The reactivatibility of cholinesterase inhibited by VX and sarin in man.
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Biomedical subjects
Publications and source records attributed to F R Sidell.
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1. The ED50 of acetyl strophanthidin for producing ventricular arrhythmias in normal dogs was 54.5 mug/kg intravenously.2. Doses up to and including those which caused ventricular tachycardia did not produce either atrial arrhythmias or significant aberration of A-V conduction.3. Although the classic digitalis-induced rate and e.c.g. waveform changes may appear after administration of acetyl strophanthidin, their presence or absence have no value in predicting the subsequent development of ventricular arrhythmias.
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Nerve agents, highly toxic organophosphorus cholinesterase inhibitors, inhibit acetylcholinesterase and cause an accumulation of acetylcholine. Clinical effects depend on the route and amount of exposure and include miosis, bronchoconstriction, excessive secretions, vomiting, seizures, and cessation of respiratory and cardiac activity. Eye effects include miosis, engorgement of ocular vessels, pain, and decrease in light sensitivity. Therapy consists of atropine, a cholinesterase reactivator (pralidoxime), and ventilation as needed.