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作 者:郭群[1] 陈水英[1] 张作明[1] 姚秀娟[1]
机构地区:[1]第四军医大学,西安710032
出 处:《陕西医学杂志》2006年第8期932-933,941,共3页Shaanxi Medical Journal
摘 要:目的:探讨氧自由基与心肌缺血-再灌注损伤的关系。方法:采用在体大鼠心肌缺血-再灌注模型,于结扎冠状动脉前3m in,静注超氧化物歧化酶(SOD)75U/kg或等体积生理盐水(N S),观察心肌缺血-再灌注状态下心电图、心肌丙二醛(MDA)、SOD及Ca2+的变化。结果:在缺血期,8/20动物发生心律失常。再灌后,缺血再灌组全部动物发生室性心律失常,其中90%为新发生或再灌后加重的心律失常,室性早博、室速、室颤发生率分别为100%、80%和40%;心肌MDA含量明显高于假手术组(P<0.01);SOD活性从11.4±2.9降至6.9±1.6mm o l/m in.g.port(P<0.01),Ca2+含量由1.6±0.1增至2.0±0.2μm o l/g(P<0.01)。结论:心肌缺血-再灌注损伤与再灌后产生大量氧自由基有关。SOD可使室性心律失常发生率明显减少;降低MDA和Ca2+的含量。Objective: To study the association between ischemia-reperfusion myocardium injury and oxygen radials. Methods: The myocardial ischemia-reperfusion model of rats in vivo was used for the present study. ECGS of rats under ischemia-reperfusion condition were recorded. The contents of myocardial malondiald (MDA), superoxide dismutase(SOD), calcium in serum were measured. Results.. During myocardial-ischemia period, 8/20 rats had arrhythmias , 90% got arrhymias just after ischemia- reperfusion or became more serious after ischemia-reperfusion. Ventricular premature beat, ventricular tachycardia, ventricular fibrillation were 100%, 80%, and 40% respectively. MDA was more than sham operation group (P〈0. 01) ; activity of SOD decreased to 6.9±1.6 from 11.4±2.9mmol/min · g Arot(P〈0. 05); Ca^2+ increased to 2. 1±0. 2 from 1. 6± 0. 1μmol/min(P〈0. 01). Conclusion: The myocardial ischernia-reperfusion injury had an association with oxygen free radicals. SOD significantly decreased the incidence of ventricular arrhythias (P〈0.05) ; SOD decreased MDA and Ca^2+.
关 键 词:心肌缺血/并发症 心肌再灌性损伤 丙二醛 超氧化物歧化酶
分 类 号:R542.2[医药卫生—心血管疾病] R285.5[医药卫生—内科学]
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