Abstract
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.
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