磷酸肌酸预处理对糖尿病大鼠心肌缺血再灌注损伤的保护作用及其机制  

The protective effect of phosphocreatine preconditioning on myocardial ischemia-reperfusion injury in diabetic rats and its action mechanisms

作　　者：常建华[1] 景桂霞[1] 党旭云[1] 

机构地区：[1]西安交通大学医学院第一附属医院麻醉科,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2011年第2期151-154,共4页Journal of Xi’an Jiaotong University（Medical Sciences）

摘　　要：目的探讨磷酸肌酸(PCr)预处理对糖尿病大鼠心肌缺血再灌注损伤的保护作用及其机制。方法诱导糖尿病大鼠模型,2周后随机分为3组:假手术组(D1),缺血再灌注组(D2),缺血再灌注+PCr给药组(D3);观察缺血区心肌线粒体超微结构,计算凋亡指数(AI),测定心肌匀浆中磷酸腺苷和PCr的含量,并计算能荷值(EC)。结果与D2组相比,D3组线粒体肿胀变性的损伤较轻,AI降低,ATP、PCr含量和EC均升高(P<0.05)。结论 PCr通过维护心肌线粒体结构和功能的完整性,提高心肌组织内能量物质的含量,减少心肌细胞的凋亡,从而对糖尿病大鼠心肌缺血再灌注损伤起到保护作用。Objective To investigate the protective effect of phosphocreatine（PCr） preconditioning on myocardial ischemia-reperfusion injury in diabetic rats and its action mechanisms.Methods A diabetic rat model was induced first;two weeks later these rats were divided randomly into 3 groups： sham-operation group（D1）,myocardial ischemia-reperfusion group（D2） and ischemia reperfusion ＋ PCr preconditioning group（D3）.The ultrastructure of the cardiac muscle and mitochondria was observed under an electron microscope,the content of high-energy compounds in the cardiac muscle and apoptosis index（AI） were measured,and the value of energy charge（EC） was calculated.Results Compared with those in D2,the mitochondria damage was alleviated,AI decreased while adenosine triphosphate（ATP）,PCr content and EC increased in D3（P0.05）.Conclusion PCr can protect mitochondrial structure and function,enhance the content of high-energy compounds in the myocardial cells and reduce myocardial apoptosis,thus fighting against myocardial ischemia-reperfusion injury in diabetic rats.

关 键 词：磷酸肌酸 糖尿病大鼠 心肌缺血再灌注损伤 线粒体 凋亡 

分 类 号：R587.1[医药卫生—内分泌]