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作 者:袁文俊[1] 戎伟芳[1] 严云[1] 许金廉[1] 朱宝旺[1] 蒋应明[1] 杨宁[1] 吴德林[1] 侯钢星[1] 富维骏[1]
机构地区:[1]第二军医大学基础医学部生理学教研室,济南医学高等专科学校生理学教研室
出 处:《第二军医大学学报》1996年第6期539-541,共3页Academic Journal of Second Military Medical University
基 金:"八五"全军医学科研基金
摘 要:目的:探明内皮秦-1(ET-1)致心律失常作用的氧自由基机理及药物干预的作用。方法:对照组大鼠冠状动脉口、猫冠状动脉前降支(LADD)分别注射ET-1,均引起室性期前收缩及室性心动过速、心室颤动等严重心律失常;实验组分别以不同剂量超氧化物歧化酶-1(SOD-1)经大鼠冠状动脉口或猫LAD预处理5min后,再予ET-1。结果:经SOD-1处理后,相同剂量ET1(900pmol/kg)引起大鼠心律失常的发生率、心律失常评分均显著低于ET-1对照组(P<0.01),SOD-1拮抗ET-1致心律失常作用与SOD-1的剂量呈量效关系;6例猫LAD起始段注射SOD-10.1mg/kg后再予ET-160pmol/kg,其心律失常评分为0.20±0.17,显著低于同剂量ET-1对照组(5.17±1.60,P<0.01)。结论:SOD-1具有拮抗ET-1的致心律失常作用,表明ET-1引起的心律失常可能与氧自由基参与有关。To evaluate the oxygen free radical mechanism in the arrhythmogenic action of endothelin-1(ET-1) and the effect of agents on arrhythmia induced by ET-1. Methods :ET-1 was administered into the coronary ostia in rats and left anterior descending(LAD) of coronary artery in cats, respectively. The premature ventricular contraction(PVC),ventricular tachycardia(VT) and ventricular fibrillation(VF) thus elicited were observed. Results: Incidence and severity of arrhythmia decreased in rats pretreated with 0.3~1.2 mg/kg superoxide dismutase-1(SOD-1) administered into the coronary ostia 5 min before ET-1 administration(P<0. 01). The antagonistic effects of SOD-1 on arrhythmia induced by ET-1 were dose-related. And the arrhythmia score in the group pretreated with SOD-1 0.1 mg/kg administered into proxial LAD was 0.20± 0.17, significantly lower than that in the ET-1 group in cats(5. 17±1. 60,P<0. 05). Conclusion: Oxygen free radical is involved in arrhythmia caused by ET-l which could be antagonized by SOD-1.
分 类 号:R541.705[医药卫生—心血管疾病] R977.3[医药卫生—内科学]
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