect of atropine compared with cyclopentolate-tropicamide combination in children with hypermetropia

    PubMed Central

    Sani, Rabi Yahaya; Hassan, Sadiq; Habib, Saudat Garba; Ifeanyichukwu, Ebisike Philips

    2016-01-01

    Background: Cycloplegic refraction is important in assessing children with hypermetropia. Atropine, though the gold standard cycloplegic agent for refraction in children, has a long duration of action and more severe side effects compared to short-acting cycloplegic agents. The aim of the study was to compare the cycloplegic effect of atropine with cyclopentolate and tropicamide combination in children with hypermetropia. Subjects and Methods: This was a crossover interventional study in children with hypermetropia. Cycloplegic refraction using two separate regimens of cycloplegic drugs was done on all subjects. Data were analyzed using the statistical software SPSS version 22.0. The mean spherical equivalent values of regimen 1 (atropine 1%) and regimen 2 (cyclopentolate 1% and tropicamide 1%) were presented as mean and standard deviation. A P ≤ 0.05 was considered statistically significant. Results: One hundred and twenty-six eyes of 63 subjects aged 5–12 years were examined. The mean spherical equivalent values for regimen 1 and regimen 2 for the right eyes were 4.73 ± 2.1 DS and 4.54 ± 1.9 DS, respectively (P = 0.59). The mean spherical equivalent values for regimens 1 and 2 for the left eyes were 4.74 ± 2.0 DS and 4.54 ± 1.8 DS, respectively (P = 0.56). Conclusion: The combination of 1% cyclopentolate and 1% tropicamide could be a useful alternative to atropine 1% for cycloplegic refraction in children with hypermetropia. PMID:27397958

  13. A Double-Blind Atropine Trial for Active Learning of Autonomic Function

    ERIC Educational Resources Information Center

    Fry, Jeffrey R.; Burr, Steven A.

    2011-01-01

    Here, we describe a human physiology laboratory class measuring changes in autonomic function over time in response to atropine. Students use themselves as subjects, generating ownership and self-interest in the learning as well as directly experiencing the active link between physiology and pharmacology in people. The class is designed to…

  14. Permanent alterations in muscarinic receptors and pupil size produced by chronic atropinization in kittens

    SciTech Connect

    Smith, E.L.; Redburn, D.A.; Harwerth, R.S.; Maguire, G.W.

    1984-02-01

    Chronic mydriasis was induced in six kittens (four monocular, two binocular) and two adult cats (both monocular) by the daily topical application of atropine. Both the kittens and the adult cats were atropinized for a 13-week period with the treatment regimen beginning at the time of eye opening for the kittens. Pupil size measurements, obtained 1 year after the atropinization were discontinued, revealed that, although the pupils of the adult cats were normal, the pupils of the kittens' treated eyes were consistently smaller than pupils in control eyes. The status of the muscarinic receptors in the kittens' irides was investigated using /sup 3/H-QNB binding assays. In comparison with iris muscle homogenates from the control eyes, those from the treated eyes demonstrated an eightfold increase in the number of receptor binding sites. The results indicate that pupil size can be altered permanently by chronic mydriasis initiated early in the life of a kitten and that the permanent change in pupil size may result, in part, from a type of permanent supersensitivity response in the muscle following chronic blockade of muscarinic transmission by atropine.

  15. Enhanced accumulation of atropine in Atropa belladonna transformed by Rac GTPase gene isolated from Scoparia dulcis.

    PubMed

    Asano, Kyouhei; Lee, Jung-Bum; Yamamura, Yoshimi; Kurosaki, Fumiya

    2013-12-01

    Leaf tissues of Atropa belladonna were transformed by Sdrac2, a Rac GTPase gene, that is isolated from Scoparia dulcis, and the change in atropine concentration of the transformants was examined. Re-differentiated A. belladonna overexpressing Sdrac2 accumulated considerable concentration of atropine in the leaf tissues, whereas the leaves of plants transformed by an empty vector accumulated only a very low concentration of the compound. A. belladonna transformed by CASdrac2, a modified Sdrac2 of which translate was expected to bind guanosine triphosphate (GTP) permanently, accumulated very high concentrations of atropine (approximately 2.4-fold excess to those found in the wild-type plant in its natural habitat). In sharp contrast, the atropine concentration in transformed A. belladonna prepared with negatively modified Sdrac2, DNSdrac2, expected to bind guanosine diphosphate instead of GTP, was very low. These results suggested that Rac GTPases play an important role in the regulation of secondary metabolism in plant cells and that overexpression of the gene(s) may be capable of enhancing the production of natural products accumulated in higher plant cells. PMID:23852262

  16. Cocaine Intoxication and Thyroid Storm

    PubMed Central

    Lacy, Mary E.

    2014-01-01

    Introduction. Cocaine, a widely used sympathomimetic drug, causes thermoregulatory and cardiac manifestations that can mimic a life-threatening thyroid storm. Case. A man presented to the emergency department requesting only cocaine detoxification. He reported symptoms over the last few years including weight loss and diarrhea, which he attributed to ongoing cocaine use. On presentation he had an elevated temperature of 39.4°C and a heart rate up to 130 beats per minute. Examination revealed the presence of an enlarged, nontender goiter with bilateral continuous bruits. He was found to have thyrotoxicosis by labs and was treated for thyroid storm and cocaine intoxication concurrently. The patient was ultimately diagnosed with Graves’ disease and treated with iodine-131 therapy. Conclusion. Cocaine use should be considered a possible trigger for thyroid storm. Recognition of thyroid storm is critical because of the necessity for targeted therapy and the significant mortality associated with the condition if left untreated. PMID:26425625

  17. Dose-response effects of atropine and HI-6 treatment of organophosphorus poisoning in guinea pigs

    SciTech Connect

    Koplovitz, I.; Menton, R.; Matthews, C.; Shutz, M.; Nalls, C.

    1995-12-31

    H1-6 (1-2-hydrnxyiminomethyl-1 pyridino-3-(4-carbameyl- 1--pyddino)-2- oxaprnpane dichioride) has been evaluated as an oxime alternative to pralidoxime, and toxogonin in the treatment of organophosphorus (OP) poisoning. The dose response effects of atropine (ATR) and HI-6 were investigated to more fully explore the interaction of these compounds in the treatment of OP poisoning. ATR, HI-6 and various combinations of the two drugs were evaluated against lethal poisoning by soman (GD) and tabun (GA) in guinea pigs. The effect of adjunctive diazepam treatment on the efficacy of atropine and HI-6 against soman was also investigated. Animals of either sex were challenged s.c. with OP and treated i.m. 1 min later with ATR and/or HI-6. When used, diazepam was injected immediately after ATR+HI6. LD50s of each treatment were calculated from probit models based on 24-hour survival against 5 levels of nerve agent and 6 animals per challenge level. A protective index (PI) was calculated by dividing the nerve agent LD50 in the presence of treatment by the LD50 in the absence of treatment. Treatment with HI-6 alone had little effect on the toxicity of either OP. Treatment with ATR alone was more effective than HI-6 alone and was significantly more effective against soman than against tabun. When used in combination atropine and HI-6 had a strong synergistic effect against both agents. The dose of atropine used with HI-6 was critical in determining the efficacy of HI-6 against either agent. The slopes of the dose-lethality curves were minimally affected by the dose of ATR or HI-6. Adjunctive treatment with diazepam enhanced the efficacy of HI-6 and atropine against soman.

  18. Opposing effects of atropine and timolol on the color and luminance emmetropization mechanisms in chicks.

    PubMed

    Goldberg, Laura A; Rucker, Frances J

    2016-05-01

    This study analyzed the luminance and color emmetropization response in chicks treated with the nonselective parasympathetic antagonist atropine and the sympathetic β-receptor blocker timolol. Chicks were binocularly exposed (8h/day) for 4days to one of three illumination conditions: 2Hz sinusoidal luminance flicker, 2Hz sinusoidal blue/yellow color flicker, or steady light (mean 680lux). Atropine experiments involved monocular daily injections of either 20μl of atropine (18nmol) or 20μl of phosphate-buffered saline. Timolol experiments involved monocular daily applications of 2 drops of 0.5% timolol or 2 drops of distilled H2O. Changes in the experimental eye were compared with those in the fellow eye after correction for the effects of saline/water treatments. Atropine caused a reduction in axial length with both luminance flicker (-0.078±0.021mm) and color flicker (-0.054±0.017mm), and a reduction in vitreous chamber depth with luminance flicker (-0.095±0.023mm), evoking a hyperopic shift in refraction (3.40±1.77D). Timolol produced an increase in axial length with luminance flicker (0.045±0.030mm) and a myopic shift in refraction (-4.07±0.92D), while color flicker caused a significant decrease in axial length (-0.046±0.017mm) that was associated with choroidal thinning (-0.046±0.015mm). The opposing effects on growth and refraction seen with atropine and timolol suggest a balancing mechanism between the parasympathetic and β-receptor mediated sympathetic system through stimulation of the retina with luminance and color contrast. PMID:26971621

  19. Symptoms and signs in interpreting Gamma-hydroxybutyrate (GHB) intoxication - an explorative study

    PubMed Central

    2014-01-01

    Background Acute poisoning with gamma-hydroxybutyrate (GHB) has been a serious medical and social problem in different parts of the world including Sweden. GHB is a drug of abuse which acts primarily as central nervous system (CNS) depressants. GHB has serious toxicity, although many young users do not recognise GHB as a dangerous drug. The aim of this pilot study was to explore how symptoms with risk of failure in vital functions would be valued among professionals that encounter GHB intoxication in the emergency phase. Methods A web-based survey focusing on the assessment of vital clinical signs for possible GHB intoxication using a numeric scale was carried out during April and May 2011. The participants, n 105, are all professionals who encounter GHB intoxicated in the emergency phase, but have different levels of training in GHB intoxication, mainly Registered Nurses (RNs) in southwest Sweden, employed in pre-hospital or emergency departments at somatic and most psychiatric health care facilities, as well as police officers who in their work come into contact with drug users. Responses in the survey were scored according to risk of GHB intoxication with serious failure of vital functions. The score value was then referred to a so-called evidence based priority (EBP) scale and analysed using descriptive statistics and Fisher's exact test. Results Cardiac arrest, coma, hypoxia, general convulsions, slow respiratory and heart rate and pale skin are symptoms with the highest risk of serious failure in vital physical functions and were predominantly recognised as such. Conclusion Despite the professionals' different levels of training in GHB intoxication, all of them were relatively well aware of and in accordance regarding the most risky symptoms. The interpretation score for the less risky symptoms and signs of GHB intoxication varied depending on their degree of training. The results should be viewed cautiously, as the size of the professional groups and their

  20. Economic Contraction, Alcohol Intoxication and Suicide: Analysis of the National Violent Death Reporting System

    PubMed Central

    Kaplan, M.S.; Huguet, N.; Caetano, R.; Giesbrecht, N.; Kerr, W.C.; McFarland, B.H.

    2014-01-01

    Objectives Although there is a large and growing body of evidence concerning the impact of contracting economies on suicide mortality risk, far less is known about the role alcohol consumption plays in the complex relationship between economic conditions and suicide. The aims were to compare the postmortem alcohol intoxication rates among male and female suicide decedents before (2005–07), during (2008–09), and after (2010–11) the economic contraction in the United States. Methods Data from the restricted National Violent Death Reporting System 2005–11 for male and female suicide decedents aged 20 years and older were analyzed by Poisson regression analysis to test whether there was significant change in the fractions of suicide decedents who were acutely intoxicated at the time of death (defined as blood alcohol concentration ≥ 0.08 g/dl) prior, during, and after the downturn. Results The fraction of all suicide decedents with alcohol intoxication increased by 7% after the onset of the recession from 22.2% in 2005–07 to 23.9% in 2008–11. Compared to the years prior to the recession, male suicide decedents showed a 1.09-fold increased risk of alcohol intoxication within the first two years of the recession. Surprisingly, there was evidence of a lag effect among female suicide decedents, who had a 1.14-fold (95% CI, 1.02 to 1.27) increased risk of intoxication in 2010–11 compared to 2005–07. Conclusions These findings suggest that acute alcohol intoxication in suicide interacts with economic conditions, becoming more prevalent during contractions. PMID:25024394

  1. Dihydromyricetin As A Novel Anti-Alcohol Intoxication Medication

    PubMed Central

    Shen, Yi; Lindemeyer, A. Kerstin; Gonzalez, Claudia; Shao, Xuesi M.; Spigelman, Igor; Olsen, Richard W.; Liang, Jing

    2012-01-01

    Alcohol use disorders (AUD) constitute the most common form of substance abuse. The development of AUD involves repeated alcohol use leading to tolerance, alcohol withdrawal syndrome (AWS), physical and psychological dependence, with loss of ability to control excessive drinking. Currently there is no effective therapeutic agent for AUD without major side-effects. Dihydromyricetin (DHM, 1 mg/kg, i.p. injection), a flavonoid component of herbal medicines, counteracted acute alcohol (EtOH) intoxication, and also withdrawal signs in rats including tolerance, increased anxiety and seizure susceptibility; DHM greatly reduced EtOH consumption in an intermittent voluntary EtOH intake paradigm in rats. GABAA receptors (GABAARs) are major targets of acute and chronic EtOH actions on the brain. At the cellular levels, DHM (1 μM) antagonized both acute EtOH-induced potentiation of GABAARs and EtOH exposure/withdrawal-induced GABAAR plasticity, including alterations in responsiveness of extra- and post-synaptic GABAARs to acute EtOH, and most importantly, increases in GABAAR α4 subunit expression in hippocampus and cultured neurons. DHM anti-alcohol effects on both behavior and CNS neurons were antagonized by flumazenil (10 mg/kg in vivo, 10 μM in vitro), the benzodiazepine (BZ) antagonist. DHM competitively inhibited BZ-site [3H]flunitrazepam binding (IC50, 4.36 μM), suggesting DHM interaction with EtOH involves the BZ-sites on GABAARs. In summary, we determined DHM anti-alcoholic effects on animal models, and determined a major molecular target and cellular mechanism of DHM for counteracting alcohol intoxication and dependence. We demonstrated pharmacological properties of DHM consistent with those expected to underlie successful medical treatment of AUD; therefore DHM is a therapeutic candidate. PMID:22219299

  2. Effects of ethanol intoxication on speech suprasegmentals

    NASA Astrophysics Data System (ADS)

    Hollien, Harry; Dejong, Gea; Martin, Camilo A.; Schwartz, Reva; Liljegren, Kristen

    2001-12-01

    The effects of ingesting ethanol have been shown to be somewhat variable in humans. To date, there appear to be but few universals. Yet, the question often arises: is it possible to determine if a person is intoxicated by observing them in some manner? A closely related question is: can speech be used for this purpose and, if so, can the degree of intoxication be determined? One of the many issues associated with these questions involves the relationships between a person's paralinguistic characteristics and the presence and level of inebriation. To this end, young, healthy speakers of both sexes were carefully selected and sorted into roughly equal groups of light, moderate, and heavy drinkers. They were asked to produce four types of utterances during a learning phase, when sober and at four strictly controlled levels of intoxication (three ascending and one descending). The primary motor speech measures employed were speaking fundamental frequency, speech intensity, speaking rate and nonfluencies. Several statistically significant changes were found for increasing intoxication; the primary ones included rises in F0, in task duration and for nonfluencies. Minor gender differences were found but they lacked statistical significance. So did the small differences among the drinking category subgroups and the subject groupings related to levels of perceived intoxication. Finally, although it may be concluded that certain changes in speech suprasegmentals will occur as a function of increasing intoxication, these patterns cannot be viewed as universal since a few subjects (about 20%) exhibited no (or negative) changes.

  3. A double-blind atropine trial for active learning of autonomic function.

    PubMed

    Fry, Jeffrey R; Burr, Steven A

    2011-12-01

    Here, we describe a human physiology laboratory class measuring changes in autonomic function over time in response to atropine. Students use themselves as subjects, generating ownership and self-interest in the learning as well as directly experiencing the active link between physiology and pharmacology in people. The class is designed to concomitantly convey the importance of bias in experimentation by adopting a double-blind placebo-controlled approach. We have used this class effectively in various forms with ∼600 students receiving atropine over the last 16 yr. This class has received favorable feedback from staff and students of medicine, pharmacy, and neuroscience, and we recommend it for such undergraduates. The learning objectives that students are expected to achieve are to be able to 1) know the ethical, safety, and hygiene requirements for using human volunteers as subjects; 2) implement and explain a double-blind placebo-controlled trial; 3) design, agree, and execute a protocol for making (and accurately recording) precise reproducible measurements of pulse rate, pupil diameter, and salivary flow; 4) evaluate the importance of predose periods and measurement consistency to detect effects (including any reversibility) after an intervention; 5) experience direct cause-and-effect relationships integrating physiology with pharmacology in people; 6) calculate appropriate summary statistics to describe the data and determine the data's statistical significance; 7) recognize normal variability both within and between subjects in baseline physiological parameters and also recognize normal variability in response to pharmacological treatment; 8) infer the distribution and role of muscarinic receptors in the autonomic nervous system with respect to the heart, eye, and mouth; 9) identify and explain the clinical significance of differences in effect due to the route and formulation of atropine; 10) produce and deliver a concise oral presentation of

  4. Fatal Intoxication with Acetyl Fentanyl.

    PubMed

    Cunningham, Susan M; Haikal, Nabila A; Kraner, James C

    2016-01-01

    Among the new psychoactive substances encountered in forensic investigations is the opioid, acetyl fentanyl. The death of a 28-year-old man from recreational use of this compound is reported. The decedent was found in the bathroom of his residence with a tourniquet secured around his arm and a syringe nearby. Postmortem examination findings included marked pulmonary and cerebral edema and needle track marks. Toxicological analysis revealed acetyl fentanyl in subclavian blood, liver, vitreous fluid, and urine at concentrations of 235 ng/mL, 2400 ng/g, 131 ng/mL, and 234 ng/mL, respectively. Acetyl fentanyl was also detected in the accompanying syringe. Death was attributed to recreational acetyl fentanyl abuse, likely through intravenous administration. The blood acetyl fentanyl concentration is considerably higher than typically found in fatal fentanyl intoxications. Analysis of this case underscores the need for consideration of a wide range of compounds with potential opioid-agonist activity when investigating apparent recreational drug-related deaths. PMID:26389815

  5. Histamine, histamine intoxication and intolerance.

    PubMed

    Kovacova-Hanuskova, E; Buday, T; Gavliakova, S; Plevkova, J

    2015-01-01

    Excessive accumulation of histamine in the body leads to miscellaneous symptoms mediated by its bond to corresponding receptors (H1-H4). Increased concentration of histamine in blood can occur in healthy individuals after ingestion of foods with high contents of histamine, leading to histamine intoxication. In individuals with histamine intolerance (HIT) ingestion of food with normal contents of histamine causes histamine-mediated symptoms. HIT is a pathological process, in which the enzymatic activity of histamine-degrading enzymes is decreased or inhibited and they are insufficient to inactivate histamine from food and to prevent its passage to blood-stream. Diagnosis of HIT is difficult. Multi-faced, non-specific clinical symptoms provoked by certain kinds of foods, beverages and drugs are often attributed to different diseases, such as allergy and food intolerance, mastocytosis, psychosomatic diseases, anorexia nervosa or adverse drug reactions. Correct diagnosis of HIT followed by therapy based on histamine-free diet and supplementation of diamine oxidase can improve patient's quality of life. PMID:26242570

  6. Combined approach to demonstrate acetylcholinesterase activity changes in the rat brain following tabun intoxication and its treatment.

    PubMed

    Bajgar, Jiri; Hajek, Petr; Kassa, Jiri; Slizova, Dasa; Krs, Otakar; Karasova, Jana Zdarova; Fusek, Josef; Capek, Lukas; Voicu, Victor A

    2012-01-01

    Reactivation effects of K203 and currently available oximes (obidoxime, HI-6) in combination with atropine on acetylcholinesterase activities in the brain parts of rats poisoned with tabun were studied. The activity was determined by quantitative histochemical and biochemical methods correlating between them very well. The tabun-induced changes in acetylcholinsterase activity as well as in reactivation potency of reactivators used were different in various parts of the brain. Pontomedullar area seems to be important for observed changes following tabun intoxication and its treatment. From the oximes studied, the reactivation effect of K203 was comparable with obidoxime; HI-6 was ineffective. Combination of bio- and histochemical methods allow fine differentiation among the action of different oximes following tabun poisoning. PMID:21851296

  7. Physiological responses wearing MOPP-IV after atropine and pralidoxime administration in warm and cool environments

    SciTech Connect

    Kolka, M.A.; Cadarette, B.S.

    1988-04-01

    The effect of cholinolytic and oxime (2 mg atropine + 600 mg pralidoxime) therapy on temperature regulation was evaluated in 8 subjects wearing chemical warfare protective clothing (MOPP-level IV). Subjects were tested in two environments: 35 c, 60% rh and 13 C, 44% rh during very light physical activity (1-2 Met) over a six-hour period. Sweating was suppressed approximately 40% by atropine and pralidoxime, and heart rate increased approximately 30 beats/min with drug treatment. At 13 C, all eight subjects completed 350 minutes of exposure in both drug and control experiments. Rectal temperature (t sub re) averaged 38.24 C in both treatments when subjects terminated their exposure at 35 C. Mean skin temperature averaged 37.42 C for both groups at termination. The treatment of subjects with atropine and pralidoxime when wearing chemical protective clothing does not adversely affect the length of time individuals can remain in a cool environment during very light work. However, the wearing of chemical protective clothing will decrease exposure time significantly (approx. 40%) in both control and drug treated subjects in a warm environment.

  8. [Acute poisoning by pesticides in children].

    PubMed

    Leveau, P

    2016-07-01

    Acute pesticide poisoning in children is rare but potentially serious. Some clinical patterns (toxidromes) are suggestive of the drug class: cholinergic crisis for organophosphate or carbamate insecticides; neurological syndrome for rodenticides; digestive and respiratory syndrome for herbicides. Treatment is symptomatic and only a few patients are treated with an antidote: atropine and pralidoxime for organophosphate insecticides, vitamin K for anticoagulant rodenticides. PMID:27266642

  9. Two Fatal Intoxications with Cyanohydrins.

    PubMed

    Zheng, Shuiqing; Yuan, Xiaoliang; Wang, Wei; Liang, Chen; Cao, Fangqi; Zhang, Runsheng

    2016-06-01

    Cyanohydrins, also be called cyanoalcohols, are important industrial precursors to carboxylic acids and some amino acids. Acetone cyanohydrin (ACH) and formaldehyde cyanohydrin (glycolonitrile, FCH), which are the typical examples of cyanohydrins, are classified as extremely hazardous substances. As the cyanohydrins can readily decompose, and it is hard to find cyanohydrins in gastric contents and heart blood, the determination study in biological samples can be divided into two parts: the first is the determination of HCN by using a Prussian blue reaction and the HS-GC-MSD after derivatization by chloramine-T. The second is the determination of acetone or formaldehyde. In this part, headspace gas chromatography with flame ionization detector (HS-GC-FID) and solid phase microextraction (SPME)-gas chromatography with mass spectrometric detectors (GC-MSD) had been used. In this report, we reported two fatal intoxication cases of ACH and FCH; one person was killed by his wife by poisoning his food and the other was suicide by poison. Two real cases of ACH and FCH in human blood and gastric contents have been analyzed by using the above-mentioned method. The Prussian blue reaction was positive in the two cases. The peaks of acetone with retention times of 0.998 min appear in specimens of the deceased are consistent with the retention times of pure acetone. The peaks of formaldehyde with a retention time of 1.658 min appear in heart blood of the deceased, and the retention time of formaldehyde of the liquid is 1.674 min, which are consistent with the retention times of pure formaldehyde (1.673 min). PMID:27026650

  10. Beneficial effects of TCP on soman intoxication in guinea pigs: seizures, brain damage and learning behaviour.

    PubMed

    de Groot, D M; Bierman, E P; Bruijnzeel, P L; Carpentier, P; Kulig, B M; Lallement, G; Melchers, B P; Philippens, I H; van Huygevoort, A H

    2001-12-01

    Poisoning with the potent nerve agent soman produces a cascade of central nervous system (CNS) effects characterized by severe convulsions and eventually death. In animals that survive a soman intoxication, lesions in the amygdala, piriform cortex, hippocampus and thalamus can be observed. In order to examine the mechanisms involved in the effects of soman and to evaluate possible curative interventions, a series of behavioural, electrophysiological and neuropathological experiments were carried out in the guinea pig using the NMDA antagonist N-[1-(2-thienyl)cyclohexyl] piperidine (TCP) in conjunction with atropine and pyridostigmine. The NMDA antagonist TCP appeared to be very effective in the treatment of casualties who suffered from soman-induced seizures for 30 min: (i)Seizures were arrested within minutes after the TCP injection, confirmed by quantitative electroencephalogram (EEG), after fast Fourier analysis. Three hours after TCP the quantitative EEGs were completely normal in all frequency bands and remained normal during the entire 3-week intoxication period. The power shift to the lower (delta) frequency bands, indicative for neuropathology and found in control animals intoxicated only by soman, was not observed in the soman-TCP group. (ii)The gross neuropathology found in soman control animals within 48 h after soman was prevented in soman-TCP animals and was still absent in 3-week survivors. Instead, ultrastructural changes were observed, indicative of defense mechanisms of the cell against toxic circumstances. (iii)Twenty-four hours after soman, soman-TCP animals were able to perform in the shuttle box and Morris water maze. The beneficial effects of TCP on the performance in these tests during the 3-week intoxication period were very impressive, notwithstanding (minor) deficits in memory and learning. (iv)The increase in excitability after TCP was confirmed by an increase in the acoustic startle response. Taken together, these results confirmed the

  11. Systemic Delivery of Atropine Sulfate by the MicroDose Dry-Powder Inhaler

    PubMed Central

    Venkataramanan, R.; Hoffman, R.M.; George, M.P.; Petrov, A.; Richards, T.; Zhang, S.; Choi, J.; Gao, Y.Y.; Oakum, C.D.; Cook, R.O.; Donahoe, M.

    2013-01-01

    Abstract Background Inhaled atropine is being developed as a systemic and pulmonary treatment for the extended recovery period after chemical weapons exposure. We performed a pharmacokinetics study comparing inhaled atropine delivery using the MicroDose Therapeutx Dry Powder Inhaler (DPIA) with intramuscular (IM) atropine delivery via auto-injector (AUTO). Methods The MicroDose DPIA utilizes a novel piezoelectric system to aerosolize drug and excipient from a foil dosing blister. Subjects inhaled a 1.95-mg atropine sulfate dose from the dry powder inhaler on one study day [5 doses×0.4 mg per dose (nominal) delivered over 12 min] and received a 2-mg IM injection via the AtroPen® auto-injector on another. Pharmacokinetics, pharmacodynamic response, and safety were studied for 12 hr. Results A total of 17 subjects were enrolled. All subjects completed IM dosing. One subject did not perform inhaled delivery due to a skin reaction from the IM dose. Pharmacokinetic results were as follows: area under the curve concentration, DPIA=20.1±5.8, AUTO=23.7±4.9 ng hr/mL (means±SD); maximum concentration reached, DPIA=7.7±3.5, AUTO=11.0±3.8 ng/mL; time to reach maximum concentration, DPIA=0.25±0.47, AUTO=0.19±0.23 hr. Pharmacodynamic results were as follows: maximum increase in heart rate, DPIA=18±12, AUTO=23±13 beats/min; average change in 1-sec forced expiratory volume at 30 min, DPIA=0.16±0.22 L, AUTO=0.11±0.29 L. The relative bioavailability for DPIA was 87% (based on output dose). Two subjects demonstrated allergic responses: one to the first dose (AUTO), which was mild and transient, and one to the second dose (DPIA), which was moderate in severity, required treatment with oral and intravenous (IV) diphenhydramine and IV steroids, and lasted more than 7 days. Conclusions Dry powder inhalation is a highly bioavailable route for attaining rapid and consistent systemic concentrations of atropine. PMID:22691110

  12. The influence of aerosol retention and pattern of deposition on bronchial responsiveness to atropine and methacholine in humans

    SciTech Connect

    Gillett, M.K.; Briggs, B.A.; Snashall, P.D. )

    1989-12-01

    We have examined the influence of total intrapulmonary deposition and its pattern on the bronchial response to aerosolized methacholine and atropine in 10 normal and 12 asthmatic subjects. On Day 1 we performed a dose-response challenge to methacholine and defined responsiveness as the provocative dose (PD35) needed to cause a 35% decrease in specific airway conductance (SGaw). On Day 2 we repeated methacholine challenge after premedication with aerosolized atropine, and we defined the response to atropine as dose ratio-1 (DR-1) where DR = PD35 after atropine/PD35 without atropine. On Day 3 we imaged intrapulmonary aerosol deposition by mixing 99mtechnetium with methacholine aerosol and scanning the thorax with a gamma camera during the development of bronchoconstriction. Total pulmonary aerosol deposition varied considerably between individuals (1.2 to 23.6% of nebulized dose) but there was no difference between normal and asthmatic subjects, and no correlation between deposition and baseline SGaw or PD35; there was a significant positive correlation between deposition and DR-1. Deposition of aerosol in central lung zones was inversely related to SGaw and correlated positively with DR-1; there was no significant relationship with PD35. Total intrapulmonary aerosol deposition and its pattern partially determine bronchial responsiveness to atropine, but we have not demonstrated any significant effect on responsiveness to methacholine.

  13. Accidental salinomycin intoxication in calves

    PubMed Central

    Omidi, Arash; Aslani, Mohammad R.; Movassaghi, Ahmad R.; Mohri, Mehrdad; Dadfar, Mohammad

    2010-01-01

    Twenty-four 10- to 16-week-old calves in a dairy herd in Birjand, Iran, inadvertently received an excessive dose of salinomycin mixed with barley grain. There was 58% mortality within 10 d. The calves had high serum AST, LDH, and CK activities; histopathologic lesions in myocardium, liver, and kidneys; and clinical signs associated with acute and congestive heart failure. PMID:21197208

  14. [Suicidal salicylate intoxications and unintentional percutaneous poisoning with salicylic ointment].

    PubMed

    Chodorowski, Zygmunt; Anand, Jacek Sein; Waldman, Wojciech

    2003-01-01

    Suicidal salicylate poisonings are presented in 49 patients, 33 women and 16 men, aged from 18 to 71 (mean 37) years. Mixed poisonings with multiple agents were four times more frequent, had more severe clinical course and demanded longer hospitalisation than acute intoxications with salicylates alone. Four patient were over 65 years old (8.2%). Difficult economic situation of geriatric population in Poland had no effect on frequency of suicidal attempts in the studied cohort. There were no fatalities in the studied group. There were two unintentional systemic poisonings due to topical administration of the 10% salicylic acid ointment for wide spread skin lesions (more than 80% of body surface) in two patients with exudative psoriasis. PMID:14569910

  15. [Safety problems of occupational activity during alcoholic intoxication].

    PubMed

    Ushakov, I B; Popov, V I

    1999-01-01

    It has been established that work efficiency of persons occupied by machine operating duties degrades markedly under the action of an acute alcoholic intoxication--less on real machines and more on simulators and when operating simple technical devices. Work efficiency degradation is manifested by the task execution time increase (to a lesser degree) and by erroneous action quantity increase after taking alcohol, i.e. by work reliability decease. Most heavily it is manifested during the first 0.7-1.5 hr. After taking alcohol. And direct work efficiency index is usually improved 12-16 hr. after taking alcohol. Increase of erroneous action quantity is caused probably by a series of physiological, psychophysiological and psychological changes in the condition of a man under the action of alcohol. Time of the day when the activity takes place after taking that dose of alcohol is practically non valid for changing work efficiency index. PMID:11965736

  16. Double, suicidal intoxication with hydroxycarbamide--a case report.

    PubMed

    Waldman, Wojciech; Kabata, Piotr; Sein Anand, Jacek

    2012-01-01

    Hydroxycarbamide (HCB), also known as hydroxyurea, is an urea derivative used mainly as antineoplastic and antisickling agent. We described a 31 yrs. female, with essential thrombocythemia, who was admitted to our clinic because of double suicidal ingestion of hydroxycarbamide. First time it was 7.5 g of HCB with coingestion of 50 mg of diazepam, and several glasses of wine, second time it was 10 g of HCB, with coingestion of 100 mg paroxetine and few glasses of vodka. Both suicidal attempts were triggered by multiple reactive factors. At the time of admissions the patient was conscious, restless, with decreased mood. Transient decrease of total leukocyte count was noted on fourth day of first overdose. The second overdose led to no significant changes in blood count. There were no other abnormalities in biochemical results. According to the best of our knowledge this is the first report of acute suicidal intoxication with hydroxy-carbamide in an adult. PMID:23243936

  17. [Suicidal intoxication with sodium azide--a case report].

    PubMed

    Wiergowski, Marek; Galer-Tatarowicz, Katarzyna; Krzyzanowski, Maciej; Jankowski, Zbigniew; Sein Anand, Jacek

    2012-01-01

    Sodium azide (NaN3) is an inorganic matrix compound with a very high toxicity. Mechanism of action is not clarified, and it is assumed to interfere with the processes of oxidative phosphorylation. The acute intoxications with sodium azide are extremely rare. We described a case of 19-year-old man who was found dead. In the course of prosecution the empty container, with label "NaN3, 20 g", was found near the body. There were traces of white powder detected in the container. Azide ions were determined by derivatization, i.e. they were transformed to pentafluorobenzaldehyde azide compound. Analysis of the final extract after derivatization was performed by gas chromatography coupled with mass spectrometry GC/MS. The largest concentration of azide ions were determined in the stomach content and vitreous humour, and much less one in whole blood, urine and kidney fluid. PMID:23243931

  18. Possible fatal acetaminophen intoxication with atypical clinical presentation.

    PubMed

    De-Giorgio, Fabio; Lodise, Maria; Chiarotti, Marcello; d'Aloja, Ernesto; Carbone, Arnaldo; Valerio, Luca

    2013-09-01

    Acetaminophen or paracetamol, a commonly used over-the-counter analgesic, is known to elicit severe adverse reactions when taken in overdose, chronically at therapeutic dosage or, sporadically, following single assumptions of a therapeutic dose. Damage patterns including liver damage and, rarely, acute tubular necrosis or a fixed drug exanthema. We present a case of fatal acetaminophen toxicity with postmortem blood concentration 78 μg/mL and unusual clinical features, including a visually striking and massive epidermolysis and rhabdomyolysis, disseminated intravascular coagulation and myocardial ischemia. This case is compared with the most similar previous reports in terms of organ damage, clinical presentation, and cause of death. We conclude that a number of severe patterns of adverse effects to acetaminophen are emerging that were previously greatly underestimated, thus questioning the adequacy of the clinical spectrum traditionally associated with acetaminophen intoxication and leading to the need to review this spectrum and the associated diagnostic criteria. PMID:23822653

  19. [Clinical cases of occupational chronic manganese intoxication].

    PubMed

    Konstantinova, T N; Lakhman, O L; Katamanova, E V; Kartapol'tseva, N V; Meshcheriagin, V A; Rusanova, D V; Andreeva, O K

    2009-01-01

    Classic symptoms of manganese intoxication are very rarely seen nowadays. Clinic in Angarsk Research Institute for Occupational medicine and Human ecology registered two cases of stage I and II chronic manganese intoxication over 10 years among electric welders. The cases were diagnosed with consideration of long length of exposure to manganese with the ambient air level exceeding the MAC 1.5 times, the disease manifestation at middle age, high manganese level in serum and urine, characteristic neurologic symptoms in association with organic psychopathologic defects and polyneuropathy of limbs. PMID:19278189

  20. Gangliosides, or sialic acid, antagonize ethanol intoxication

    SciTech Connect

    Klemm, W.R.; Boyles, R.; Matthew, J.; Cherian, L.

    1988-01-01

    Because ethanol elicits a dose-dependent hydrolysis of brain sialogangliosides, the authors tested the possibility that injected gangliosides might antagonize intoxicating doses of ethanol. Clear anti-intoxication effects were seen at 24 hr post-injection of mixed mouse-brain gangliosides at 125-130 mg/kg, but not at lower or higher doses. Sleep time was reduced on the order of 50%, and roto-rod agility was significantly enhanced. Sialic acid (SA) similarly antagonized ethanol; however, the precursor of SA, N-acetyl-D-mannosamine, as well as ceramide and asialoganglioside did not.

  1. Children with alcohol intoxication in Cracow, Poland.

    PubMed

    Kościelniak, Barbara; Tomasik, Przemysław J

    2016-01-01

    Alcoholism among minors is a serious social problem. The aim of the current study was to analyze alcohol intoxication in children based on hospitalizations in the University Children's Hospital in Cracow between the years 2007 and 2015. During these 9 years, 381 patients were hospitalized due to excessive alcohol consumption. Most patients were junior high school or high school students. The highest blood alcohol concentrations in hospitalized patients were found in a 16-year-old boy (BAC .41%) and a 15-year-old girl (BAC .37%). Alcohol consumption and severe intoxication are linked to a wide variety of familial, social, and personal problems. PMID:26745242

  2. 7 CFR 500.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2010 CFR

    2010-01-01

    ... 7 Agriculture 6 2010-01-01 2010-01-01 false Intoxicating beverages and narcotics. 500.7 Section... Intoxicating beverages and narcotics. (a) Entering USNA property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or a narcotic drug, is prohibited....

  3. 7 CFR 500.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2012 CFR

    2012-01-01

    ... 7 Agriculture 6 2012-01-01 2012-01-01 false Intoxicating beverages and narcotics. 500.7 Section... Intoxicating beverages and narcotics. (a) Entering USNA property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or a narcotic drug, is prohibited....

  4. 30 CFR 57.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 30 Mineral Resources 1 2013-07-01 2013-07-01 false Intoxicating beverages and narcotics. 57.20001... Miscellaneous § 57.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  5. 30 CFR 56.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 30 Mineral Resources 1 2011-07-01 2011-07-01 false Intoxicating beverages and narcotics. 56.20001... § 56.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  6. 30 CFR 56.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 30 Mineral Resources 1 2014-07-01 2014-07-01 false Intoxicating beverages and narcotics. 56.20001... § 56.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  7. 31 CFR 407.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 31 Money and Finance: Treasury 2 2014-07-01 2014-07-01 false Intoxicating beverages and narcotics... TREASURY ANNEX § 407.8 Intoxicating beverages and narcotics. Entering or being on the property, or operating a motor vehicle thereon, by a person under the influence of intoxicating beverages or...

  8. 7 CFR 501.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2013 CFR

    2013-01-01

    ... 7 Agriculture 6 2013-01-01 2013-01-01 false Intoxicating beverages and narcotics. 501.7 Section... § 501.7 Intoxicating beverages and narcotics. Entering Research Center property or the operating of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic...

  9. 7 CFR 501.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2012 CFR

    2012-01-01

    ... 7 Agriculture 6 2012-01-01 2012-01-01 false Intoxicating beverages and narcotics. 501.7 Section... § 501.7 Intoxicating beverages and narcotics. Entering Research Center property or the operating of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic...

  10. 7 CFR 502.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2011 CFR

    2011-01-01

    ... 7 Agriculture 6 2011-01-01 2011-01-01 false Intoxicating beverages and narcotics. 502.8 Section..., MARYLAND § 502.8 Intoxicating beverages and narcotics. Entering BARC property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic drug,...

  11. 7 CFR 500.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2011 CFR

    2011-01-01

    ... 7 Agriculture 6 2011-01-01 2011-01-01 false Intoxicating beverages and narcotics. 500.7 Section... Intoxicating beverages and narcotics. (a) Entering USNA property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or a narcotic drug, is prohibited....

  12. 7 CFR 500.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2013 CFR

    2013-01-01

    ... 7 Agriculture 6 2013-01-01 2013-01-01 false Intoxicating beverages and narcotics. 500.7 Section... Intoxicating beverages and narcotics. (a) Entering USNA property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or a narcotic drug, is prohibited....

  13. 7 CFR 501.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2010 CFR

    2010-01-01

    ... 7 Agriculture 6 2010-01-01 2010-01-01 false Intoxicating beverages and narcotics. 501.7 Section... § 501.7 Intoxicating beverages and narcotics. Entering Research Center property or the operating of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic...

  14. 31 CFR 407.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 31 Money and Finance:Treasury 2 2011-07-01 2011-07-01 false Intoxicating beverages and narcotics... TREASURY ANNEX § 407.8 Intoxicating beverages and narcotics. Entering or being on the property, or operating a motor vehicle thereon, by a person under the influence of intoxicating beverages or...

  15. 30 CFR 56.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 30 Mineral Resources 1 2010-07-01 2010-07-01 false Intoxicating beverages and narcotics. 56.20001... § 56.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  16. 7 CFR 501.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2011 CFR

    2011-01-01

    ... 7 Agriculture 6 2011-01-01 2011-01-01 false Intoxicating beverages and narcotics. 501.7 Section... § 501.7 Intoxicating beverages and narcotics. Entering Research Center property or the operating of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic...

  17. 30 CFR 56.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 30 Mineral Resources 1 2012-07-01 2012-07-01 false Intoxicating beverages and narcotics. 56.20001... § 56.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  18. 30 CFR 56.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 30 Mineral Resources 1 2013-07-01 2013-07-01 false Intoxicating beverages and narcotics. 56.20001... § 56.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  19. 7 CFR 501.7 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2014 CFR

    2014-01-01

    ... 7 Agriculture 6 2014-01-01 2014-01-01 false Intoxicating beverages and narcotics. 501.7 Section... § 501.7 Intoxicating beverages and narcotics. Entering Research Center property or the operating of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic...

  20. 7 CFR 502.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2013 CFR

    2013-01-01

    ... 7 Agriculture 6 2013-01-01 2013-01-01 false Intoxicating beverages and narcotics. 502.8 Section..., MARYLAND § 502.8 Intoxicating beverages and narcotics. Entering BARC property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic drug,...

  1. 30 CFR 57.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 30 Mineral Resources 1 2010-07-01 2010-07-01 false Intoxicating beverages and narcotics. 57.20001... Miscellaneous § 57.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  2. 30 CFR 57.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 30 Mineral Resources 1 2012-07-01 2012-07-01 false Intoxicating beverages and narcotics. 57.20001... Miscellaneous § 57.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  3. 30 CFR 57.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 30 Mineral Resources 1 2014-07-01 2014-07-01 false Intoxicating beverages and narcotics. 57.20001... Miscellaneous § 57.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  4. 31 CFR 407.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 31 Money and Finance:Treasury 2 2013-07-01 2013-07-01 false Intoxicating beverages and narcotics... TREASURY ANNEX § 407.8 Intoxicating beverages and narcotics. Entering or being on the property, or operating a motor vehicle thereon, by a person under the influence of intoxicating beverages or...

  5. 31 CFR 407.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 31 Money and Finance: Treasury 2 2010-07-01 2010-07-01 false Intoxicating beverages and narcotics... TREASURY ANNEX § 407.8 Intoxicating beverages and narcotics. Entering or being on the property, or operating a motor vehicle thereon, by a person under the influence of intoxicating beverages or...

  6. 31 CFR 407.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 31 Money and Finance:Treasury 2 2012-07-01 2012-07-01 false Intoxicating beverages and narcotics... TREASURY ANNEX § 407.8 Intoxicating beverages and narcotics. Entering or being on the property, or operating a motor vehicle thereon, by a person under the influence of intoxicating beverages or...

  7. 30 CFR 57.20001 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 30 Mineral Resources 1 2011-07-01 2011-07-01 false Intoxicating beverages and narcotics. 57.20001... Miscellaneous § 57.20001 Intoxicating beverages and narcotics. Intoxicating beverages and narcotics shall not be permitted or used in or around mines. Persons under the influence of alcohol or narcotics shall not...

  8. 7 CFR 502.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2014 CFR

    2014-01-01

    ... 7 Agriculture 6 2014-01-01 2014-01-01 false Intoxicating beverages and narcotics. 502.8 Section..., MARYLAND § 502.8 Intoxicating beverages and narcotics. Entering BARC property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic drug,...

  9. 7 CFR 502.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2012 CFR

    2012-01-01

    ... 7 Agriculture 6 2012-01-01 2012-01-01 false Intoxicating beverages and narcotics. 502.8 Section..., MARYLAND § 502.8 Intoxicating beverages and narcotics. Entering BARC property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic drug,...

  10. 7 CFR 502.8 - Intoxicating beverages and narcotics.

    Code of Federal Regulations, 2010 CFR

    2010-01-01

    ... 7 Agriculture 6 2010-01-01 2010-01-01 false Intoxicating beverages and narcotics. 502.8 Section..., MARYLAND § 502.8 Intoxicating beverages and narcotics. Entering BARC property or the operation of a motor vehicle thereon, by a person under the influence of intoxicating beverages or narcotic drug,...