Cason B A, Gamperl A K, Slocum R E, Hickey R F
University of California, San Francisco, Department of Anesthesia, Veterans Affairs Medical Center, 94121, USA.
Anesthesiology. 1997 Nov;87(5):1182-90. doi: 10.1097/00000542-199711000-00023.
Experimental evidence suggests that ATP-sensitive potassium channels are involved in myocardial ischemic preconditioning. Because some pharmacologic effects of isoflurane are mediated by K(ATP) channels, the authors tested the hypothesis: Isoflurane administration, before myocardial ischemia, can induce or mimic myocardial preconditioning.
Myocardial infarct size was measured in three groups of propofol-anesthetized rabbits, each subjected to 30 min of anterolateral coronary occlusion followed by 3 h of reperfusion. Groups differed in their pretreatment: Group 1 (control, N = 13) no pretreatment, Group 2 (ischemic preconditioning, N = 8), 5 min of coronary occlusion and 15 min of reperfusion; Group 3 (isoflurane pretreatment; N = 15), 15 min of isoflurane (1.1% end-tidal) and 15 min of washout. Hemodynamics were monitored serially. Myocardial infarct size and the area at risk were defined using triphenyltetrazolium chloride staining and fluorescent microspheres, respectively, and both were measured using computerized planimetry.
Infarct size expressed as a percentage of area at risk was 23.4 +/- 8.5% (mean +/- SD) in the isoflurane group compared with 33.1 +/- 13.3% in controls, and 8.7 +/- 6.2% in the ischemia-preconditioned group. Analysis for coincidental regressions, followed by tests for equality of slope and elevation, showed that the linear relationship between infarct size and area at risk was significantly (P < 0.05) different in all three groups because of differences in line elevation. Minor differences in hemodynamic variables were found between groups, which were unlikely to account for the significant differences in infarct size.
Preadministration of isoflurane, before myocardial ischemia, reduces myocardial infarct size, and mimics myocardial preconditioning.
实验证据表明，ATP敏感性钾通道参与心肌缺血预处理。由于异氟烷的某些药理作用是由K（ATP）通道介导的，作者检验了以下假设：在心肌缺血前给予异氟烷可诱导或模拟心肌预处理。
在三组丙泊酚麻醉的兔中测量心肌梗死面积，每组均接受30分钟的前外侧冠状动脉闭塞，随后再灌注3小时。各组预处理不同：第1组（对照组，N = 13）未预处理；第2组（缺血预处理组，N = 8），冠状动脉闭塞5分钟，再灌注15分钟；第3组（异氟烷预处理组，N = 15），吸入15分钟异氟烷（呼气末浓度1.1%），然后冲洗15分钟。连续监测血流动力学。分别使用氯化三苯基四氮唑染色和荧光微球确定心肌梗死面积和危险区域面积，并均采用计算机图像分析测量。
异氟烷组梗死面积占危险区域面积的百分比为23.4±8.5%（均值±标准差），对照组为33.1±13.3%，缺血预处理组为8.7±6.2%。经共线性回归分析，随后进行斜率和截距相等性检验，结果显示，由于截距不同，三组梗死面积与危险区域面积之间的线性关系存在显著差异（P < 0.05）。各组间血流动力学变量存在微小差异，不太可能解释梗死面积的显著差异。
在心肌缺血前给予异氟烷可减小心肌梗死面积，模拟心肌预处理。
