Kischer C W, Thies A C, Chvapil M
Hum Pathol. 1982 Sep;13(9):819-24. doi: 10.1016/s0046-8177(82)80078-6.
Microvessels in normal skin, granulation tissue, hypertrophic scar, keloid, and mature scar from human subjects were studied by transmission electron microscopy. Comparative observations suggested that most microvessels in hypertrophic scar and keloid are occluded or partially occluded, apparently owing to an excess of endothelial cells. Endothelial cell contraction was also supported by the observations, and perivascular satellite cells (pericytes), some of which were identified as myofibroblasts, were observed in hypertrophic scars and keloids. Among findings from statistical analyses were that 1) the patency of microvessels in hypertrophic scar and granulation tissue is similar, as is that of microvessels in keloid and mature scar, but the patency of all these microvessels is significantly less than that of microvessels in normal skin, and 2) endothelial cell density is greater in nonpatent vessels than in patent vessels. The observed extent of microvascular occlusion supports a previously published theory that hypoxia is involved in the generation of hypertrophic scar.
通过透射电子显微镜对来自人类受试者的正常皮肤、肉芽组织、增生性瘢痕、瘢痕疙瘩和成熟瘢痕中的微血管进行了研究。比较观察结果表明,增生性瘢痕和瘢痕疙瘩中的大多数微血管被阻塞或部分阻塞,这显然是由于内皮细胞过多所致。观察结果也支持内皮细胞收缩,并且在增生性瘢痕和瘢痕疙瘩中观察到血管周围卫星细胞(周细胞),其中一些被鉴定为肌成纤维细胞。统计分析结果包括:1)增生性瘢痕和肉芽组织中微血管的通畅率相似,瘢痕疙瘩和成熟瘢痕中微血管的通畅率也相似,但所有这些微血管的通畅率均显著低于正常皮肤中的微血管,以及2)非通畅血管中的内皮细胞密度高于通畅血管。观察到的微血管阻塞程度支持了先前发表的一种理论,即缺氧参与了增生性瘢痕的形成。