Influence of Ischemic-Simulation on the Action Potential Characteristics in Rat Atrial Fibers

Background:To investigate the mechanisms of myocardial ischemia induced changes of electrophysiological properties, influences of various ischemic-simulated Tyrode’s solutions on the changes of action potential characteristics were examined. Method:Action potential characteristics were measured during superfusion with various ischemic-simulated solutions (modified physiologic salt solution;MPSS) by the method of conventional microelectrode technique in rat atrial fibers. Results:Hypoxic-, hyperkalemic-, and mixed-MPSS decreased ‘maximum diastolic potential’(MDP) and ‘action potential amplitude’ (APA), however, no significant changes of MDP and APA were observed by acidicand glucose-free-MPSS.‘Maximum velocity of phase 0 depolarization’(dV/dtmax) and ‘time for 90% repolarization’ (APD90) significantly decreased during hypoxicand mixedMPSS superfusion, and hyperkalemic-MPSS also decreased the dV/dtmax and APD90. However, no significant changes in dV/dtmax and APD90 were observed by acidicand glucose-free-MPSS. The decreasing effects of dV/ dt max and APD 90 by the MPSSes were attenuated when the MPSSes were replaced with normal Tyrode’s solution. DPCPX (2×10 M), a purinergic antagonist, inhibited the decreasing effects of APD90 at 5, 10, and 20 min superfusion of the mixed-MPSS, and glibenclamide (10 M), a KATP channel blocker, inhibited those at 10 and 20 min superfusion of the mixed-MPSS. Diclofenac (10 M), a cyclooxygenase inhibitor inhibited only those at 20 min superfusion of the mixed-MPSS. Conclusion:The primary factors for changing the electrophysiological characteristics during ischemic insults could be hypoxia and high-extracellular K, and the mechanisms of the electrophysiological changes are inferred that adenosine through purinoceptors is involved initially, and followed by KATP channel and prostanoids. (Korean Circulation J 1999;29(11):1225-1233)