药物预处理对缺血再灌注心肌的保护作用

Protective Effects of Pharmacological Preconditioning on Ischemic Reperfusion Injury

目的:本实验旨在讨论心肌缺血再灌注损伤的发生机理,观察药物预处理对心肌缺血再灌注损伤保护作用。方法:采用在体兔心肌缺血再灌注模型,结扎兔冠状动脉前降支,缺血20 min再灌注30 min。将健康家兔30只随机分为三组:Ⅰ组为对照组(SC);Ⅱ组为腺苷预处理组(Adopc);Ⅲ组为去甲肾上腺素预处理组(NEPC)。观察指标包括:①心功能各参数;②心律失常发生;③血肌酸激酶(CK);④心肌超微结构。结果:实验结果表明,再灌注期间Ⅱ、Ⅲ组左室最大压力变化速率(±dp/dtmax)较Ⅰ组有显著改善(P<0.05)。Ⅱ、Ⅲ组再灌注心律失常的发生率较Ⅰ组均明显降低(P<0.05)。再灌注血肌酸激酶Ⅱ、Ⅲ组明显低于Ⅰ组(P<0.05)。心肌超微结构的改善Ⅱ、Ⅲ组优于Ⅰ组。结论:本实验研究表明,药物预处理对心肌缺血再灌注损伤有明显的保护作用,他们是通过激发机体内源性保护机制而发挥其心肌保护作用。

Objective： The purpose of this study is to explore the mechanisms underlying ischemia - reperfu- sion injury of the heart. To investigate the protective effects of pharmacological preconditioning （PPC） on ischemia - reperfution injury. Methods： The heart of rabitts were used to made ischemia - repel＇fusion model in our experiment. All hearts were subject to 20 minutes local ischemia ;then were reperfused for 30 minutes . Thirty rabitts were randomly divided into three groups： Ⅰ Sham control group （SC） ; Ⅱ Adenosine preconditioning group （Adopc） ; m Norepinephrine preconditioning （NEPC） . Observed indexes include： （1） myocardial contractility. （2）the incidence of arrhythmia. （3）CK in blood .（4）yocardial ultrastructure observation . Results ： The re- sults showed that Ⅱ 、 Ⅲ group , Significantly improved myocardial contractility （ ＋ dp/dtmax） as compared with Ⅰ group during repel-fusion period（P 〈 0.05）, The incidence of reperfusion arrhythmia was higher in group Ⅱ and m than in group Ⅰ （P〈0.01） . CK leakage was remarkably reduced in group Ⅱ and m （P〈0.05） . My- ocardial electron microscope observation demonstrated that myocardial ultrastucture of group Ⅱ and m was better than of group Ⅰ .Conclusion ： This study suggested pharmacological preconditioning can remarkably enhance cardio - protecive effects on ischemia- reperfusion injury, The cardio - protective effects of PPC were carried out by activating themselves endogenous protective mechanism.