Hale S L, Dave R H, Kloner R A
Heart Institute, Good Samaritan Hospital, Los Angeles, California 90017, USA.
Basic Res Cardiol. 1997 Oct;92(5):351-7. doi: 10.1007/BF00788947.
Previously, we observed that reducing myocardial temperature in the risk region before coronary artery occlusion caused a profound reduction in infarct size. It is unknown whether lowering myocardial temperature after ischemia has already begun, or just before reperfusion, is also effective in reducing infarct size. This study tests the hypothesis that reducing myocardial temperature locally, after coronary occlusion, reduces infarct size.
Anesthetized rabbits received 30 min of coronary artery occlusion and three hours of reperfusion. Myocardial temperature in the risk zone was monitored. Rabbits were randomly assigned to one of three groups: group 1, topical myocardial cooling starting 10 min after coronary occlusion (n = 11); group 2, cooling starting 25 min after coronary occlusion (n = 11); or group 3, control, no intervention (n = 10).
Hemodynamic parameters and regional myocardial blood flow were equivalent in all groups. Risk zone temperature was similar in all groups at occlusion. The cooling maneuver produced a rapid reduction in temperature in the risk region. In group 1, myocardial temperature was reduced an average of 6.3 degrees C between 10 and 15 min of coronary artery occlusion; myocardial temperature in group 2 was reduced an average of 5.9 degrees C between 25 and 30 min of coronary artery occlusion. Cooling was maintained until 15 min of reperfusion. Myocardial temperature in group 3 remained within 0.3 degree C of baseline during coronary artery occlusion and into reperfusion. Core temperature was similar in all groups. Although the ischemic risk region was comparable in all groups, early cooling (group 1) resulted in a significant reduction in infarct size, expressed as a fraction of the risk region, compared with the control group (0.23 +/- 0.04 vs. 0.44 +/- 0.04 of the risk region); however, cooling just before reperfusion (group 2) failed to modify infarct size compared with the controls (0.43 +/- 0.04 and 0.44 +/- 0.04 of the risk region, respectively).
These results support our hypothesis that reducing myocardial temperature reduces infarct size. However, it is important the reduction in temperature be produced as early as possible following coronary artery occlusion.
此前，我们观察到在冠状动脉闭塞前降低危险区域的心肌温度可使梗死面积显著减小。目前尚不清楚在缺血已经开始后或再灌注前降低心肌温度是否也能有效减小梗死面积。本研究检验冠状动脉闭塞后局部降低心肌温度可减小梗死面积这一假设。
将麻醉的兔子冠状动脉闭塞30分钟，再灌注3小时。监测危险区域的心肌温度。兔子被随机分为三组之一：第1组，冠状动脉闭塞10分钟后开始局部心肌降温（n = 11）；第2组，冠状动脉闭塞25分钟后开始降温（n = 11）；或第3组，对照组，不进行干预（n = 10）。
所有组的血流动力学参数和局部心肌血流量相当。闭塞时所有组的危险区域温度相似。降温操作使危险区域温度迅速降低。在第1组中，冠状动脉闭塞10至15分钟期间心肌温度平均降低6.3℃；在第2组中，冠状动脉闭塞25至30分钟期间心肌温度平均降低5.9℃。降温持续至再灌注15分钟。第3组在冠状动脉闭塞期间及进入再灌注时心肌温度保持在基线的0.3℃以内。所有组的核心温度相似。尽管所有组的缺血危险区域相当，但与对照组相比，早期降温（第1组）导致梗死面积显著减小，以危险区域的比例表示（危险区域的0.23±0.04对0.44±0.04）；然而，再灌注前降温（第2组）与对照组相比未能改变梗死面积（分别为危险区域的0.43±0.04和0.44±0.04）。
这些结果支持我们的假设，即降低心肌温度可减小梗死面积。然而，重要的是在冠状动脉闭塞后尽早降低温度。
