TRANSIENT OUTWARD CURRENT IN HUMAN VENTRICULAR MYOCYTES OF SUBEPICARDIAL AND SUBENDOCARDIAL ORIGIN

TRANSIENT OUTWARD CURRENT IN HUMAN VENTRICULAR MYOCYTES OF SUBEPICARDIAL AND SUBENDOCARDIAL ORIGIN
复制标题

DOI:
10.1161/01.res.75.3.473
复制
发表时间:
1994-09-01
影响因子:
20.1
通讯作者:
RAVENS, U
RAVENS, U
中科院分区:
医学1区
文献类型:
--
作者:
WETTWER, E;AMOS, GJ;RAVENS, U

文献摘要

被引文献

相似文献

在各种哺乳动物中,由于瞬时外向电流(I-to)的差异,心脏壁内动作电位的形状各不相同。在人心室肌细胞中存在一个突出的I-to,但细胞尚未根据其原始定位进行分离。从分离的心外膜下和内膜下组织中分离出人心室肌细胞,并研究了I-to的区域变化。心外膜下细胞的I-to大于心内膜下细胞。在+60 mV下,心外膜下细胞的电流密度为7.9+/-0.7 pA/pF(n=28),内膜下细胞的电流密度为2.3+/-0.3 pA/pF(n=16)。当比较移植后衰竭和非衰竭供体心脏的细胞时,心外膜下细胞的I-to没有差异;然而,来自非衰竭心脏的内膜下细胞的I-to较大。心内膜下细胞(+25.6 +/- 3.5 mV,n=15)的半数最大激活电位(V-0.5)比心外膜下细胞(+9.2 +/- 1.8 mV,n=28)更阳性。衰竭和非衰竭心脏的细胞之间的V-0.5没有差异。I-to失活在所有细胞类型中是相似的,并且独立于膜去极化(时间常数[tau]=在22 ℃下约60毫秒)。在所有细胞类型中,半数最大稳态失活的可能性相似。心外膜下细胞在-100 mV(tau=24+/-4毫秒,n=6)时I-to失活恢复较快,短暂超过对照值(过冲),在-40 mV时恢复较慢,无过冲(tau=638+/-91毫秒,n=6)。在内膜下细胞中,I-to在-100 mV下恢复,具有快相(tau=25毫秒)和慢相(tau = 328毫秒),并且在-100 mV下6秒后恢复不完全。总之,心外膜下和心内膜下细胞之间的I-to区域差异可能对心力衰竭期间的节律紊乱具有临床意义。
In various mammalian species, shapes of action potentials vary within the cardiac wall because of differences in transient outward current (I-to). A prominent I-to exists in human ventricular myocytes, but cells have not been separated according to their original localization. Human ventricular myocytes were isolated from separated subepicardial and subendocardial tissue, and regional variations in I-to were studied. I-to was larger in subepicardial than subendocardial cells. Current density at +60 mV was 7.9+/-0.7 pA/pF (n=28) in subepicardial cells and 2.3+/-0.3 pA/pF (n=16) in subendocardial cells. When cells from explanted failing and nonfailing donor hearts were compared, I-to was not different in subepicardial cells; however, it was larger in subendocardial cells from nonfailing hearts. The potential of half-maximal activation (V-0.5) was more positive in subendocardial cells (+25.6 +/- 3.5 mV, n=15) than in subepicardial cells (+9.2 +/- 1.8 mV, n=28). There was no difference in V-0.5 between cells from failing and nonfailing hearts. I-to inactivation was similar in all cell types and independent of membrane depolarization (time constant [tau]=approximate to 60 milliseconds at 22 degrees C). The potential of half-maximal steady-state inactivation was similar in all cell types. Recovery from inactivation of I-to was fast in subepicardial cells at -100 mV (tau=24+/-4 milliseconds, n=6), exceeding control values transiently (overshoot), and slow at -40 mV without overshoot (tau=638+/-91 milliseconds, n=6). In subendocardial cells, I-to recovered at -100 mV with a fast phase (tau=25 milliseconds) and a slow phase (tau-328 milliseconds), and recovery was not complete after 6 seconds at -100 mV. In conclusion, regional differences in I-to between subepicardial and subendocardial cells may have clinical implications with respect to rhythmic disturbance during heart failure.