卡马西平对离体蛙心心功能的影响

Effects of carbamazepine on isolated frog hearts

目的:观察卡马西平对离体蛙心心肌收缩力和心率的影响及其初步机制。方法:根据斯氏蛙心插管方法,蛙心插管内液体恒定体积为1ml,以卡马西平溶液100μl对离体蛙心进行一次加药灌流,使其终浓度为10.58μmol·L^(-1)、21.16μmol·L^(-1)、42.32μmol·L^(-1),采用BL-420生物机能实验系统记录第2分钟内离体蛙心心率、心力峰峰值、心肌平均收缩力的变化;以乙酰胆碱100μl对离体蛙心进行一次加药灌流,使其终浓度为1mg·L^(-1)、以艾司洛尔100μl对离体蛙心进行一次加药灌流,使其终浓度为10 mg·L^(-1)、以乙酰胆碱与卡马西平溶液各50μl同时灌流离体蛙心,使乙酰胆碱和卡马西平终浓度分别为1mg·L^(-1)和21.16μmol·L^(-1)1、以艾司洛尔与卡马西平溶液各50μl同时灌流离体蛙心,使艾司洛尔和卡马西平终浓度分别为10 mg·L^(-1)和21.16μmol·L^(-1),记录第2分钟内离体蛙心心力峰峰值的变化。结果:10.58μmol·L^(-1)、21.16μmol·L^(-1)、42.32μmol·L^(-1)浓度的卡马西平溶液对蛙心心率无影响,但是可以增强离体蛙心心肌自发性收缩的心力峰峰值和平均收缩力(P<0.01),且具有一定浓度依赖性;21.16μmol·L^(-1)卡马西平可明显拮抗乙酰胆碱抑制蛙心心肌收缩峰峰值的作用(P<0.01),同时也可明显拮抗艾司洛尔抑制蛙心心肌收缩峰峰值的作用(P<0.01)。结论:卡马西平可以明显增强心肌收缩力,其机制可能与其兴奋β1受体、阻断M2受体有关。

Objective：To observe the effects and mechanisms of carbamazepine on heart rate and myocardial contractility of isolated frog hearts.Methods：According to the spa＇s frog heart intubation method,the constant volume of liquid in the frog heart cannula was 1 ml.And the isolated frog heart was full of C Masi Bing solution 100μl.The final concentration of carbamazepine was 10.58μmol·L^（-1）,21.16μmol·L^（-1）,and 42.32μmol·L^（-1）.The heart rate and peak of the frogs in the second minute were recorded by the BL-420 biological function experimental system.The changes of the peak value and the mean systolic force of the myocardium were achieved by an addition of acetylcholine 100μl to the isolated frog hearts with a final concentration of 1 mg·L^（-1）,and an addition of esmolol 100μl to the isolated frog heart.The final concentration was 10 mg·L^（-1）,and the 50μl of acetylcholine and C Masi Bing solution was administered to the isolated frog heart at the same time.The final concentration of acetylcholine and C Masi Bing was 1 mg·L^（-1） and 21.16μmol·L^（-1）,respectively,with each 50μl of esmolol and C Masi Bing solution at the same time.The final concentration of esmolol and C Masi Bing was 10 mg·L^（-1） and21.16μmol·L^（-1）,respectively.Results：Carbamazepine had no effect on the heart rate of frog in the concentration of10.58μmol·L^（-1）,21.16μmol·L^（-1）,42.32μmol·L^（-1）.But it could dose-dependently enhance the peak of spontaneous contraction and the mean contractility（P〈0.01）of the isolated frog hearts.Carbamazepine at the concentration of 21.16μmol·L^（-1） could obviously antagonize the inhibition of acetylcholine.Conclusion：Carbamazepine can obviously strengthen the myocardial contractility.The mechanism may be induced by excitingβ1 receptors and blocking the M2 receptors.