摘要
目的 了解二氮嗪预处理对未成熟兔心脏有无保护作用,并探讨其机制。方法 大耳白幼兔(小于28 d)21只随机分成三组:对照组(Ⅰ组n=8):K-H缓冲液灌注30 min后St.ThomasⅡ号停跳液(STH)停跳;二氮嗪预处理组(Ⅱ组n=8):二氮嗪(100μmol/L)灌注5 min,再K-H液灌注10min后STH停跳;二氮嗪+5-HD组(Ⅲ组n=5):二氮嗪和5-HD(均100μmol/L)共同灌注5 min后停跳。在LangendOrff模型上进行离体心脏常温缺血/再灌注(I/R)实验。观察再灌后血液动力学恢复、冠脉流出液心肌酶、心肌组织内ATP含量及心肌超微结构变化。结果 再灌后Ⅱ组左室发展压(LVDP)、左室压力上升和下降最大速率(±dp/dtmax)的恢复率在多个时间点上均高于Ⅰ组,再灌末心肌组织ATP含量也高于Ⅰ组(P<0.01),冠脉流出液中的三种心肌酶值均较Ⅰ组降低(P<0.01)。Ⅱ组的线粒体评分低于Ⅰ组(P<0.01),Ⅲ组线粒体评分回到Ⅰ组水平(P>0.05)。结论 二氮嗪能通过开放线粒体ATP敏感性通道而发挥对幼兔心肌的保护作用。
Objective To investigate whether diazoxide preconditioning can exert protective effect on myocardium against ischemia-reperfusion injury in immature rabbits and the possible mechanism. Methods Twenty-one healthy 3-4 week old white rabbits of either sex were randomly divided into 3 groups : group Ⅰ control ( n = 8) ; group Ⅱ diazoxide preconditioning ( n = 8) and group Ⅲ diazoxide + 5-HD preconditioning ( n = 5) . The animals were anesthetized with intraperitoneal pentobarbital 50 mg·kg-1 and heparized (150 IU·kg-1). The hearts were excised and connected to Langendorff apparatus and passively perfused with normothermic (37℃), oxygenated (95% O2 , 5% CO2) Krebs-Henseleit buffer (KHB) at a constant perfusion pressure of 70cmH2O. A latex balloon was inserted via left atrium into left ventricle and filled with water. The left ventricular end-diastolic pressure (LVEDP) was maintained at 10 mm Hg. In group I cardiac arrest was induced with St Thomas Ⅱ solution after the heart was perfused with KHB for 30 min. In group 11 after being perfused with KHB for 15 min, the hearts were perfused with diazoxide 100μmol·L-1 for 5 min followed by 10 min wash-out with KHB , then cardiac arrest was induced as in group Ⅰ . In group Ⅲ after being perfused with KHB for 15 min, the hearts were perfused with diazoxide 100μmol·L-1 and 5-HD 100μmol·L-1 for 5 min, followed by 10 min wash-out with KHB, then the cardiac arrest was induced as in group Ⅰ and Ⅱ . All hearts were subjected to 30 min ischemia followed by 45 min reperfusion after cardiac arrest. Coronary flow (CF), HR, left ventricular developed pressure (LVDP) and dp / dt max were measured after the hearts were perfused with KHB for 15 min (baseline) and at 5, 10, 15, 30, 45 min after reperfusion was resumed. Coronary effluent was collected at 5 min after reperfusion was resumed for determination of myocardial enzymes, CK, LDH and AST. At the end of experiment myocardial specimen was obtained for determination of ATP content and ultrastructure examination.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2003年第12期905-907,共3页
Chinese Journal of Anesthesiology
