Recovery of the conduction system from ischemic arrest and cardioplegia in perfused rat heart.

Normothermic ischemic arrest of the perfused rat heart for 1 h was followed by severe reperfusion arrhythmias, depressed excitability, atrioventricular (AV) node and sinoatrial (SA) node conduction blocks and by marked impairment of contractility. Excitability and conduction recovered within 10 to 15 mins whereas contractility remained greatly depressed. This finding is in agreement with a theoretically based assumption of lesser sensitivity of conduction system to ischemia compared to the working myocardium. When the hearts were exposed to ischemia at 20 degrees C, the sinus rhythm recovered instantaneously upon reperfusion; excitability and SA node conduction times were not significantly different from control; and contractility was much less depressed than after 34 degrees C ischemia. However, AV node conduction times did not normalize even after 15 mins of reperfusion. Potassium cardioplegia (34 degrees C) did not prevent post ischemic arrhythmias but evidently protected both SA node and AV node conduction. Optimum recovery of the conduction system and contractility was achieved by hypothermic (20 degrees C) potassium cardioplegia. Other cardioplegic additives did not further improve the hypothermic potassium protection of the conduction system.