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为观察环孢霉素 (syclosporinA)对缺血预处理心脏保护作用的影响 ,探讨Calcineurin信号通路在心脏缺血预处理中的作用 ,制备离体大鼠心肌缺血 再灌注模型 ,测定心功能和心肌Calcineurin活性。结果发现 ,缺血预处理明显减轻缺血 再灌注的心功能抑制 ,与单纯缺血 再灌注比较 ,冠状动脉灌流量、收缩期左室内压最大变化速率和舒张期左室内压最大变化速率分别减少 39% (P <0 .0 5 )、33 % (P <0 .0 1)和 5 2 % (P <0 .0 5 ) ,心肌钙含量下降2 1% (P <0 .0 1)。Calcineurin抑制剂环孢霉素A可抵消缺血预处理的心肌保护作用。此外 ,缺血 45min 再灌 15min使心肌Calcineurin活性升高 ,与对照组相比较 ,Calcineurin活性增加 1.9倍 (P <0 .0 1)。单纯缺血预处理组心肌Cal cineurin的活性较对照组增加 2 .3倍 (P <0 .0 1)。环孢霉素A预先处理心脏则完全阻断了缺血预处理诱导的Calci neurin激活 ,与缺血预处理组相比较 ,其活性下降 75 % (P <0 .0 1)。以上提示Calcineurin途径介导了缺血预处理的心脏保护作用
To investigate the effect of syclosporin A on the cardioprotection induced by ischemic preconditioning, to explore the role of calcineurin signaling in cardiac ischemic preconditioning and to establish an isolated rat model of myocardial ischemia reperfusion, Calcineurin activity in myocardium. The results showed that ischemic preconditioning can significantly reduce the cardiac function inhibition of ischemia-reperfusion, compared with ischemia-reperfusion, the maximum rate of change of coronary perfusion, systolic left ventricular pressure and diastolic left ventricular pressure were decreased (P <0. 05), 33% (P <0. 01) and 52% (P <0. 05) respectively, and the myocardial calcium content decreased by 21% (P <0.01). Calcineurin inhibitor cyclosporin A can counteract the myocardial protective effect of ischemic preconditioning. In addition, calcineurin activity increased after 45 min of ischemia and 15 min of reperfusion, and the activity of Calcineurin increased 1.9-fold (P <0.01) compared with the control group. Compared with the control group, the activity of Cal cineurin in myocardial ischemic preconditioning group increased by 2.3 times (P <0.01). Cyclosporine A pretreatment of the heart completely blocked ischemic preconditioning-induced Calci neurin activation by 75% (P <0.01) compared with the ischemic preconditioning group. The above suggests that the Calcineurin pathway mediates cardioprotection of ischemic preconditioning