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目的从氧化应激和线粒体介导的凋亡方面探讨异丙酚对大鼠离体心脏缺血再灌注损伤的保护作用。方法40只SD大鼠随机分为对照组、缺血再灌注(I/R)组和异丙酚15、30、60μmol·L-1组,每组8只。应用Langendorff离体心脏灌注系统建立心脏缺血再灌注损伤模型,经主动脉用Lock氏平衡灌注。除对照组外,各组均全心缺血25 min再灌注30 min。记录平衡灌注末、缺血前即刻及再灌注30 min时心率(HE)、左室收缩压(LVSP)、左室舒张末压(LVDEP)、左室压力变化速率(±dp/dtmax)、冠脉流量(CF);测定冠脉流出液中乳酸脱氢酶(LDH)、磷酸肌酸激酶(CK)活性及心肌线粒体活力、膜肿胀度、丙二醛(MDA)含量及心肌细胞凋亡率、半胱天冬酶(caspase)-3蛋白的表达。结果与I/R组比较,异丙酚30、60 μmol·L-1组再灌注30min时LVDEP升高,LVDP、±dp/dtmax、CF均降低,冠脉流出液中LDH、CK活性降低,心肌线粒体膜肿胀度、MDA含量降低,线粒体活力升高,心肌细胞凋亡率降低,caspase-3表达降低(P<0.05或0.01)。结论30、60/μmol·L-1异丙酚对大鼠离体心脏缺血再灌注损伤有一定的保护作用,减少缺血再灌所致的氧化应激,保护线粒体,抑制心肌细胞凋亡可能是其作用机制之一。
Objective To investigate the protective effect of propofol on isolated rat hearts from ischemia-reperfusion injury induced by oxidative stress and mitochondria-mediated apoptosis. Methods Forty SD rats were randomly divided into control group, ischemia / reperfusion (I / R) group and propofol 15,30,60μmol·L-1 group (n = 8). The Langendorff isolated heart perfusion system was used to establish the model of ischemia-reperfusion injury in the heart. BALF was perfused via the aorta. Except the control group, all groups were subjected to 25 min reperfusion for 30 min. The heart rate (HE), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVDEP), left ventricular pressure change rate (± dp / dtmax) (CF). The levels of lactate dehydrogenase (LDH), creatine phosphokinase (CK), myocardial mitochondrial activity, membrane swelling, malondialdehyde (MDA) and myocardial cell apoptosis , Caspase-3 protein expression. Results Compared with the I / R group, the LVDEP, ± dp / dtmax and CF of the 30,60 μmol·L-1 propofol groups were increased at 30 min after reperfusion, the activities of LDH and CK in the coronary effluent decreased, Myocardial mitochondrial membrane swelling, decreased MDA content, increased mitochondrial activity, decreased cardiomyocyte apoptosis, caspase-3 expression decreased (P <0.05 or 0.01). Conclusion Propofol at 30, 60 / μmol·L-1 can protect rat hearts from ischemia-reperfusion injury and reduce oxidative stress induced by ischemia-reperfusion, protect mitochondria and inhibit cardiomyocyte apoptosis It may be one of the mechanisms of action.