Courtade E T, Tsuda T, Thomas C R, Dannenberg A M
Am J Pathol. 1975 Feb;78(2):243-60.
Dermal tuberculous lesions were produced in rabbits by the intradermal injection of BCG. At various times after infection, anesthetized animals were perfused with a gelatin-colloidal carbon medium via the abdominal aorta. The capillary density of the nonnecrotic granulation tissue in the lesions was determined quantitatively by counting the capillaries under an ocular grid of a microscope. The capillary density in normal skin near the lesions was 3.8 plus or minus 0.5 in millimetersof capillary lengths per square millimeter in 250-mu tissue sections. The capillary density of the nonnecrotic tissue in BCGlesions averaged 6.1 plus or minus 0.6 mm/sq mm, an increase of 60%. The capillary density remained more or less constant as the BCG lesions grew and then regressed. The development of delayed hypersensitivity seemed to increase the capillary density, but this increase may have been a response to an extension of the necrosis at the time delayed hypersensitivity developed. Capillary densities in tuberculin reactions resembled those in BCG lesions. In the early stages, the increaseed capillary network of dermal BCG lesions was derived mainly from the subpapillary vascular plexus of the deep dermis supplied branches that surrounded the lower half of the caseous necrotic center and anastomosed with capillaries from the subpapillary plexus supplying the upper half. When the necrotic center extended, nearby capillaries thrombosed and in turn became necrotic. Peripherally, new capillaries formed and anastomosed with existing capillaries. From these vessels, mononuclear phagocytes emigrated, destroyed the tubercle bacilli, and enabled the lesion to heal. In the BCG lesions at all stages of development and healing, the capillary network in the nonnecrotic areas seemed adequate to supply and nourish the defense cells controlling the infection.
通过皮内注射卡介苗在兔身上产生皮肤结核病变。在感染后的不同时间，对麻醉的动物经腹主动脉灌注明胶 - 胶体碳介质。通过在显微镜目镜网格下计数毛细血管来定量测定病变中非坏死肉芽组织的毛细血管密度。在250微米组织切片中，病变附近正常皮肤的毛细血管密度为每平方毫米3.8±0.5毫米毛细血管长度。卡介苗病变中非坏死组织的毛细血管密度平均为6.1±0.6毫米/平方毫米，增加了60%。随着卡介苗病变的生长然后消退，毛细血管密度或多或少保持恒定。迟发型超敏反应的发展似乎增加了毛细血管密度，但这种增加可能是对迟发型超敏反应发生时坏死扩展的一种反应。结核菌素反应中的毛细血管密度与卡介苗病变中的相似。在早期，皮肤卡介苗病变中增加的毛细血管网络主要来自真皮深层的乳头下血管丛，该血管丛供应围绕干酪样坏死中心下半部分的分支，并与供应上半部分的乳头下丛的毛细血管吻合。当坏死中心扩展时，附近的毛细血管血栓形成并继而坏死。在周边，新的毛细血管形成并与现有毛细血管吻合。单核吞噬细胞从这些血管中移出 , 破坏结核杆菌 , 使病变愈合。在卡介苗病变发展和愈合的所有阶段，非坏死区域的毛细血管网络似乎足以供应和滋养控制感染的防御细胞。
