摘要
目的 :研究血管紧张素转换酶抑制剂 (ACEI)卡托普利 (captopril)在家兔心肌缺血再灌注时的心脏保护作用。方法 :采用冠状动脉左前降支结扎放松法制作模型。家兔随机分为 3组 ,即假手术组 (S)、模型组 (M)、卡托普利治疗组 (C)。结扎 30分钟 ,再灌注 6 0分钟后测定血乳酸 ,血清磷酸肌酸激酶 MB同功酶 (CK- MB)、乳酸脱氢酶(L DH)、一氧化氮合成酶 (NOS)活性 ;血清一氧化氮 (NO)含量 ;心肌匀浆超氧歧化酶 (SOD)活性、丙二醛 (MDA)及血管紧张素 (Ang )含量 ;并观察心肌结构以及细胞超微结构的变化 ,比较 3组受损线粒体所占的比例。结果 :S组、C组血乳酸浓度、血清 L DH、CK- MB、NOS活性、血清 NO含量均低于 M组 ,S组、C组之间无显著性差异 ;心肌 SOD活性 S组、 C组明显高于 M组 ,S组明显高于 C组 ;S组、C组心肌 MDA、Ang 含量均低于 M组 ,S组与 C组相比无显著性差异。S组心肌结构及超微结构大致正常 ,C组损伤较 M组轻。M组受损线粒体所占比例明显高于 S组、C组 ;S组与 C组相比无显著差异。结论 :肾素 -血管紧张素系统 (RAS)参与了心肌缺血再灌注损伤。卡托普利可以阻断心肌局部 RAS,通过 NO释放增加 ,减少自由基生成 ,对心肌缺血再灌注损伤起到保护作用。
Objective: To investigate the cardioprotective effects of angiotensin converting enzyme inhibitor (ACEI) on ischemic and reperfused rabbit hearts. Methods: The study was conducted using a MIRI model by left anterior descending coronary artery ligation for 30 minutes, and then reperfusion for 60 minutes in rabbits. The rabbits are randomly divided into three groups: shan operated group (S), model group (M) and captopril treated group (C). At the end of the experiment, blood lactic acid, activity of serum creatinekinase MB (CK MB), lactic dehydrogenase (LDH), the nitric oxide synthase (NOS), the concentration of serum nitric oxide (NO), contents of myocardial angiotensin Ⅱ(AngⅡ), malondialdehyde (MDA), activity of superoxide dismutase (SOD) are measured, the structure of myocardium and the ultramicro structure of myocardial cells are observed, and the rate of injured mitochondrion of three groups are compared. Result: The blood lactic acid, the serum LDH , CK MB, NOS activity and the content of NO in group S and group C are lower than those in group M. The contents of cardiac MDA, AngⅡ in group S and group C are lower than those in group M. There is no difference between group S and group C. The activity of cardiac SOD in group S and group C are higher than that in group M. The activity of cardiac SOD in group S is higher than that in group C. The myocardial structure and ultramicro structure in group S is almost normal, while in group C shows some mild injury, and in group M the injury is the most serious. The rate of injuried mitochondrion in group M is higher than those in group S and group M. There is no difference between group S and group C. Conclusion: When myocardial ischemia reperfusion injury (MIRI) occurs, the cardiac local RAS is activated, and activated local RAS participate MIRI. After using Captopril, it can block local RAS, and can present cardioprotective effects by increasing NO synthesize, reducing the production of free radicals.
出处
《天津药学》
2001年第5期30-33,共4页
Tianjin Pharmacy
关键词
心肌缺血
再灌注损伤
血管紧张素Ⅱ
一氧化氮
卡托普利
myocardial ischemia reperfusion injury (MIRI), angiotensin Ⅱ,nitric oxide (NO), captopril
