Profound structural alterations of the extracellular collagen matrix in postischemic dysfunctional ("stunned") but viable myocardium.
Profound structural alterations of the extracellular collagen matrix in postischemic dysfunctional ("stunned") but viable myocardium.
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缺血后功能失调（“震惊”）但存活的心肌中细胞外胶原基质的深刻结构改变。
DOI：
10.1016/s0735-1097(87)80137-7
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发表时间：
1987
影响因子：
24
通讯作者：
Eng,C
中科院分区：
文献类型：
--
作者：
Zhao,MJ;Zhang,H;Robinson,TF;Factor,SM;Sonnenblick,EH;Eng,C
使用扫描、常规和高压透射电子显微镜和光学显微镜对“震惊”的心肌进行细胞外胶原基质的超微结构研究。左冠状动脉前降支 12 次连续 5 分钟闭塞，中间间隔 10 分钟再灌注，造成局部心肌功能障碍。最后 90 分钟的再灌注期记录了持续的心肌功能障碍。在最后的再灌注期结束时，通过声测微计测量的收缩期缩短百分比显着降低至基线的 35 ± 9%。然后对心脏进行灌注固定，并从对照区域和击晕区域采集样本。在击晕区域中没有发现与不可逆细胞损伤相关的变化。然而，震惊区域的扫描电子显微镜显示，细胞外胶原基质发生了深刻的结构变化。胶原蛋白线变得粗糙、展开且不连续。肌细胞表面经常可见线性凹槽，表明胶原索完全丧失。肌细胞周围通常致密的胶原蛋白编织变得不规则或消失。肌细胞到肌细胞的支柱稀疏且经常缺失，残留的结节状或块状结构表明断裂。击晕区域的高压电子显微镜显示，胶原蛋白支柱不连续，呈空泡状，尖端呈圆形。震惊组织的银染色切片的光学显微镜显示大片片状区域不含银，表明不存在胶原蛋白基质。在每次连续冠状动脉闭塞期间，收缩期膨胀百分比逐渐增加，表明心肌顺应性增加。这些结果表明，心肌胶原基质因可逆性缺血性细胞损伤而严重受损。顿挫心肌中较大的心肌顺应性和较低的有效收缩力可能在结构基础上得到解释：细胞外胶原基质提供的机械耦合功能的破坏。
Ultrastructural studies of the extracellular collagen matrix were made on the “stunned” myocardium using scanning, conventional and high voltage transmission electron microscopy and light microscopy. Regional myocardial dysfunction was produced by 12 sequential 5 minute occlusions of the left anterior descending coronary artery, separated by 10 minute intervals of reperfusion. A final 90 minute reperfusion period documented persistent myocardial dysfunction. At the end of the final reperfusion period, the percent systolic shortening, measured by sonomicrometers, was depressed significantly to 35 ± 9% of baseline. The heart was then perfusion fixed, and samples were taken from both control and stunned areas.No changes associated with irreversible cellular damage were noted in the stunned region. However, scanning electron microscopy of the stunned area showed that the extracellular collagen matrix underwent profound structural changes. Collagen cables were roughened, uncoiled and discontinuous. Linear grooves on the surface of the myocytes were frequently seen, indicating complete loss of collagen cables. The usual dense collagen weave surrounding myocytes became patchy or absent. Myocyte to myocyte struts were sparse and frequently absent, with remnant nodular or nublike structures indicative of breakage. High voltage electron microscopy of the stunned area showed that the collagen struts were discontinuous and vacuolated with rounded tips. Light microscopy of silver-stained sections of the stunned tissue demonstrated large patchy areas that were devoid of silver, indicating absence of the collagen matrix. There was a progressive increase in percent systolic bulging during each sequential coronary occlusion, suggesting increasing myocardial compliance.These results indicate that the myocardial collagen matrix is severely damaged from reversible ischemic cell injury. The greater myocardial compliance and less effective contractile effort in the stunned myocardium might be explained on a structural basis: disruption of the mechanical coupling function provided by the extracellular collagen matrix.