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[Organophosphate poisoning and myocardial necrosis].
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A man (46 years-old) was admitted to the intensive care unit (ICU) with a history that eight hours before he had voluntarily drank 100 ml of malathion. He complained of a burning pain on the anterior thorax and was confused. His cardiovascular evaluation was normal and his breathing was heavy with
Tumor necrosis factor-alpha induces a biphasic effect on myocardial contractility in conscious dogs.
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Tumor necrosis factor-alpha (TNF-alpha) likely plays a role in the pathophysiology of myocardial depression observed in septic shock. To evaluate the hemodynamic effects of TNF-alpha in vivo while eliminating the influence of altered sympathetic tone, eight conscious chronically instrumented dogs
Effects of phenytoin, ketamine, and atropine methyl nitrate in preventing neuromuscular toxicity of acetylcholinesterase inhibitors soman and diisopropylphosphorofluoridate.
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Toxic manifestations of acetylcholinesterase inhibitors (AChE-I) include muscle twitching and muscle fiber necrosis, in addition to muscarinic manifestations of acetylcholine excess. The AChE-Is pinacolyl methylphosphonofluoridate (soman) or diisopropylphosphorofluoridate (DFP) were administered to
Efficacy of an adenosine A1 receptor agonist compared with atropine and pralidoxime in a rat model of organophosphate poisoning.
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The objective of this study was to evaluate the effects of an adenosine A1 agonist, phenylisopropyl adenosine (PIA), on metamidophos poisoning compared to specific antidotes. Rats were poisoned with metamidophos (30 mg/kg, oral) and observed for 24 hours. One group received sodium chloride (1 mL/kg)
Comparison between dobutamine echocardiography and thallium-201 scintigraphy in detecting residual stenosis, ischemia, and necrosis in patients with prior myocardial infarction.
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BACKGROUND
Following the first attempts to detect myocardial ischemia with two-dimensional echocardiography stress testing, pharmacologic stress using dobutamine infusion has become an alternative to echocardiography exercise testing for evaluation of coronary artery disease. It has been shown that
Histopathologic effects of the single intramuscular injection of ketamine, atropine and midazolam in a rat model.
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Ketamine and atropine are often combined in a single syringe for im injection for pediatric conscious sedation; however, the effort of adding midazolam to this combination has not been studied. We investigated the single im injection of ketamine, atropine and midazolam (KAM) to determine if it
[Postischemic dysfunction and persistent ischemia in the early postinfarction period. Evaluation by echo-dobutamine-atropine test].
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OBJECTIVE
To study post-ischemic dysfunction and persistent ischemia in early post-infarction, by means of Echo-dobutamine-Atropine stress test (ECHO-DOB). Methods. We studied 138 patients (pts) aged < or = 75 yrs (mean 59.2 +/- 9.8) at their first uncomplicated myocardial infarction (AMI), treated
Efficacy of antidotes (midazolam, atropine and HI-6) on nerve agent induced molecular and neuropathological changes.
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BACKGROUND
Recent alleged attacks with nerve agent sarin on civilians in Syria indicate their potential threat to both civilian and military population. Acute nerve agent exposure can cause rapid death or leads to multiple and long term neurological effects. The biochemical changes that occur
Pesticide induced muscle necrosis: mechanisms and prevention.
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The nerve agent soman, as well as other organophosphates such as paraoxon and phospholine in concentrations that caused cholinergic symptoms induced a progressive dose-related necrosis in rat skeletal muscle fibers. The severity of the myopathy depended on a critical decrease in activity and
Prevention of phospholine-induced myopathy with d-tubocurarine, atropine sulfate, diazepam, and creatine phosphate.
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Acute administration of phospholine [diethyl-S-(2-dimethyl aminoethyl)phosphorothioate] at 0.2 mg/kg sc produces a myopathy characterized by initial focal changes in the subsynaptic area of the skeletal muscle. The onset of the myopathy is associated with fasciculations of high frequency. Agents
Acrylonitrile-induced gastric mucosal necrosis: role of gastric glutathione.
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Acrylonitrile [vinyl cyanide (VCN)] induces acute hemorrhagic focal superficial gastric mucosal necrosis or gastric erosions. In this report the authors have studied the mechanism of the VCN-induced gastric erosions. VCN-induced gastric lesions are coupled with a marked decrease of gastric reduced
Acetylcholine inhibits tumor necrosis factor α activated endoplasmic reticulum apoptotic pathway via EGFR-PI3K signaling in cardiomyocytes.
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Previous findings have shown that acetylcholine (ACh) decreased hypoxia-induced tumor necrosis factor alpha (TNF α) production, thus protected against cardiomyocyte injury. However, whether and how ACh affects TNF α-induced endoplasmic reticulum (ER) stress and cell apoptosis remain poorly defined.
Isoflurane attenuates pulmonary interleukin-1beta and systemic tumor necrosis factor-alpha following mechanical ventilation in healthy mice.
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BACKGROUND
Mechanical ventilation (MV) induces an inflammatory response in healthy lungs. The resulting pro-inflammatory state is a risk factor for ventilator-induced lung injury and peripheral organ dysfunction. Isoflurane is known to have protective immunological effects on different organ
MRI findings in 6 cases of children by inadvertent ingestion of diphenoxylate-atropine.
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OBJECTIVE
Compound diphenoxylate (diphenoxylate-atropine) poisoning can cause toxic encephalopathy in children, and magnetic resonance imaging (MRI) of the brain in this condition has not been reported. This study is to analyze brain MRI findings and to investigate the relations between MRI features
Acetylcholine inhibits hypoxia-induced tumor necrosis factor-α production via regulation of MAPKs phosphorylation in cardiomyocytes.
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Recent findings have reported that up-regulation of tumor necrosis factor-alpha (TNF-α) induced by myocardial hypoxia aggravates cardiomyocyte injury. Acetylcholine (ACh), the principle vagal neurotransmitter, protects cardiomyocytes against hypoxia by inhibiting apoptosis. However, it is still
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