Vracko R, Thorning D, Frederickson R G, Cunningham D
Laboratory Service, Veterans Administration Medical Center, Seattle, Washington.
Lab Invest. 1988 Jul;59(1):104-14.
To better understand the apparent tendency of myocardium to heal by scarring rather than by restoration of normal structure, we have examined by light and electron microscopy the basic reactions of rat ventricular myocytes and their interactions with the extracellular matrix. Using three different types of necrotizing injuries, we found that necrotic myocytes separated from viable myocytes at intercalated discs leaving blunt-ended stumps at the edge of each lesion; the basal lamina of necrotic myocytes remained largely intact and spanned the gap between viable myocytes on opposite sides of each lesion. A small number of stumps were capped off by a new layer of basal lamina and showed no evidence of proliferative activity. The majority of the stumps developed cell processes that extended along the acellular myocyte basal lamina sheaths. These processes had one of two different fates. Some became apposed to similar processes, formed intercalated disc attachments, increased myofibrillar mass, and appeared to be associated with muscle reconstruction. Others developed elongate tapered ends, which terminated in myotendinous connections to scar tissue. The outcome of healing necrotic myocardium, like the healing of noncardiac necrotic tissue injuries, appears to be a function of cell growth and extracellular framework guidance; however, unlike healing of noncardiac tissues, healing of myocardium is uniquely complicated by continuing muscle contractions. We think the rhythmic pulling at the edges of necrotic lesions induces formation of myotendinous attachments, which anchor myocytes to scar tissue and probably prevent further growth.
为了更好地理解心肌倾向于通过瘢痕形成而非正常结构恢复来愈合的明显趋势，我们通过光学显微镜和电子显微镜检查了大鼠心室肌细胞的基本反应及其与细胞外基质的相互作用。使用三种不同类型的坏死性损伤，我们发现坏死的心肌细胞在闰盘处与存活的心肌细胞分离，在每个损伤边缘留下钝端残端；坏死心肌细胞的基膜在很大程度上保持完整，并跨越每个损伤两侧存活心肌细胞之间的间隙。少数残端被一层新的基膜覆盖，没有增殖活动的迹象。大多数残端形成了沿着无细胞心肌细胞基膜鞘延伸的细胞突起。这些突起有两种不同的命运。一些与类似的突起并列，形成闰盘连接，增加肌原纤维质量，似乎与肌肉重建有关。另一些则形成细长的锥形末端，终止于与瘢痕组织的肌腱连接。坏死心肌愈合的结果，与非心脏坏死组织损伤的愈合一样，似乎是细胞生长和细胞外框架引导的结果；然而，与非心脏组织的愈合不同，心肌的愈合因持续的肌肉收缩而独具复杂性。我们认为坏死损伤边缘的节律性牵拉诱导了肌腱连接的形成，将心肌细胞锚定在瘢痕组织上，并可能阻止进一步生长。
