Prostaglandins have been shown to contribute to the pathogenesis, progression and exacerbation of ischemic heart disease. Prostaglandins have also reported to contribute to the arrhythmogenesis of lethal arrhythmias during ischemia and reperfusion. In this review article, The electrophysiologic effects of prostacyclin, its stable analogues, thromboxane A2 and its stable analogue were reviewed, and described the in vitro effects of a stable analogue of prostaglandin, and a stable analogue of thromboxane A2 in our laboratory. Finally, the electrophysiologic and metabolic effects of a thromboxane A2 synthetase inhibitor on the coronary artery occlusion/reperfusion model were studied in our laboratory. The prostacyclin analogue shortened the action potential duration in a normal Tyrode′s solution, and shifted the Vmax - resting membrane potential curve rightward. The TXA2 analogue did not exhibit any electrophysiologic effects on the normal, high K+, and simulated ischemia conditions. Intracoronary administration of the TXA2 analogue led to marked surface and epicardial ECG ST segment elevation and the subsequent development of ventricular tachycardia. The thromboxane A2 synthetase inhibitor elicited significant reduction of ventricular premature contractions and tended to reduce reperfusion-induced ventricular fibrillation. The rise in extracellular K+ concentration of the ischemic myocardium was markedly decreased in the thromboxane A2 synthetase inhibitortreated group. Therefore, prostacyclin may be antiarrhythmic through its direct electrophysiologic effects, i.e., recovery of Vmax leading to improvement of conduction delay during ischemia, and thromboxane A2 may be arrhythmogenic not through its direct electrophysiologic effects on the ischemic myocardium, but through exacerbation of ischemia due to its potent vaso-constrictive effects.
