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目的:探讨卡托普利介导缓激肽诱导预适应对大鼠缺血再灌注心肌保护作用的机制。方法:将60只Wistar大鼠随机分成正常对照组、缺血再灌注(IR)组、卡托普利预处理组、缓激肽β_2受体拮抗剂B1650加卡托普利组。麻醉大鼠冠脉结扎30min后,再灌注60 min,观察各组缺血再灌注前后心功能及一氧化氮合酶(NOS)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)活性以及丙二醛(MDA)和一氧化氮(NO)含量的变化。结果:IR组心肌原生型NOS(cNOS)活性及总NOS活性显著下降(P均<0.01),NO产生减少(P<0.05～0.01);卡托普利组缺血再灌注期间NO水平高于IR组(p<0.01),再灌注30 min心肌cNOS活性(P<0.01)及总NOS活性(p<0.05)显著高于IR组,心肌损害较IR组减轻。先静注B1650后再给予卡托普利,则卡托普利对心肌损伤的保护作用明显减弱。结论:NO产生不足是心肌再灌注损伤的主要因素;卡托普利通过调节缓激肽活性,维持正常NO水平对缺血再灌注心肌损伤大鼠可产生药理预适应保护作用,该作用可由缓激肽所介导。
Objective: To investigate the mechanism of captopril-mediated bradykinin-induced preconditioning on myocardial protection in rats with ischemia-reperfusion. Methods: Sixty Wistar rats were randomly divided into normal control group, ischemia reperfusion group, captopril preconditioning group and bradykinin β_2 receptor antagonist B1650 plus captopril group. After anesthetized rats were ligated for 30 min with coronary artery occlusion for 60 min, the changes of cardiac function, nitric oxide synthase (NOS), glutathione peroxidase (GSH-PX), superoxide The activity of SOD and the content of malondialdehyde (MDA) and nitric oxide (NO) were measured. Results: The activities of NOS (cNOS) and total NOS in myocardium of IR group were significantly decreased (P <0.01), NO production was decreased (P <0.05 ~ 0.01), while the level of NO in the captopril group was higher than that of ischemia-reperfusion IR group (p <0.01). The myocardial cNOS activity (P <0.01) and total NOS activity (p <0.05) at 30 min after reperfusion were significantly higher than those in IR group. The first intravenous injection of captopril B1650, captopril myocardial injury was significantly weakened. Conclusions: The lack of nitric oxide (NO) is the main factor of myocardial reperfusion injury. Captopril can protect rats with myocardial ischemia-reperfusion injury by regulating bradykinin activity and maintaining normal NO level, Kinin mediated.