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目的探讨缺血预处理(ischemic preconditioning,IP)对缺血再灌注损伤大鼠心肌线粒体心磷脂(cardiolipin)及心功能的影响。方法清洁级SD大鼠72只,体质量200～300g,雌雄各半,用随机数字表法分为正常组、对照组、缺血预处理组(IP组)、5-羟葵酸(5-HD)拮抗缺血预处理组(HD组),每组18只。采用Langendorff灌流装置建立大鼠离体心脏缺血再灌注模型,正常组灌注平衡20min,持续灌注100min;对照组灌注平衡20min,持续灌注30min,缺血40min,再灌注30min;IP组灌注平衡20min后,给予2次间断缺血预处理,每次缺血5min再灌注5min,余缺血再灌注同对照组;HD组在预处理前灌注5-HD10min,余同IP组。各组分别于灌注平衡末(T1)、缺血前即刻(T2)、再灌注末(T3)记录心率(HR)、左心室发展压(LVDP)和左心室舒张末压(LVEDP),采用高效液相色谱仪测定心肌线粒体心磷脂含量。结果与T1、T2时比较,各组T3时HR、LVDP明显降低,LVEDP明显升高,心肌线粒体心磷脂含量明显降低(P<0.05,P<0.01);与正常组比较,余3组T3时HR、LVDP明显降低,LVEDP明显升高,心肌线粒体心磷脂含量明显降低(P<0.05,P<0.01);与对照组比较,IP组及HD组T3时HR、LVDP明显升高,LVEDP明显降低,心肌线粒体心磷脂含量明显升高(P<0.05,P<0.01);与IP组比较,HD组T3时HR、LVDP明显降低,LVEDP明显升高,心肌线粒体心磷脂含量明显降低(P<0.05,P<0.01)。结论IP可维护心肌线粒体心磷脂含量的相对稳定,改善大鼠离体缺血再灌注心脏功能,其机制主要与mito-KATP通道的激活有关。
Objective To investigate the effect of ischemic preconditioning (IP) on myocardial mitochondrial cardiolipin and cardiac function in rats with ischemia-reperfusion injury. Methods Seventy-two SD rats were divided into normal group, control group, ischemic preconditioning group (IP group), 5-hydroxynitrite (5- HD) antagonized ischemic preconditioning group (HD group), each group of 18. The rats were perfused with Langendorff perfusion device for 20min, and then perfused for 100min. The control group was perfused for 20min, then perfused for 30min, then perfused for 40min and reperfused for 30min. The perfusion equilibrium in IP group was 20min , Given two intermittent ischemic preconditioning, each ischemia 5min reperfusion 5min, ischemia and reperfusion with the control group; HD group before pretreatment perfusion 5-HD10min, with the same IP group. The heart rate (HR), left ventricular development pressure (LVDP) and left ventricular end diastolic pressure (LVEDP) were recorded at the end of perfusion equilibrium (T1), immediately before ischemia (T2) and at the end of reperfusion Determination of Myocardial Mitochondria Cardiolipin by Liquid Chromatography. Results Compared with T1 and T2, the HR, LVDP and the LVEDP of T3 in each group were significantly decreased (P <0.05, P <0.01), while those in T3 and T2 (P <0.05, P <0.01). Compared with the control group, the HR and LVDP at T3 and the LVEDP in the IP and HD groups were significantly decreased and the LVEDP and LVEDP were significantly increased (P <0.05, P <0.01). Compared with the IP group, the HR, LVDP and the LVEDP of the T3 group were significantly lower than those of the IP group (P <0.05) , P <0.01). Conclusions IP can maintain the relative stability of myocardial mitochondrial cardiolipin and improve the cardiac function in vitro. The mechanism is mainly related to the activation of mito-KATP channel.