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目的：探讨心肌缺血预处理（Ischemicpreconditioning，IPC）的心肌保护作用机制。方法：通过大鼠在体心肌缺血预处理模型，观察预处理（PC）对缺血再灌注心肌钠泵（Na+-K+-ATP酶）、钙泵（Ca(2+)-ATP酶）活性、Na+、Ca(2+)浓度及超氧化物歧化酶（SOD）、丙二醛（MDA）的影响。结果：与单纯缺血再灌注组相比，PC组缺血再灌注心肌钠泵、钙泵的活性降低幅度小（P＜0．01），心肌钠钙离子浓度降幅较大（P＜0．01），且SOD活性升高，MDA含量下降。结论：心肌缺血预处理通过提高缺血再灌注区心肌钠泵、钙泵的活性，减少心肌钠钙超载及氧自由基的产生而达到保护心肌的作用。
Objective: To investigate the mechanism of myocardial protection in ischemic preconditioning (IPC). Methods: Rat preconditioning model of myocardial ischemia was used to observe the effect of preconditioning (PC) on Na + -K + -ATPase activity and Ca (2 +) - ATPase activity in myocardial ischemia-reperfusion rats , Na +, Ca (2+) concentration and superoxide dismutase (SOD), malondialdehyde (MDA). Results: Compared with ischemia / reperfusion group, the activity of sodium pump and calcium pump in myocardial ischemia-reperfusion group decreased less (P <0.01) and the concentration of sodium and calcium in myocardial tissue decreased significantly (P <0. 01), and SOD activity increased MDA content decreased. Conclusion: Myocardial ischemic preconditioning can protect myocardium by increasing the activity of sodium pump and calcium pump in myocardial ischemia-reperfusion area and decreasing the overload of sodium and calcium and the production of oxygen free radicals.