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目的 观察远处其它器官短暂缺血是否能保护心肌及机制的探讨。方法 Wistar大鼠48只,随机分为6组。采用免疫组化方法检测 PKCα、PKCδ亚型在心肌细胞内转移及转位。结果 心肌缺血预处理组（IPC），肠系膜动脉阻塞 （MAO）15min组，股动脉阻塞（FAO）15min组,对心肌都有保护作用。灯盏花素乙(Bre.)不能消除FAO、MAO对心肌的保护作用。免疫组化检测结果除IPC组外,MAO组、FAO组、Bre.干预组心肌细胞内均未见PKCα、PKCδ亚型转位。结论 短暂的肠系膜动脉、 股动脉阻塞和心肌缺血预处理一样能有效保护心肌组织被长时间缺血-再灌注损伤,但其机制与IPC不同,它们并不是经激活PKC信息通道而发挥作用的。
Objective To investigate whether transient ischemia in other organs can protect myocardium and its mechanism. Methods Wistar rats 48, were randomly divided into 6 groups. Immunohistochemistry was used to detect PKCα and PKCδ subtypes in cardiomyocytes. Results Myocardial ischemic preconditioning (IPC), mesenteric artery occlusion (MAO) 15min and femoral artery occlusion (FAO) 15min had protective effect on myocardium. Breviscapine B (Bre.) Can not eliminate the protective effect of FAO and MAO on myocardium. Immunohistochemical results in addition to IPC group, MAO group, FAO group, Bre. Intervention group myocardial cell PKCα, PKCδ subtype translocation. Conclusions Short-term mesenteric artery, femoral artery occlusion and myocardial ischemic preconditioning can effectively protect myocardium from long-term ischemia-reperfusion injury. However, its mechanism is different from that of IPC in that it does not play a role in activation of PKC signaling pathway .