Ghadhanfar Elham A, Juggi Jasbir S
Department of Physiology, Faculty of Medicine, Kuwait University, Kuwait.
Exp Clin Cardiol. 2007 Spring;12(1):11-6.
Myocardial ischemic preconditioning (PC) is a protective intervention that aims to reduce the deleterious effects of ischemia-reperfusion injury.
: To assess the comparative efficacy of ischemic PC induced at hypothermic, normothermic and hyperthermic temperatures on the postischemic recovery of left ventricular contractile and coronary vascular functions in the aortic perfused rat heart model.
An isolated aorta-perfused (Langendorff) rat heart model was used. Hearts were studied in eight different groups (n=5 each). Unprotected ischemia for 60 min served as control. For the remaining seven groups, ischemia was preceded by PC at 10 degrees C, 20 degrees C, 30 degrees C, 34 degrees C, 37 degrees C, 40 degrees C and 42 degrees C achieved by two episodes of 5 min ischemia at the designated PC temperature and 10 min of reperfusion, respectively. The postischemic recovery in contractile (maximum developed pressure and left ventricular end-diastolic pressure) and coronary vascular functions (coronary flow and coronary vascular resistance) was assessed at the end of 30 min reperfusion.
Hyperthermic PC provided optimal preservation and resulted in a 25% increase in the myocardial and 15% increase in the coronary vascular tolerance to ischemia. Normothermic PC resulted in a 21% increase in myocardial and 14% increase in coronary vascular tolerance to ischemia. Hypothermic PC was comparatively less effective and resulted in 11% increase in myocardial and 15% increase in the coronary vascular tolerance to ischemia. The temperature-dependence of PC may be summarized as: PC-42 degrees C > PC-40 degrees C > PC-37 degrees C > PC-34 degrees C > PC-30 degrees C > PC-20 degrees C > PC-10 degrees C.
The results of the present study indicate that the extent of reversibility of the ischemic damage depends on the PC temperature and that optimal preservation occurred at the ideal PC temperature between 40 degrees C and 42 degrees C.
心肌缺血预处理（PC）是一种旨在减轻缺血再灌注损伤有害影响的保护性干预措施。
评估在低温、常温及高温下诱导的缺血预处理对主动脉灌注大鼠心脏模型缺血后左心室收缩功能和冠状血管功能恢复的比较效果。
采用离体主动脉灌注（Langendorff）大鼠心脏模型。将心脏分为八个不同组（每组n = 5）。以60分钟的无保护缺血作为对照。对于其余七组，在指定的PC温度下通过两次5分钟缺血及10分钟再灌注实现PC，PC温度分别为10℃、20℃、30℃、34℃、37℃、40℃和42℃。在再灌注30分钟结束时评估缺血后收缩功能（最大收缩压和左心室舒张末期压力）和冠状血管功能（冠脉流量和冠状血管阻力）的恢复情况。
高温预处理提供了最佳的保护，使心肌对缺血的耐受性提高25%，冠状血管对缺血的耐受性提高15%。常温预处理使心肌对缺血的耐受性提高21%，冠状血管对缺血的耐受性提高14%。低温预处理效果相对较差，使心肌对缺血的耐受性提高11%，冠状血管对缺血的耐受性提高15%。预处理的温度依赖性可总结为：PC-42℃>PC-40℃>PC-37℃>PC-34℃>PC-30℃>PC-20℃>PC-10℃。
本研究结果表明，缺血损伤的可逆程度取决于预处理温度，且在40℃至42℃的理想预处理温度下可实现最佳保护。
