[The electrophysiologic effect of atenolol and nitrendipine on normal and ischemic rabbit myocardium in situ. I. Effects on transmembrane potential].
Transmembrane potential recording technique was achieved by using microelectrode with multiple impalement. The results showed that atenolol, both in normal and ischemic ventricular cells, produced significant lengthening of APD, but no apparent effects on APA, RS, OS and dv/dt max. Nitrendipine exerted no significant influences on all the parameters in normal and ischemic cells. Thus, it is suggested that beta-receptor blocker, atenolol possessed the characteristics of class III antiarrhythmic drug action on normal and ischemic rabbit heart in situ. This in situ action may provide some explanations for the mechanisms through which beta-blockers afford their beneficial effects of reducing the incidence of sudden death in postmyocardial infarction patients. Another interesting finding was that different parts of the repolarization phase of action potentials responded differently to interfering factors. According to the results obtained by analysing various parts of repolarization, we proposed three new parameters, APD0-50 (action potential duration from 0 to 50% of repolarization), APD50-100 (action potential duration from 50 to 100% of repolarization) and RI (repolarization index), to describe the different changes in various parts of repolarization. Discussion of the significance of these three is presented.
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D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D009568:Nitrendipine / Q000494:pharmacology / Q000627:therapeutic use*; D011817:Rabbits
D001262:Atenolol; D009568:Nitrendipine