Abrahams C, Janicki J S, Weber K T
Lab Invest. 1987 Jun;56(6):676-83.
The collagen skeleton in the myocardium of 37 non-human primates (Macaca fascicularis) was studied by scanning electron microscopy. Twenty-one hypertensive animals had "pressure-overload" myocardial hypertrophy of 4 to 80 weeks duration induced by unilateral perinephric cellophane insertion and 16 were normotensive controls. The purpose of the study was to examine possible remodeling of the collagen matrix of the hypertrophied pressure overloaded M. fascicularis myocardium. An extensive collagen matrix was demonstrated in nonoperated macaques, consisting of a weave which sequestered groups of myocytes and which was joined to the epimysium by long collagen tendons, and of numerous intermyocyte and myocyte to capillary struts. In addition, strands of collagen were seen crossing interfascicular planes. This collagen skeleton was studied at three periods of perinephritis-induced hypertension with hypertrophy: at 4 weeks (evolutionary); at 32 weeks with mild to moderate hypertension (early compensatory); and at 80 weeks with moderately severe hypertension (late compensatory). These sequential studies revealed that the matrix was remodeled. At 4 weeks there was slight thickening and increase in density of the weave. At 32 weeks, in addition to changes in the weave, the collagen strands became thick and pillar-like and the tendons increased in numbers and thickness, and at 80 weeks some myocytes became encased in collagen. The geometrical arrangement of the normal collagen matrix of the myocardium is similar to series and parallel elastic elements with respect to myocytes, and, accordingly, it may be responsible for the mechanical properties of the myocardium during diastole and systole. The structural alterations in the collagen skeleton which we observed in hypertrophy may play a significant role in deleteriously affecting ventricular function of the pressure-overloaded myocardium.
通过扫描电子显微镜对37只非人灵长类动物(食蟹猴)心肌中的胶原骨架进行了研究。21只高血压动物通过单侧肾周插入玻璃纸诱导产生了持续4至80周的“压力超负荷”心肌肥大,16只为血压正常的对照动物。本研究的目的是检查压力超负荷的食蟹猴心肌肥大时胶原基质可能发生的重塑。在未手术的猕猴中发现了广泛的胶原基质,其由包裹成组心肌细胞的编织结构组成,该编织结构通过长胶原束与肌外膜相连,还有许多心肌细胞间以及心肌细胞与毛细血管间的支柱。此外,可见胶原束穿过束间平面。在肾炎性高血压伴心肌肥大的三个阶段对该胶原骨架进行了研究:4周时(演变期);32周时伴有轻度至中度高血压(早期代偿期);80周时伴有中度至重度高血压(晚期代偿期)。这些连续研究表明基质发生了重塑。4周时,编织结构略有增厚且密度增加。32周时,除了编织结构的变化外,胶原束变粗且呈柱状,束的数量和厚度增加,80周时一些心肌细胞被胶原包裹。心肌正常胶原基质的几何排列在心肌细胞方面类似于串联和并联弹性元件,因此,它可能负责心肌在舒张期和收缩期的力学性能。我们在心肌肥大中观察到的胶原骨架结构改变可能在有害地影响压力超负荷心肌的心室功能方面起重要作用。