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作 者:张殿新[1,2] 张荣庆[2] 程何祥[2] 黄岚[1] 王海昌[2] 郭文怡[2] 刘兵[2] 张清[2] 李伟杰[2] 秦涛[2]
机构地区:[1]第三军医大学新桥医院心内科 [2]第四军医大学西京医院心内科,西安710032
出 处:《中国临床医学》2005年第3期392-394,共3页Chinese Journal of Clinical Medicine
摘 要:目的:观察AngⅡ对人心房肌细胞膜钙通道电流的影响及卡维地洛的拮抗作用,为应用卡维地洛治疗房性心律失常提供实验基础。方法:急性分离单个人心房肌细胞,采用全细胞膜片钳方法记录L-型钙电流(LCaL)。实验分4组:对照组,AngⅡ(0.1μmol/L)组,卡维地洛(1μmol/L)组,AngⅡ+卡维地洛组。结果:与对照组相比,0.1μmol/LAngⅡ使人心房肌细胞膜LCaL峰值电流密度明显增加(-12.74±1.65vs-5.78±0.82pA/pF,P<0.05)。1μmol/L卡维地洛对人心房肌细胞膜ICa-L无明显影响(-5.72±0.77pA/pF).但可拮抗AngⅡ的作用;AngⅡ+卡维地洛组的ICa-L峰值电流密度(-8.03±0.84pA/pF)与AngⅡ组相比有显著差异(P<0.05)。结论:AngⅡ对人心房肌细胞具有明显的电生理学作用,0.1μmol/LAngⅡ可促进人心房肌细胞膜ICaL.卡维地洛可拮抗AngⅡ对人心房肌细胞膜ICaL的作用。Objective: To observe the effects of angiotensm Ⅱ(AngⅡ) on calcium channel current of human atrial myocyte and its antagonism by carvedilol, and to provide a laboratory basis for application of carvedilol to treat atrial arrhythmias. Methods: Single human atrial myocyte was isolated,and conventional whole-cell configuration of the patch-clamp technique was used to detect membrane ICa-L. The experiment comprised four groups, ie,control group, AngⅡ group, carvedilol group and AngⅡ + carvedilol group. Results: Compared with con trol group, Angll 0. 1 μmol/L significantly increased the peak density of ICa L in human atrial myocyte(-12. 74 ± 1.65 vs -5.78 ± 0.82 pA/ pF,P<0. 05). Carvedilol of 1 μmol/L had no significant effect on ICa L. in human atrial myocyte( - 5. 72 ± 0. 77)pA/pF. but it could antago mze the effects of Angll. In Angll + carvedilol group, the peak density of ICa-L was ( - 8. 03 ?0. 84)pA/pF, which had a significant difference compared with the Angll group(P<0. 05). Conclusion: Angll has significant electrophysiological effects on human atrial myocyte. Angll of 0. 1 μmol/L can significantly increase the peak density of ICa-L. Carvedilol can antagonize the effects of Angll on human atrial myocyte.
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