Cyclic adenosine monophosphate, ventricular fibrillation, and antiarrhythmic drugs.
It is proposed that the development of ventricular fibrillation in the context of ischaemic heart-disease and myocardial infarction can be related to accumulation of cyclic adenosine 3',5' monophosphate (A.M.P.) in the ischaemic zone. The known electrophysiological and metabolic actions of cyclic A.M.P. are consonant with the hypothesis, which also provides a framework for the better understanding of the action of antiarrhythmic drugs.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002118:Calcium / Q000378:metabolism; D003327:Coronary Disease / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D000242:Cyclic AMP / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D000882:Haplorhini; D008012:Lidocaine / Q000627:therapeutic use; D050356:Lipid Metabolism; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000517:prevention & control
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D006003:Glycogen; D008012:Lidocaine; D000242:Cyclic AMP; D011188:Potassium; D002118:Calcium