Peters N S, Green C R, Poole-Wilson P A, Severs N J
Department of Cardiac Medicine, National Heart and Lung Institute, London, England.
Circulation. 1993 Sep;88(3):864-75. doi: 10.1161/01.cir.88.3.864.
Gap junctions are a determinant of myocardial conduction. Disturbances of gap-junctional content may account for abnormalities of impulse propagation, contributing to the arrhythmic tendency and mechanical inefficiency of ischemic and hypertrophied myocardium. The aim of this study was to characterize gap junction organization in normal human ventricular myocardium and to establish whether abnormalities exist in myocardium of chronically ischemic and hypertrophied hearts.
Cardiac gap-junctional connexin43 antibodies and confocal microscopy were used in a quantitative immunohistochemical study of surgical myocardial samples to explore the structural basis of electromechanical ventricular dysfunction in chronic ischemic and hypertrophic heart diseases. Normal adult human left ventricular myocardium had a gap-junctional surface area of 0.0051 micron2/micron3 myocyte volume; gap junctions were confined to intercalated disks, of which there was a mean of 11.6 per cell. The right ventricle showed similar gap junction surface area. Left ventricular myocardium from ischemic hearts (distant from any fibrotic scarring), despite normal numbers of intercalated disks per cell, had a reduced gap junction surface area (0.0027 micron2/micron3; P = .02), as did hypertrophied myocardium (0.0031 micron2/micron3; P = .05). The cardiac myocytes in the pathological tissues were larger than normal, and estimated gap-junctional content per cell was reduced in ischemic ventricle (P = .02) compared with normal.
Gap junctions in normal adult human working ventricular myocardium occupy an area of 0.0051 micron2/micron3 myocyte volume. This surface area is reduced in ventricular myocardium from hearts subject to chronic hypertrophy and ischemia, despite a normal number of intercellular abutments, and this alteration may contribute to abnormal impulse propagation in these hearts.
缝隙连接是心肌传导的一个决定因素。缝隙连接成分的紊乱可能导致冲动传播异常，进而导致缺血性和肥厚性心肌的心律失常倾向及机械效率低下。本研究的目的是描述正常人心室心肌中缝隙连接的组织结构，并确定慢性缺血和肥厚心脏的心肌中是否存在异常。
采用心脏缝隙连接蛋白43抗体和共聚焦显微镜对手术获取的心肌样本进行定量免疫组织化学研究，以探讨慢性缺血性和肥厚性心脏病中机电性心室功能障碍的结构基础。正常成人左心室心肌的缝隙连接表面积为0.0051平方微米/立方微米心肌细胞体积；缝隙连接局限于闰盘，每个细胞平均有11.6个闰盘。右心室显示出相似的缝隙连接表面积。缺血心脏的左心室心肌（远离任何纤维化瘢痕），尽管每个细胞的闰盘数量正常，但缝隙连接表面积减少（0.0027平方微米/立方微米；P = 0.02），肥厚心肌也是如此（0.0031平方微米/立方微米；P = 0.05）。病理组织中的心肌细胞比正常细胞大，与正常相比，缺血心室中每个细胞的缝隙连接含量估计减少（P = 0.02）。
正常成人心室工作心肌中的缝隙连接占心肌细胞体积的面积为0.0051平方微米/立方微米。尽管细胞间连接数量正常，但慢性肥厚和缺血心脏的心室心肌中该表面积减少，这种改变可能导致这些心脏中冲动传播异常。
