ENDOTHELIAL PROLIFERATION IN INFLAMMATION .2. AUTORADIOGRAPHIC STUDIES IN X-IRRADIATED LEUKOPENIC RATS AFTER THERMAL INJURY TO SKIN

  • 1 January 1978
    • journal article
    • research article
    • Vol. 91  (2) , 229-+
Abstract
The effect of leukocyte depletion on endothelial proliferation in the microvasculature of skin sites of acute inflammation was studied. Leukocytes were suppressed by 800 rad of whole-body irradiation 2 or 4 days prior to producing necrotizing thermal injuries (60.degree. C, 20 s) on a shielded area of skin. Endothelial proliferation was assayed 3 days after thermal injury by quantitating the labeling index after injection of 3H-thymidine. Circulating mononuclear cells were depressed to 1.3% of pre-irradiation levels by 2 days and remained at similar levels at 5 days. Lesions developing over this interval were devoid of mononuclear infiltrate, although neutrophils emigrated as usual. Three-day lesions without mononuclear infiltrate had a mean endothelial-labeling index of 8.97%, and this was not significantly different from controls (9.42%). Lesions induced at 4 days, when circulating neutrophils were also suppressed, had reduced infiltration of neutrophils, but endothelial-labeling indexes were similar to those of controls. Infiltration of monocytes is apparently not a necessary stimulus for endothelial proliferation or new vessel growth in sites of nonimmunologic acute inflammation.