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.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
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
关键词
超氧化物歧化酶
内皮素
心律失常
superoxide dismutase
endothelin
arrhythmia
rats
cats
