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作 者:赵临[1] 尹永强[1] 吴红[1] 康毅[1] 娄建石[1]
出 处:《中国新药与临床杂志》2013年第4期311-314,共4页Chinese Journal of New Drugs and Clinical Remedies
基 金:国家自然科学基金资助项目(30672458)
摘 要:目的观察牛磺酸镁配合物(TMCC)对哇巴因致大鼠心室肌细胞心律失常钠电流(INa)的作用。方法采用酶解法分离大鼠单个心室肌细胞。5μmol.L-1哇巴因诱发细胞水平心律失常,实验分为正常组,100、200、400μmol.L-1TMCC组,胺碘酮(24.24μmol.L-1)组,哇巴因(5μmol.L-1)组,哇巴因+100、200、400μmol.L-1TMCC组,哇巴因+胺碘酮组。采用全细胞膜片钳技术,在电压钳模式下记录INa的变化。结果与正常组INa密度(46.78±1.37)pA.pF-1相比,100、200、400μmol.L-1TMCC组INa密度呈浓度依赖性降低,分别为(42.42±4.75)pA.pF-1、(39.71±1.63)pA.pF-1、(37.59±4.75)pA.pF-1(P<0.05),胺碘酮组电流密度减少到(32.27±1.68)pA.pF-1(均P<0.05)。哇巴因组INa密度为(35.33±1.29)pA.pF-1,哇巴因+100μmol.L-1TMCC组能显著增加哇巴因诱导INa的减少,哇巴因+胺碘酮组INa密度减小到(28.47±1.65)pA.pF-1(均P<0.05)。结论 INa是TMCC抗心律失常作用的离子靶点之一,100μmol.L-1TMCC能够恢复哇巴因减少的INa,作用效果优于胺碘酮。[ ABSTRACT] AIM To investigate the effect of taurine magnesium coordination abnormal sodium current (/No) induced by ouabain in rat cardiomyocytes. METHODS compound (TMCC) on Enzymatic dissociation was used to get single rat cardiomyocyte cells. The experiment groups included the normal group, 100, 200, 400 μmol·L-1 TMCC groups, amiodarone (24.24 μmol·L-1) group, ouabain (5μmol·L-1) group, ouabain + 100, 200, 400 μmol·L-1 TMCC groups, ouabain + amiodarone group. Whole-cell patch clamp was used to record INa in normal cardiomyocytes and abnormal INa induced by ouabain. RESULTS Compared with the normal group 4.75) , INa was blocked by 100, 200, 400μmol·L-1 TMCC in a concentration-dependent manner (42.42 ± pA-pF-1, (39.71 ± 1.63) pA-pF-1, (37.59 ± 4.75) pA.pF-1 vs. (46.78 ± 1.37) pA.pF-1, (P 〈 0.05) . INa was decreased to (32.27 ± 1.68) pA pF-1 in the amiodarone group. INa of the ouabain group was (35.33 ± 1.29) pA pF-l. IN, could be restore in ouabain + 100 μmol·L-1 TMCC group (P 〈 0.05) , and decrease in the ouabain + amiodarone group (28.47 ± 1.65) pA.pF-1 (P 〈 0.05) . CONCLUSION IN, is one of ion targets of antiarrhythmia effect by TMCC. 100 μmol·L-1 TMCC can restore INa, which is decreased by ouabain, and the effect is better than amiodarone.
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