Transient prolongation of ventricular action potential duration after metabolic inhibition.

Transient prolongation of the action potential duration was observed in canine ventricular muscle during the reoxygenation period following metabolic inhibition. We investigated the effects of verapamil, lanthanum (La3+), and hexamethyleneamiloride (HMA) on the recovery time course of the action potential and its rebound prolongation. The time course of the intracellular resistivity was estimated from the conduction velocity and electrograms. The action potentials of canine left ventricular trabeculae were recorded by the conventional microelectrode technique. After a control tracing was obtained, the preparation was perfused with a hypoxic, acidic solution for 20 min and then reoxygenated with regular Tyrode's solution. After reoxygenation, action potential prolongation exceeding the control value by 21.0 +/- 7.3% was observed depending on the degree of metabolic inhibition. Verapamil depressed the rebound prolongation when it was added before the start of metabolic inhibition, but not when added after reoxygenation was started. La3+ and HMA depressed the rebound phenomenon. Intracellular resistivity was increased during metabolic inhibition, but showed no significant changes during the period of action potential prolongation. It was concluded that the rebound action potential prolongation was related to the accumulation of intracellular Ca2+ during metabolic inhibition. Other ions, such as Na+ and H+ may also contribute to the phenomenon by modulating outward currents.