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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。
Intravenous injection of berberine (Ber) 1 ~ 4mg / kg significantly reduce the incidence of ischemia-reperfusion arrhythmia, significantly inhibited the abnormal increase in myocardial LPO levels. Ber 1, 3, and 10 μmol / L shifted the Phe dose-response curve of right anus tail muscle parallel to the right, with the maximum response unchanged. The regression slope of Iog (x-1) versus -log [B] was -1.06, indicating competitive antagonism Role; but left myocardial Phe dose-effect curve. Ber 30μmol / L obviously inhibited the delayed depolarization induced by hypoxia-reoxygenation and completely abolished the abnormal electrical activity. Therefore, Ber anti-ischemia and reperfusion arrhythmia an important mechanism is to prevent the damage of myocardial oxygen free radicals and delayed depolarization produced, West and α 1 receptor has nothing to do.