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目的研究3-硝基丙酸(3-NPA)化学预处理对大鼠离体心脏缺血-再灌注损伤的保护作用及其机制。方法16只Wistar大鼠随机分为2组,每组8只。实验组(3-NPA组):腹腔注射3-NPAmg·kg-1预处理24h;对照组(C组):腹腔注射等体积生理盐水。采用Langendorff离体心脏灌流模型,两组行常温缺血30min-再灌注60min模拟心肌缺血-再灌注损伤。观察各组缺血前(基础值)和再灌注后30、60min时心率(HR)、左心室发展压(LVDP)、左心室压力上升和下降最大变化速率(±dp/dtmax),测定再灌注后15min时冠脉流出液肌酸激酶(CK)和乳酸脱氢(LDH)活性,测定再灌注后60min时心肌丙二醛(MDA)含量和超氧化物岐化酶(SOD)活性。结果与C组比较,3-NPA组LVDP、+dp/dtmax再灌注后30、60min、-dp/dtmax再灌注后60min时升高(P<0.01或0.05),HR组间比较差异无统计学意义(P>0.05),灌注后15min时冠脉流出液CK和LDH活性降低,再灌注后60min时心肌SOD活性明显升高,心肌MDA含量降低。结论4mg·kg-13-NPA预处理对大鼠离体心脏缺血-再灌注损伤具有一定的保护作用,其机制可能是减少氧自由基的产生和提高SOD活性。
Objective To investigate the protective effect and mechanism of 3-nitropropionic acid (3-NPA) preconditioning on isolated rat hearts from ischemia-reperfusion injury. Methods Sixteen Wistar rats were randomly divided into 2 groups with 8 rats in each group. The experimental group (3-NPA group): pretreatment with 3-NPA mg · kg -1 for 24 hours; control group (C group): intraperitoneal injection of equal volume of normal saline. The Langendorff perfusion model was used. The ischemia-reperfusion injury was simulated by ischemia-reperfusion 30 min-60 min reperfusion in both groups. The changes of heart rate (HR), left ventricular development pressure (LVDP), left ventricular pressure rise and the maximum rate of decline (± dp / dtmax) were observed before ischemia (basal) and at 30 and 60 minutes after reperfusion Coronary flow creatine kinase (CK) and lactate dehydrogenase (LDH) activity were measured at 15 min after ischemia. The contents of MDA and superoxide dismutase (SOD) were measured at 60 min after reperfusion. Results Compared with group C, the LVDP and + dp / dtmax of 3-NPA group were significantly increased at 60 and 60 min after reperfusion (P <0.01 or 0.05) at 30 and 60 min after reperfusion, respectively. There was no significant difference between HR groups (P> 0.05). The activities of CK and LDH in coronary effluent were decreased at 15 min after perfusion. The activity of SOD in myocardium was significantly increased and the content of MDA in myocardium was decreased at 60 min after reperfusion. Conclusion Pretreatment with 4 mg · kg-13-NPA may have a protective effect on isolated rat hearts from ischemia-reperfusion injury. The mechanism may be to reduce the production of oxygen free radicals and increase the activity of SOD.