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作 者:张文杰[1] 宣丽颖[1] 贺永峰[1] 曹玉凤[1] 赵春燕[1] 谭文佳[1]
机构地区:[1]吉林大学基础医学院生理学教研室,吉林长春130021
出 处:《吉林大学学报(医学版)》2009年第3期427-430,共4页Journal of Jilin University:Medicine Edition
基 金:吉林省科技厅科研基金资助课题(200705367)
摘 要:目的:观察1-磷酸鞘氨醇(S1P)对豚鼠心室肌细胞单通道延迟整流钾电流的影响,探讨S1P在室性心律失常中的作用。方法:Langendorff离体心脏逆向灌流法分离豚鼠心室肌细胞,随机选取心室肌细胞分为正常对照组、S1P(2.2μmol.L-1)组及S1P(2.2μmol.L-1)+Suramin(200μmol.L-1)组。应用细胞贴附式记录方式记录心室肌细胞延迟整流钾电流(IK)。结果:细胞贴附式记录及通道动力学分析,S1P组心室肌细胞通道开放时间及开放概率明显低于正常对照组(P<0.05),关闭时间明显高于正常对照组(P<0.05);S1P+Suramin组通道开放时间、开放概率以及关闭时间与正常对照组比较差异无显著性(P>0.05)。结论:S1P抑制心室肌细胞延迟整流钾电流外流,该作用通过缩短开放时间、延长关闭时间、降低开放概率实现,且通过膜受体介导。Objective To investigate the effects of sphingosine-l-phosphate (S1P) on single-aisle delayed rectifier K^+ current in heart ventricular myocytes of guinea pigs Methods The Langendorff perfusion method was used and explore the role of S1P in ventricular arrhythmia. to isolate ventricular myocytes of guinea pigs and the ventricular myocytes were randomly divided into normal control group, S1P (2.2μmol·L^-1) group and S1P (2.2 μmol·L^-1)+ Suramin (200 μmol·L^-1) group. The current of delayed rectifier potassium channel was recorded by cell-attached recording. Results Compared with normal control group by cell-attached recording and respecting the channel dynamics, the opening dwell time and the opening probability decreased, while the closing dwell time increased in S1P group (P〈0.05) ; and there was no obviously difference between S1P+Suramin group and normal control group while respecting the channel dynamics (P〉 0.05). Conclusion S1P inhibits delayed rectifier potassium current of ventricular myocytes of guinea pigs by shortening its opening dwell time, extending its closing dwell time and reducing the opening probability. And the functions above are mediated by membrane receptor.
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