我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

胺碘酮对家兔急性心肌缺血左室跨壁复极离散度的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第5期
页码:
561-564
栏目:
基础研究
出版日期:
2011-10-25

文章信息/Info

Title:
Effect of amiodarone on electrophysiological characteristics in acute ischemic rabbit left ventricle
作者:
刘 峰1; 周 筠2; 孙小霞1; 兰燕平1; 杜克莘3; 于晓江2; 崔长琮1
西安交通大学医学院:1.第一附属医院心内科，2.药理学系,3.机能中心，陕西 西安 710061
Author(s):
LIU Feng1;  ZHOU Jun2;  SUN Xiao-xia1;  LAN Yan-ping1;  DU Ke-xin3;  YU Xiao-jiang2;  CUI Chang-cong1
Department of Pharmacology, Medical College, Xi’an Jiaotong University, Xi’an 710061, Shaanxi, China
关键词:
心肌缺血; 动作电位时程; 跨壁复极离散度; 心律失常; 家兔
Keywords:
cardiac ischemia;  action potential duration;  transmural dispersion of repolarization;  arrhythmia
分类号:
R541.73
DOI:
-
文献标识码:
A
摘要:
目的:探讨胺碘酮对家兔急性缺血左室心肌楔形组织块电生理特性和跨壁复极离散度（TDR）的影响及其抗缺血心律失常的机制。方法： 建立冠状小动脉灌注家兔左室心肌楔形组织块模型，应用浮置玻璃微电极和心电图同步记录技术，观察急性无灌流心肌缺血时，胺碘酮对内外层心肌细胞的动作电位时程（APD）、TDR和心律失常的影响。结果： ①左心室楔形组织块停止灌注后，胺碘酮组内、外膜心肌细胞的APD较对照组明显延长[(228±19) ms vs.(212±6) ms,P<0.05］，且外膜APD的延长更明显[(203±15) ms vs.(180±5) ms,P<0.05］。②急性缺血各时间段，APD较缺血前均缩短，以外膜APD缩短更明显，导致TDR增大。用药后TDR明显短于对照组。结论： 胺碘酮可延长内、外膜心肌细胞的APD，且外膜APD的延长明显，并可减小急性缺血心肌的TDR，这可能是其抗心律失常机制的细胞电生理基础。
Abstract:
AIM:To study the transmural dispersion of repolarization (TDR) and electrophysiological characteristics in left ventricle of rabbits during acute ischemia and to explore the mechanism of the antiarrhythmic effect of amiodarone. METHODS: The effects of amiodarone in acute nonflow cardiac ischemia on action potential duration (APD) of epi- and endomyocardial cells, TDR and arrhythmia were observed using floating glass microelectrode and recording electrocardiogram. RESULTS: 1) After 5, 10, and 15 min of acute ischemia, in rabbit left ventricular wedge preparation, amiodarone produced a greater prolongation of APD in cardiac cells of the endo- and epicardium ［(228±19) msec and (203±15) msec］ respectively, compared with control group ［(212±6) msec and (180±5) msec］ respectively, especially in epicardium. 2) During acute ischemia, two-layer cells APD shortened and the shortening in epicardium was greater than that of the endocardium, thus leading to increased TDR. TDR in amiodarone group was significantly lower than control group. CONCLUSION: Amiodarone causes a prolongation in APD and a decrease in TDR in arterially perfused rabbit left ventricular wedge preparation in acute cardiac ischemia. This may be an important cellular electrophysiological foundation of anti-arrhythmia mechanism.

参考文献/References

[1]Rubulis A,Jensen J,Lundahl G,et al.Ischemia induces aggravation of baseline repolarization abnormalities in left vent ricular hypert rophy: a delete rious interaction[J].J Appl Physiol,2006, 101(1):102-110.

[2]苏显明,王东琦,于忠祥,等.急性心肌缺血犬心肌细胞瞬时外向钾电流和跨壁复极离散度变化致心律失常机制研究[J].临床心血管病志,2006,22(3):140-144.

[3]姚青海,吴尚勤,孙 姗,等. 急性缺血对兔左心室跨壁复极离散度的影响[J].中华心律失常学杂志,2006,10(5):370-370.

[4]Yan GX, Joshi A,Guo D,et al.Phase 2 reentry as a trigger to initiate ventricular fibrillation during early acute myocardial ischemia[J].Circulation,2004,110(9):1036-1041.

[5]周 筠,臧伟进,杜克莘,等. 胺碘酮对犬左心室M细胞动作电位和心室跨壁复极离散度的影响[J].心脏杂志,2006,18(2):155-158.

[6]陈哲新.胺碘酮抗心律失常临床应用进展[J].临床医药实践,2009,18(5):323-325.

[7]魏立业,夏 岳,戚国庆.胺碘酮或氯沙坦及两者合用对急性心房颤动患者心房重构的干预[J].临床心血管病杂志,2008,24(3):162-164.

[8]Furukawa T,Kimura S,Furukawa N,et al.Role of cardiac ATP-regulated potassium channels in differential responses of endocardial and epicarial cells to ischemia[J].Circ Res,1991,68(6):1693-1702.

[9]Kimura S,Bassett AL,Furukawa T,et al.Difference in the effect of metabolic inhibition on action potential and calcium currents in endocardial and epicardial cells[J].Circulation,1991,84(2):768-777.

[10]Tanabe T,Usui K,Kusuzaki S,et al.Differences in refractory period response of canine subendocardium and subepicardium to bunazosin, an alpha1-adrenoceptor antagonist, and propranolol during myocardial ischemia[J].J Cardiovasc Pharmacol,1997,30(6):824-830.

[11]Carmeliet E.Cardiac ionic currents and acute ischemia from channels to arrhythmia[J].Physiological Review,1999,79(3):917-1017.

[12]Vermeulen JT,Tan HL,Rademaker H,et al.Electrophysiologic and extracellular changes during acute ischemia in failing and normal rabbit myocardium[J].J Mol Cell Cardiol,1996,28(1):123 -131.

备注/Memo

备注/Memo:
收稿日期：2011-01-05.基金项目：国家自然科学基金重点项目资助（30930105）；中央高校基本科研业务费专项资金资助（XJJ20100036） 通讯作者：周筠，副教授，主要从事心血管药理学的研究Email:jzhou829@yahoo.com.cn 作者简介：刘峰，主治医师，硕士Email:lfhappy8@126.com
更新日期/Last Update: 2011-11-03