蛋白激酶C在硝酸甘油诱导的心肌延迟保护中的作用观察

目的蛋白激酶C在硝酸甘油（NTG）对大鼠在体缺血再灌注（I/R）心肌延迟保护中的作用。方法 建立在体大鼠心脏缺血再灌注模型。40只大鼠随机分成5组：生理盐水 I/R组、NTG I/R组、NTG 白屈菜红碱 I/R组、白屈菜红碱 I/R组及假手术组。以心肌梗塞范围、血清肌酸激酶（CK）活性及心肌组织丙二醛（MDA）含量为观察指标。结果 与对照组相比，NTG可显著缩小24小时后缺血再灌注心肌的梗塞范围(P＜0.01），而且血清CK活性、心肌MDA含量亦显著降低(P＜0.01）；而在I/R前给予白屈菜红碱可抑制NTG的保护作用，且血清CK、心肌MDA含量与对照组相比差异无显著性。结论 NTG的延迟心肌保护效应可能由PKC通路介导。

Effects of PKC in Second Window of Cardioprotection Induced by Nitroglycerin

Objective To assess the potential involvement of PKC signal transduction pathway in the delayed cardioprotection induced by nitroglycerin. Methods 40 rats were randomly divided into 5 groups. Rats in Group1 to 4 were subjected to 30 minutes of ischemia and 50 minutes of reperfusion (I/R). Group1 and 2 were injected with saline or NTG 24 hours before I/R respectively; IN Group3, NTG preconditioned rats were given the PKC pathway blocker chelerythrine (CHR) 30 minutes before I/R; IN Group4, nonpreconditioned rats were given the same dose of CHR as in groop3. Changes in myocardial infarct size, creatine kinase (CK) in serum and MDA of myocardium were investigated. Results NTG pretreatment significantly reduced infarct size/area at risk (IS/AAR) , and decreased the content of CK and MDA; while CHR abrogated the cardioprotective effect induced by NTG. Conclusion NTG pretreatment, 24 hours before an ischemic insult, produce a delayed cardioprotective effect that is possibly the result of PKC signal transduction pathway.