卡马西平对离体蛙心心功能的影响
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摘要
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.
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.
引文
1杨宝峰.药理学第8版[M].北京:人民卫生出版社,2014,125.
2 周珏倩.卡马西平重症药疹危险因素的临床分析[J].药物不良反应杂志,2008(03):158-162.
3 陈新谦.新编药物学,17版[M].北京:人民卫生出版社,2011,215.
4 邹蓉.卡马西平在临床应用现状[J].大家健康(学术版),2016,10(05):172-173.
5 明振学.卡马西平在临床常见的药物不良反应分析[J].北方药学,2015,12(06):173-174.
6 郑倩.医学机能学实验,第2版[M].北京:科学出版社,2013,129-133.
7 陈宝,郑思嘉,吴传斌.卡马西平制剂的研究进展[J].国际药学研究杂志,2008,(01):46-49.
8 李世文.老药新用途,第6版[M].北京:河南科学技术出版社,2017,62-65.
9 吴铁.药理学,第1版[M].北京:科学出版社,2015,70.
10 阎飞.卡马西平的临床应用进展[J].中国实用精神病杂志,2010,13(21):72-73.
11 戴体俊.简明药理学[M].北京:人民卫生出版社,2014,96-97.
12 松熔,张兴凯,王建生,等.卡马西平治疗快速心律失常的临床观察[J].中国综合临床,2000,16(3):221-222.
2 周珏倩.卡马西平重症药疹危险因素的临床分析[J].药物不良反应杂志,2008(03):158-162.
3 陈新谦.新编药物学,17版[M].北京:人民卫生出版社,2011,215.
4 邹蓉.卡马西平在临床应用现状[J].大家健康(学术版),2016,10(05):172-173.
5 明振学.卡马西平在临床常见的药物不良反应分析[J].北方药学,2015,12(06):173-174.
6 郑倩.医学机能学实验,第2版[M].北京:科学出版社,2013,129-133.
7 陈宝,郑思嘉,吴传斌.卡马西平制剂的研究进展[J].国际药学研究杂志,2008,(01):46-49.
8 李世文.老药新用途,第6版[M].北京:河南科学技术出版社,2017,62-65.
9 吴铁.药理学,第1版[M].北京:科学出版社,2015,70.
10 阎飞.卡马西平的临床应用进展[J].中国实用精神病杂志,2010,13(21):72-73.
11 戴体俊.简明药理学[M].北京:人民卫生出版社,2014,96-97.
12 松熔,张兴凯,王建生,等.卡马西平治疗快速心律失常的临床观察[J].中国综合临床,2000,16(3):221-222.