Pinto J M, Yuan F, Wasserlauf B J, Bassett A L, Myerburg R J
Department of Medicine, University of Miami School of Medicine, Florida 33101-6189, USA.
J Cardiovasc Electrophysiol. 1997 May;8(5):548-60. doi: 10.1111/j.1540-8167.1997.tb00823.x.
Abnormal action potentials in myocytes adjacent to > 2-month-old feline LV myocardial infarcts (MI) may reflect alterations in Ca2+ currents (Ica).
We compared ICa, at 36 degrees C, in subendocardial myocytes isolated from areas adjacent to MI and to ICa in cells from remote areas (> 4 mm away; REM) and control cells from similar regions in normal hearts. Control (CON) myocytes had membrane capacitance of 234 +/- 10 pF (n = 81 cells) compared to 305 +/- 14 pF in REM (71 cells; P < 0.05 from CON) and 237 +/- 11 pF (n = 55 cells) in MI (not different from CON). From Vh = -40 mV; peak ICa elicited by test potentials (-35 to +70 mV) were significantly larger in CON (-1746 +/- 123 pA) and REM (-1795 +/- 142 pA) compared to MI (-1352 +/- 129 pA) (P < 0.05). Peak ICa density was significantly reduced in REM (-6.0 +/- 0.4 pA/pF) or MI (-5.7 +/- 0.4 pA/pF, P < 0.05) compared to CON (-7.5 +/- 0.4 pA/pF). Double exponential ICa decay was similar among groups. Half-inactivation potential (V0.5) was significantly shifted (hyperpolarizing direction) for MI (-29.1 +/- 2.6 mV) and REM (-24.6 +/- 1.2 mV) myocytes compared to -20.3 +/- 1.0 mV in CON. MI slope factor (k; 9.0 +/- 0.5) was significantly different from CON (6.8 +/- 0.3) and REM (7.3 +/- 0.4). No differences in time course of recovery from inactivation were noted. Five millimolar Ba2+o produced significant increases in ICa in CON and REM but an attenuated response in MI. Bay K8644 (1 microM) produced similar ICa increase in all groups. ICa increase due to isoproterenol (1 microM) in MI and REM was half that in CON, but there were no differences in increased ICa responses among groups following phenylephrine (10 microM).
Reduced ICa density in REM reflects cell hypertrophy, whereas altered ICa of MI may reflect altered channel structure and/or function.
在超过2个月大的猫左心室心肌梗死（MI）附近的心肌细胞中，异常动作电位可能反映钙电流（Ica）的改变。
我们比较了在36℃时，从MI附近区域分离的心内膜下心肌细胞的Ica与远离MI区域（>4mm；REM）的细胞以及正常心脏相似区域的对照细胞的Ica。对照（CON）心肌细胞的膜电容为234±10pF（n = 81个细胞），而REM心肌细胞的膜电容为305±14pF（71个细胞；与CON相比P < 0.05），MI心肌细胞的膜电容为237±11pF（n = 55个细胞）（与CON无差异）。从静息电位（Vh）=-40mV开始；测试电位（-35至+70mV）诱发的Ica峰值在CON（-1746±123pA）和REM（-1795±142pA）中显著大于MI（-1352±129pA）（P < 0.05）。与CON（-7.5±0.4pA/pF）相比，REM（-6.0±0.4pA/pF）或MI（-5.7±0.4pA/pF，P < 0.05）中的Ica峰值密度显著降低。双指数Ica衰减在各组之间相似。与CON中的-20.3±1.0mV相比，MI（-29.1±2.6mV）和REM（-24.6±1.2mV）心肌细胞的半失活电位（V0.5）显著向超极化方向偏移。MI的斜率因子（k；9.0±0.5）与CON（6.8±0.3）和REM（7.3±0.4）显著不同。未观察到失活恢复时间过程的差异。5mM的细胞外钡离子（Ba2+o）使CON和REM中的Ica显著增加，但MI中的反应减弱。Bay K8644（1μM）在所有组中产生相似的Ica增加。MI和REM中异丙肾上腺素（1μM）引起的Ica增加是CON中的一半，但去氧肾上腺素（10μM）后各组Ica增加反应无差异。
REM中Ica密度降低反映细胞肥大，而MI中Ica改变可能反映通道结构和/或功能改变。
