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急性心肌梗死对心室肌细胞钾电流的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2003年第1期
页码:
1-3
栏目:
实验研究
出版日期:
2003-01-01

文章信息/Info

Title:
Alteration of transient outward K+ current and inward rectifier K+ current in ventricular myocytes from acute infarcted heart
作者:
丁超; 何振山; 齐书英; 崔俊玉; 石巧; 杨丽; 胡丽叶
解放军白求恩国际和平医院心内科,河北 石家庄050082
Author(s):
DINGChao; HEZhen-shan; QIShu-ying; CUIJun-yu; SHIQiao; YANGLi; HULi-ye
DepartmentofCardiology,BethuneInternationalPeaceHospitalofPLA,Shijiazhuang,Hebei050082,Chin
关键词:
心肌梗塞; 瞬时外向钾电流; 内向整流性钾电流; 心室肌; 膜片钳
Keywords:
myocardeial infarction; transient outward K+ current; inward rectifier K+ current; ventricular myocytes; patch clamp
分类号:
R541.7;R542
DOI:
-
文献标识码:
A
摘要:
目的:研究急性心肌梗死(AMI)心室肌细胞瞬时外向钾电流(Ito)和内向整流性钾电流(IK1)的变化。方法:采用结扎兔冠状动脉左前降支的方法建立AMI动物模型,应用膜片钳全细胞记录方法,记录比较AMI后1周心外膜梗死区心肌细胞Ito和IK1的变化。结果:心梗组Ito明显下降,I-V曲线明显下移。指令电位为+60mV时,Ito在心梗组为1.08±0.24nA(n=12),与对照组(2.09±0.39nA,n=16)相比,显著下降,P<0.01;心梗组IK1与对照组比较,明显下降,特别在超极化时。指令电位为-120mV时,心梗组IK1为3.01±0.49nA(n=11),对照组为4.12±0.51nA(n=10,P<0.05)。结论:AMI可引起心室肌细胞Ito和IK1的下降,从而导致动作电位平台期延长、复极异常,这可能是导致AMI后出现折返性室性心律失常的原因。
Abstract:
AIM: To study the change in transient outward K+ current(Ito) and inward rectifier K+ current (IK1) in cells from the epicardial border zone of the 1 week infarcted rabbit heart.METHODS:Rabbits were infarcted by ligation of the left anterior descending coronary artery.1 week later,Ito and IK1 were recorded by using patch-clamp techniques from infarcted heart(IZs) and compared with the noninfarcted heart(NZs).RESULTS:Ito(at+60mV) was significantly reduced in IZs(1.08±0.24nA,n=12) compared with NZs(2.09±0.39nA,n=16),P<0.01;IK1 (-120mV) was also significantly reduced in IZs(3.01±0.49nA,n=11) compared with NZs(4.12±0.51nA,n=10),P<0.05.CONCLUSION:There were changes in both Ito and IK1 in IZs,which changes might underlie the abnormallong transmembrane action potentials and repolarization of these arrhymogenic surviving ventricular fibers of the IZs.Thus contributing to reentrant arrhymias in the infarcted heart

参考文献/References

[1] Hamill OP, Marty A, Neher E, et al. Improved patch-clamp techniques for high-resolution current recording from cells and cell-free me mbrane patches [J] . Pflugers Arch, 1981, 391:85-100.

[2] Jeck C, Pinto JMB, Boyden PA, et al. Transient outward currents in subendocardial Purkinje myocytes surviving in the 24 and 48 h infarcted heart [J] . Circulation, 1995, 92:465-473.

[3] Lue WM, Boyden PA. Abnormal electrical properties of myocytes from chronically infarcted cannine heart.Alterations in Vmax and the transient outward current [J] . Circulation, 1992, 85:1175-1188.

[4] Pinto JMB, Boyden PA. Reduced inward rectifying and increased E4031 sensitive K+ channel functioin in arrhythmogenic subendocardial Purkinje myocytes from the infarcted heart [J] . J Cardiovasc Electrophysiol, 1998, 9:299-311.

[5] Kaprielian R, Wickenden AD, Kassiri Z, et al. Relationship between K+ channel down-regulation and [Ca]i in rat ventricular myocytes following myocardial infarction [J] . J Physiol, 1999, 517:229-245.

[6] Drouin E, Charpentier F, Gauthier C, et al. Electrophysiologic characteristics of cells spanning the left ventricular wall of human heart: evidence for presence of M cells [J] . J Am Coll Cardiol, 1995, 26:185-192.

[7] Aimond F, Alvarez JL, Rauzier JM, et al. Ionic basis of ventricular arrhymias in remodled rat during long term myocardial infarction [J] . Cardiovasc Res, 1999, 42:402-415.

备注/Memo

备注/Memo:
收稿日期：2002-01-23.
更新日期/Last Update: 2003-01-01