Licata A, Aggarwal R, Robinson R B, Boyden P
Department of Pharmacology, Columbia University, New York, NY, USA.
Cardiovasc Res. 1997 Feb;33(2):341-50. doi: 10.1016/s0008-6363(96)00246-5.
Myocytes that survive in the epicardial border zone of the healing canine infarcted heart provide the substrate for inducible reentrant ventricular arrhythmias. These myocytes have been shown to have altered Ca2+ currents which could impact on Cai homeostasis in these cells.
To directly measure and compare intracellular Ca2+ transients and cell shortening in myocytes dispersed from control noninfarcted hearts with those from epicardial border zone of 5 day infarcted canine hearts using the Ca2+ sensitive indicator fura-2/AM. Studies were designed to determine and compare the effects of rate and premature stimulation on intracellular Ca2+ in the two cell types.
Epicardial cells from noninfarcted hearts (1) exhibited an increase in amplitude of the fura-2 ratio with decreasing pacing cycle length (CL), while cells from the infarcted heart showed the opposite effect; (2) showed more marked acceleration of relaxation of the Cai transient with decreasing CL than myocytes from the infarcted heart; (3) exhibited little or no post rest potentiation in contrast to cells from the infarcted heart; and (4) showed a more rapid recovery during restitution protocols than cells from the infarcted heart. Cell shortening differences were also observed between cell populations in that most cells from the infarcted zone did not show any degree of cell shortening despite the reasonable intracellular Ca2+ transient.
The handling of intracellular Ca2+ in myocytes that have survived in the epicardial border zone is very different from that of normal epicardial myocytes suggesting that there may exist marked heterogeneity in intracellular Ca2+ handling in cells in the in situ healing infarcted heart. Electrophysiologic implications of these findings are discussed.
在愈合的犬梗死心脏的心外膜边缘区存活的心肌细胞为诱发性折返性室性心律失常提供了基质。这些心肌细胞已被证明具有改变的Ca2+电流，这可能会影响这些细胞内的Cai稳态。
使用Ca2+敏感指示剂fura-2/AM，直接测量并比较从对照非梗死心脏分散的心肌细胞与5天梗死犬心脏的心外膜边缘区心肌细胞的细胞内Ca2+瞬变和细胞缩短情况。研究旨在确定并比较心率和过早刺激对这两种细胞类型细胞内Ca2+的影响。
来自非梗死心脏的心外膜细胞（1）随着起搏周期长度（CL）的缩短，fura-2比率的幅度增加，而来自梗死心脏的细胞则表现出相反的效果；（2）与来自梗死心脏的心肌细胞相比，随着CL的缩短，Cai瞬变的松弛加速更为明显；（3）与来自梗死心脏的细胞相比，几乎没有或没有静息后增强；（4）在恢复方案期间比来自梗死心脏的细胞恢复更快。在细胞群体之间也观察到细胞缩短的差异，即来自梗死区的大多数细胞尽管有合理的细胞内Ca2+瞬变，但未显示任何程度的细胞缩短。
在心外膜边缘区存活心肌细胞内Ca2+的处理与正常心外膜心肌细胞非常不同，这表明在原位愈合梗死心脏的细胞内Ca2+处理中可能存在明显的异质性。讨论了这些发现的电生理意义。
