摘要
静脉注射小檗碱(Ber)1～4mg/kg显著降低缺血再灌注心律失常的发生率,明显抑制心肌LPO含量的异常升高。Ber 1、3和10μmol/L使肛尾肌Phe量效曲线平行右移,最大反应不变,Iog(x-1)对-log[B]作田的回归斜率为-1.06,表现为竞争性拮抗作用;但使心肌Phe量效曲线左移。Ber 30μmol/L明显抑制缺氧再给氧所致迟后除极,完全消除异常电活动。故Ber抗缺血再灌注心律失常作用的重要机理在于阻止心肌氧自由基的损害和迟后除极的产生,西与α_1受体无关。
Berberine(Ber, 1～4 mg/kg, iv.) significantly reduced the incidence of cardiac arrhythmias and myocardial malondialdehyde content due to reperfusion of the ischsmic myocardium in rats. In isolated rat anococcygeous muscles, Bar 1, 3 and 10 μmol/L shifted tha concentration-effect curves for phenylephrine to the right parallelly without altering the maximal response. When plotting log (E/E'-1) against -log[B], its slope was -1.06. In isolated rat ventricular muscles, Ber 1,3 and 10 μmol/L shifted the concentration-effect curves for phenylephrine to the left and intensified its maximal response. Bar 30 μmol/L was found to be able to block delayed after-depolarization and to stop abnormal automatic activity. The results indicate that antagonistic effects of Bar are duo to the depression of delayed after-depolarization and prevention of free radical injury without involvement of the cardiac a_1-adrenoceptors.
出处
《中国循环杂志》
CSCD
1992年第5期440-444,共5页
Chinese Circulation Journal
关键词
小檗碱
心律失常
再灌注
Berberine
Ischemic reperfusion
Cardiac arrhythmias
Free radicals
α_1-Adrenoceptors
Delayed after-depolarization
Anococcygeous muscle
Ventricular muscle
