Dote K, Wolff R A, Van Winkle D M
Department of Anesthesiology, Ehime University, Japan.
J Thorac Cardiovasc Surg. 1998 Aug;116(2):319-26. doi: 10.1016/s0022-5223(98)70133-3.
Both hypothermia and ischemic preconditioning are known to provide tolerance to myocardial ischemia and reperfusion. The aim of this study was to determine whether hypothermia during the ischemic preconditioning period attenuates the protective effect of ischemic preconditioning.
Experiments were performed in buffer-perfused isolated rabbit hearts. All hearts underwent 45 minutes of regional ischemia, followed by 2 hours of reperfusion. Ischemic preconditioning was elicited by either one or four periods of 5 minutes of regional ischemia. Hypothermia (25 degrees C) was induced beginning either 20 or 50 minutes before the 45-minute period of regional ischemia; normothermia (38 degrees C) was restored 10 minutes before the 45-minute period of regional ischemia. Except for the hypothermic periods noted, hearts were maintained at 38 degrees C.
Normothermic ischemic preconditioning with either one or four cycles of 5 minutes of coronary occlusion resulted in a profound reduction of infarct size (58% reduction with one cycle, p < 0.05; 95% reduction with four cycles, p < 0.01). Hypothermic ischemic preconditioning with one cycle of 5-minute coronary occlusion resulted in no reduction of infarct size but hypothermic ischemic preconditioning with four cycles of 5-minute coronary occlusions resulted in a 94% reduction of infarct size (p < 0.01). Myocardial glycogen and lactate levels were maintained near control levels during hypothermic ischemia.
From these data we conclude that hypothermia during the preconditioning period increases the threshold for eliciting the infarct limitation of ischemic preconditioning.
已知低温和缺血预处理均可使心肌对缺血及再灌注产生耐受性。本研究旨在确定缺血预处理期间的低温是否会减弱缺血预处理的保护作用。
实验在缓冲液灌注的离体兔心脏上进行。所有心脏均经历45分钟的局部缺血，随后进行2小时的再灌注。通过1个或4个周期的5分钟局部缺血来引发缺血预处理。在45分钟局部缺血期开始前20分钟或50分钟开始诱导低温（25℃）；在45分钟局部缺血期开始前10分钟恢复正常体温（38℃）。除了记录的低温期外，心脏均维持在38℃。
正常体温下，1个或4个周期的5分钟冠状动脉闭塞进行缺血预处理，均可使梗死面积显著减小（1个周期时减小58%，p<0.05；4个周期时减小95%，p<0.01）。1个周期的5分钟冠状动脉闭塞进行低温缺血预处理，梗死面积未减小，但4个周期的5分钟冠状动脉闭塞进行低温缺血预处理，梗死面积减小了94%（p<0.01）。在低温缺血期间，心肌糖原和乳酸水平维持在接近对照水平。
从这些数据我们得出结论，预处理期间的低温提高了引发缺血预处理梗死限制作用的阈值。
