Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although many cases of beta-adrenoceptor antagonist (beta-blocker) poisoning are uneventful, a proportion develop serious and sometimes fatal cardiovascular system depression with severe hypotension. As beta-adrenergic tone is not essential for cardiovascular function in health, there is no physiological reason why total beta-adrenoceptor blockade should have serious consequences in the resting individual. The toxic actions of beta-blockers appear to be related to properties such as membrane depressant activity and possibly due to actions on beta-adrenoceptors distinct from those in the cardiovascular system. Most reports of serious adverse effects following overdosage concern beta-blockers with significant membrane depressant activity, and in particular propranolol and oxprenolol, with which progressive heart block and bradycardia are features. Sotalol toxicity, with its unique electrophysiological action, is a special case. Animal experiments confirm that beta-blockers with membrane depressant activity are more toxic than the newer more selective ones, such as atenolol and nadolol. However, experimental models also reveal that artificial ventilation markedly reduces the toxicity of all beta-blockers tested, suggesting a respiratory depressant action with very high doses. Treatment of serious overdosage in man should include maintenance of adequate ventilation. High dose intravenous glucagon is recommended, because its inotropic action depends on direct stimulation of adenylate cyclase. beta-Agonists such as isoprenaline (isoproterenol) or prenalterol may be effective, but the nature of agonist-competitive antagonist interactions may necessitate the use of unrealistically large doses to overcome very high tissue beta-blocker concentrations.
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PMID:The management of acute poisoning due to beta-adrenoceptor antagonists. 256 23

The effect of glucagon in arrhythmias induced by coronary artery occlusion and ouabain was studied in dogs. Intravenous administration of glucagon (50 microgram/kg) to 6 dogs with more than 70% ectopic activity after coronary artery occlusion, resulted in significant (P less than 0.01) decrease in ectopics and increase in heart rate. Infusion of glucagon (2.5 microgram/kg/min) for 30 min caused complete elimination of ectopic activity during infusion period. In another series of 7 experiments, glucagon failed to abolish the ouabain-induced ectopic beats. In fact the hormone itself caused a significant (P less tha 0.01) increase in ectopic activity and heart rate. However, in 7 dogs with complete heart block produced after ouabain conversion to normal sinus rhythm was observed after glucagon.
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PMID:Effect of glucagon on arrhythmias induced by coronary artery occlusion and ouabain in dogs. 721 88