摘要
目的 研究地氟醚、七氟醚和异氟醚预处理对兔心肌缺血/再灌注损害的影响。方法35只大白兔,阻断左冠状动脉前降支缺血50min,开放再灌注120min,随机分为5组。3个预处理组分别吸入1.5MAC地氟醚、七氟醚和异氟醚20min,继之10min药物排出;G+地氟醚组于地氟醚预处理前10min静注KATP通道阻断剂Glybenclamide 2mg/kg;对照组无任何处理。实验中监测血流动力学变化,实验结束用氯化硝基四氮唑蓝法测定心肌梗死范围。结果 缺血和再灌注早期,HR、MAP、CO、LVSP、LVEDP和RPP各组间无统计学差异;再灌后期,对照组LVEDP明显高于各预处理组。与对照组比,地氟醚、七氟醚、异氟醚和G+地氟醚各组,分别缩小心肌梗死范围41.3％、47.2％、31.7％和17.8％,G+地氟醚组心肌梗范围明显高于地氟醚组。结论 地氟醚、七氟醚和异氟醚预处理不同程度缩小兔心肌梗死范围,KATP通道部分介导了其心肌保护。
Objective To study the effects of desflurane, sevoflurane and isoflurane preconditioning on myocardium against ischemia-reperfusion injury in rabbits. Methods Thirty-five healthy white rabbits of both sexes were randomly divided into five groups of 7 animals each: (A) desflurane group; (B) sevoflurane group; (C) isoflurane group; (D) glybenclamide + desflurane and (E) control group. The animals were anesthetized with intravenous pentobarbital 30mg-kg-1 and tracheotomized and mechanically ventilated. PaCO2 was maintained at 30-40 mm Hg. Muscle relaxation was produced by pancuronium. Right internal jugular vein was cannulated for fluid administration and femoral artery for continuous BP monitoring. ECG was continuously monitored. Chest was opened and heart and aorta were exposed. Cardiac output was measured by dopplar. Left anterior descending (LAD) artery was exposed. After the above preparation the circulation was allowed to be maintained stable for 30min, then preconditioning with 1.5MAC of desflurane (9% ) , sevoflurane (2.5%) and isoflurane (1.7%) was started and maintained for 20min, followed by 10 min wash-out. In group D (glybenclamide + desflurane ) 10min before desflurane preconditioning glybenclamide 2mg-kg-1 was given iv. LAD artery was then occluded and occlusion was confirmed by the dark blue color of the myocardium supplied by LAD, elevation of S-T segment >0. 5mv. LAD occlusion was maintained for 50min and then released for reperfusion (120min) . Myocardial infarct size was measured by nitroblue tetrazolam at the end of experiment. Results There was no statistically significant difference in HR, MAP, cardiac output (CO), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure ( LVEDP) and rate-pressure products ( RPP) among all groups during ischemia and early reperfusion period except for LVEDP in control group which was much higher than that in all preconditioning groups during the late reperfusion period. Compared with the control group, desflurane, sevoflurane, isoflurane and G+ desflurane reduced myocardial infarct size by 41%, 47%,31.7% and 17.8% respectively without significant homodynamic effects. Myocardial infarct size in G + desflurane groups was significantly larger than that in desflurane group. Conclusion Preconditioning with desflurane, sevoflurane and isoflurane reduce myocardial infarct size in rabbits to some extent. The protective effects may be partly medialed via activation of KATP channel.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2002年第11期676-680,共5页
Chinese Journal of Anesthesiology
关键词
吸入麻醉药
心肌缺血预处理
心肌再灌注损伤
Anesthetics, inhalation
Ischemic preconditioning, myocondial
Myocardial reperfusion injury
