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.

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.

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 acidic- and glucose-free-MPSS. 'Maximum velocity of phase 0 depolarization' (dV/dt(max)) and 'time for 90% repolarization' (APD90) significantly decreased during hypoxic- and mixed-MPSS superfusion, and hyperkalemic-MPSS also decreased the dV/dt(max) and APD90. However, no significant changes in dV/dt(max) and APD90 were observed by acidic- and glucose-free-MPSS. The decreasing effects of dV/dt(max) and APD90 by the MPSSes were attenuated when the MPSSes were replaced with normal Tyrode's solution. DPCPX (2x10(-6)M), a purinergic antagonist, inhibited the decreasing effects of APD90 at 5, 10, and 20 min superfusion of the mixed-MPSS, and glibenclamide (10(-6)M), a K(ATP) channel blocker, inhibited those at 10 and 20 min superfusion of the mixed-MPSS. Diclofenac (10(-6)M), a cyclooxygenase inhibitor inhibited only those at 20 min superfusion of the mixed-MPSS.

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 K(ATP) channel and prostanoids.