Valen G, Takeshima S, Vaage J
Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden.
Ann Thorac Surg. 1996 Nov;62(5):1397-403. doi: 10.1016/0003-4975(96)00499-7.
Ischemic preconditioning reduces infarct size and cardiac dysfunction during reperfusion. Preconditioning may offer myocardial protection in open heart operations.
The effect of preconditioning before ischemia and cardioplegia was investigated in Langendorff-perfused rat hearts in the following groups. First, group 1 received two episodes of 3-minute ischemia and 5-minute reperfusion before 25 minutes of global (37 degrees C) ischemia and 60 minutes of reperfusion. Group 2 served as ischemic controls to group 1. Groups 3, 5, and 7 were preconditioned as described, before 3.5, 4, or 5 hours of cold (6 degrees to 8 degrees C) St. Thomas' II cardioplegia and 1 hour of reperfusion (37 degrees C). Groups 4, 6, and 8 were cardioplegic controls to groups 3, 5, and 7 (n = 17 in groups 1 and 2, and n = 10 in groups 3 to 8).
Preconditioning before warm ischemia attenuated the ischemia-induced increase of left ventricular end-diastolic pressure (3 +/- 1 versus 17 +/- 4 mm Hg; p < 0.01) (mean +/- standard error of the mean), the reduction of coronary flow (14 +/- 1 versus 9 +/- 0.5 mL/min; p < 0.001) and heart rate (252 +/- 19 versus 198 +/- 18 beats/min; p < 0.04), and the incidence of ventricular fibrillation (2 of 17 versus 10 of 17 hearts; p < 0.04) at the start of reperfusion. However, preconditioning did not influence postischemic cardiac function or the release of lactate dehydrogenase in any of the cardioplegia groups.
Ischemic preconditioning improved post-ischemic cardiac function after warm global ischemia, but did not protect cold cardioplegic hearts, perhaps because of the time span used.
缺血预处理可减少再灌注期间的梗死面积和心脏功能障碍。预处理可能为心脏直视手术提供心肌保护。
在以下几组Langendorff灌注大鼠心脏中研究缺血和心脏停搏前预处理的效果。首先，第1组在25分钟全心缺血（37℃）和60分钟再灌注前接受两次3分钟缺血和5分钟再灌注。第2组作为第1组的缺血对照组。第3、5和7组在3.5、4或5小时冷（6℃至8℃）St. Thomas' II心脏停搏液灌注和1小时再灌注（37℃）前按上述方法进行预处理。第4、6和8组作为第3、5和7组的心脏停搏对照组（第1和2组每组n = 17，第3至8组每组n = 10）。
温缺血前预处理减轻了缺血诱导的左心室舒张末期压力升高（3±1对17±4 mmHg；p < 0.01）（均值±均值标准误）、冠状动脉血流减少（14±1对9±0.5 mL/min；p < 0.001）和心率降低（252±19对198±18次/分钟；p < 0.04），以及再灌注开始时室颤的发生率（17颗心脏中2颗对17颗心脏中10颗；p < 0.04）。然而，预处理对任何心脏停搏组的缺血后心脏功能或乳酸脱氢酶释放均无影响。
缺血预处理改善了全心温缺血后的缺血后心脏功能，但未保护冷心脏停搏的心脏，可能是由于所用的时间跨度。
