Jabr R I, Braveny P, Juggi J S
Department of Physiology, Faculty of Medicine, Kuwait University, Safat, Arabian Gulf.
Can J Cardiol. 1988 Mar;4(2):90-6.
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.
灌注大鼠心脏常温缺血停搏1小时后，出现严重的再灌注心律失常、兴奋性降低、房室（AV）结和窦房（SA）结传导阻滞以及明显的收缩力受损。兴奋性和传导在10至15分钟内恢复，而收缩力仍严重降低。这一发现与基于理论的假设一致，即与工作心肌相比，传导系统对缺血的敏感性较低。当心脏在20℃下暴露于缺血时，再灌注后窦性心律立即恢复；兴奋性和SA结传导时间与对照组无显著差异；收缩力的降低程度远低于34℃缺血后。然而，即使再灌注15分钟后，AV结传导时间仍未恢复正常。钾停搏（34℃）不能预防缺血后心律失常，但明显保护了SA结和AV结传导。低温（20℃）钾停搏可实现传导系统和收缩力的最佳恢复。其他停搏添加剂并未进一步改善低温钾对传导系统的保护作用。
