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据报道,心肌缺血——再灌损伤的机制与活性氧自由基的产生紧切相关,在大鼠心脏产生氧自由基是以黄嘌呤氧化酶(XO)途径为主.心肌中的黄嘌呤脱氢酶(XD)在Ca~(2+)激活水解酶的作用下向XD转化.而此我们设想,协同使用钙拮抗剂与超氧阴离子(O_2~1)清除剂(超氧化物歧化酶,SOD)可能加强对心肌的保护作用.本实验用电子自旋共振波谱仪(ESR)直接检测大鼠缺血——再灌心肌产生的活性氧自由基,从心脏收缩幅度,静息张力,肌酸激酶(CK)释放和心肌组织丙二醛(MDA)为指标,观察钙拮抗剂硫氮(艹卓)酮(DTZ)和SOD的分别作用和联合作用,发现两药合用可明显减少心肌活性氧自由基的产生.
It has been reported that the mechanism of myocardial ischemia-reperfusion injury is closely related to the production of reactive oxygen radicals. Oxygen free radicals are produced in the heart of the rat by the xanthine oxidase (XO) pathway. Xanthine in the heart muscle Dehydrogenase (XD) converts to XD under the action of Ca 2+ activating hydrolase. We hypothesize that the synergistic use of calcium antagonists and superoxide anion (O_2~1) scavenger (superoxide dismutase) , SOD) may enhance the protective effect on myocardium. In this experiment, the rat brain ischemia was detected directly by electron spin resonance spectroscopy (ESR)—the reactive oxygen free radicals produced by reperfusion heart muscle, the amplitude of contraction from the heart, the resting tension, Creatine kinase (CK) release and myocardial tissue malondialdehyde (MDA) were used as indicators to observe the effects and combined effects of the calcium antagonists sulfurthiazolyl (DTZ) and SOD. It was found that the combination of the two drugs can significantly reduce the myocardium The production of reactive oxygen radicals.