[Pathogenesis of arrhythmias in acute myocardial infarction].
Over the last few years, much experimental work has been done to try and elucidate the pathogenesis of disorders of rhythm in myocardial infarction. The role of bradycardia during the first few hours has been discussed, and the use of atropine has been criticised. Some light has been thrown on the importance of the Purkinje network in the infarcted zone. Some new concepts have been applied to the disturbances in exchange across membranes. The authors present the results of a series of experiments on the action of lactate and that of acidosis. The latter is responsible for upturns in the descending phase of the action potential these can cause re-excitation, and give rise to responses containing 2, 3 and even more propagated action potentials.
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000138:Acidosis / Q000503:physiopathology; D000200:Action Potentials / Q000187:drug effects; D000208:Acute Disease; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D001285:Atropine / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D004285:Dogs; D006801:Humans; D007773:Lactates / Q000494:pharmacology; D009203:Myocardial Infarction / Q000150:complications* / Q000503:physiopathology; D011690:Purkinje Fibers / Q000503:physiopathology; D014628:Vagotomy; D014630:Vagus Nerve / Q000503:physiopathology
D007773:Lactates; D001285:Atropine
Pathogénie des troubles du rythme de l'infarctus aigu du myocarde