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作 者:王增夏 解金红[2] 王贺[2] 赵亚楠 曹英杰[3] 关怀敏[2] Wang Zengxia;Xie Jinhong;Wang He(Henan University of Chinese Medicine,Zhengzhou 450000;Heart Center of the First Affiliated Hospital of Henan University of CM,Zhengzhou 450000)
机构地区:[1]河南中医药大学,郑州450000 [2]河南中医药大学第一附属医院心脏中心,郑州450000 [3]河南中医药大学第一附属医院药剂科,郑州450000
出 处:《安徽医科大学学报》2020年第1期65-69,共5页Acta Universitatis Medicinalis Anhui
基 金:国家自然科学基金(编号:81473508、81603431)
摘 要:目的观察胺碘酮对H2O2损伤大鼠单个心房肌细胞L型钙通道电流(ICaL)的作用,探讨胺碘酮对H2O2损伤后的成年SD大鼠心房肌细胞电生理特性的影响。方法使用Langendorff灌流装置系统,急性酶解法分离成年SD大鼠心房肌细胞,使用100μmol/L H2O2损伤大鼠心房肌细胞,采用全细胞膜片钳技术记录心房肌细胞ICaL,观察空白组、H2O2组、胺碘酮组ICaL密度及电生理特性的变化。结果空白组ICaL密度为(-4.99±0.35) pA/pF;H2O2组ICaL密度为(-6.97±0.60) pA/pF;胺碘酮组ICaL密度为(-3.16±0.20) pA/pF。结论 H2O2损伤大鼠心房肌细胞可使ICaL增加,胺碘酮使ICaL降低,胺碘酮可通过抑制通道的激活和失活后的恢复而降低ICaL。Objective To observe the effect of amiodarone on L-type calcium channel current in rats single atrial myocytes damaged by H2O2 and investigate the effect of amiodarone on electrophysiological characteristics of atrial myocytes. Methods The myocytes were isolated from rats atrial tissues by Langendorff perfusion apparatus,which were randomly divided into three groups: the control group(no treatment),the H2O2 group(cells cultured with 100 μmol/L H2O2 for 0.5 hour),the amiodarone group(cells cultured with 100 μmol/L H2O2 for 0.5 hour and then cultured with amiodarone for 0.5 hour). Whole cell patch clamp technique was used to record ICaL. Results Control group the peak current of ICaL density was(-4.99±0.35) pA/pF;H2O2 group increased the peak current of ICaL density to(-6.97±0.60) pA/pF;Amiodarone group reduced the peak current of ICaL density to(-3.16±0.20) pA/pF.Conclusion Amiodarone can reduce ICaL by inhibiting channel activation and recovery after inactivation.
分 类 号:R337.5[医药卫生—人体生理学]
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