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采用非创伤性下肢缺血预处理（Ｎ－ＷＩＰＣ）动物模型，研究了Ｎ－ＷＩＰＣ对大鼠心肌缺血再灌注损伤及脂质过氧化的保护效应。结果显示，Ｎ－ＷＩＰＣ可明显减少心肌组织内肌酸磷酸激酶（ＣＰＫ）的漏出，提高心肌组织超氧化物歧化酶（ＳＯＤ）的活性，降低脂质过氧化产物丙二醛（ＭＤＡ）的含量。表明非创伤性下肢缺血预处理具有抗心肌缺血再灌注损伤及脂质过氧化的作用，其机制可能是通过提高内源性心肌保护物质的水平而起作用。
The non-traumatic hypothermic ischemic preconditioning (N-WIPC) animal model was used to study the protective effects of N-WIPC on myocardial ischemia-reperfusion injury and lipid peroxidation in rats. The results showed that N-WIPC could significantly reduce the leakage of creatine phosphokinase (CPK) in myocardium, increase the activity of superoxide dismutase (SOD) and decrease the content of malondialdehyde (MDA) . The results suggest that noninvasive lower limb ischemic preconditioning has anti-myocardial ischemia-reperfusion injury and lipid peroxidation, and its mechanism may be through increasing the level of endogenous myocardial protective substances.