ALTERATIONS OF K+ CURRENTS IN ISOLATED HUMAN VENTRICULAR MYOCYTES FROM PATIENTS WITH TERMINAL HEART-FAILURE
ALTERATIONS OF K+ CURRENTS IN ISOLATED HUMAN VENTRICULAR MYOCYTES FROM PATIENTS WITH TERMINAL HEART-FAILURE
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DOI：
10.1161/01.res.73.2.379
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发表时间：
1993-08-01
影响因子：
20.1
通讯作者：
ERDMANN, E
中科院分区：
文献类型：
--
作者：
BEUCKELMANN, DJ;NABAUER, M;ERDMANN, E
动作电位的延长被假定为严重心力衰竭患者心脏舒张期松弛改变的一个主要原因。为了研究终末期心力衰竭中这种动作电位延长的电生理基础，在从16颗接受移植的患者的移植心脏中分离出的单个心室肌细胞中记录了K⁺电流。将患病心脏的结果与从6颗未患病的供体心脏中分离出的心室细胞进行了比较。心力衰竭患者的细胞动作电位时程显著延长。在大多数细胞中几乎检测不到延迟整流K⁺电流，并且如果能够记录到，在患病和未患病细胞中该电流都非常小。当将电流根据细胞表面积进行标准化时，与正常对照细胞相比，患病细胞中内向整流K⁺电流的平均电流密度显著降低（在 -100 mV时超极化，-15.9±2.2对 -9.0±1.2 μA/cm²；P<0.05）。
Prolongation of the action potential has been postulated to be a major reason for the altered diastolic relaxation of the heart in patients with severe heart failure. To investigate the electrophysiological basis for this action potential prolongation in terminal heart failure, K+ currents were recorded in single ventricular myocytes isolated from 16 explanted hearts of patients undergoing transplantation. Results from diseased hearts were compared with ventricular cells isolated from six undiseased donor hearts. Action potential duration was significantly prolonged in cells from patients with heart failure. A delayed rectifier K+ current was hardly detectable in most cells, and if it could be recorded, it was very small in both diseased and undiseased cells. When currents were normalized for cell surface area, the average current density of the inward rectifier K+ current was significantly reduced in diseased cells when compared with normal control cells (hyperpolarization at -100 mV, -15.9+/-2.2 vs -9.0+/-1.2 muA/cm2; P