Effects of Ca++-antagonists on the conduction delay observed in the ischemic myocardium were studied in open-chest anesthetized dogs. Complete occlusion of the left anterior descending coronary artery (LAD) for 5 or 10 min under a constant atrial pacing produced conduction delay in the ischemic zone. Lidocaine which was administered prior to the LD occlusion increased the conduction delay, whereas Ca++-antagonists, verapamil and diltiazem, reduced the ischemia-induced conduction delay. To determine whether the coronary vasodilating action of these Ca++-antagonists can play a role in reducing the ischemia-induced conduction delay by means of increasing the collateral blood flow, the effects of these Ca++-antagonists were compared with those of other coronary vasodilating drugs on the coronary circulation and the ischemia-induced conduction delay. Administration of verapamil, diltiazem, nifedipine, nitroglycerin+phenylephrine and dipyridamole increased both the blood flow of the left circumflex coronary artery and the regional myocardial blood flow at LAD area, whereas nitroglycerin alone decreased and isosorbide dinitrate hardly affected them. Nevertheless, only drugs possessing a slow channel blocking action, i.e. verapamil, diltiazem and a large dose of nifedipine, improved the conduction delay. Effects of verapamil on the conduction delay and potassium efflux induced by global myocardial ischemia were evaluated in isolated Langendorff-perfused rabbit hearts. Perfusion with a modified Tyrode solution containing 10-1000 ng/ml of verapamil prior to 7 min of global ischemia significantly prevented the intramyocardial conduction delay. However, the potassium efflux into the coronary effluents during ischemia and 1 min after reperfusion was not significantly reduced by verapamil. These results indicate that the favorable effect of Ca++-antagonists on the ischemia-induced conduction delay is not associated with the improvement of coronary circulation or the reduction of potassium efflux from the ischemic myocardium.