title: Endothelial proliferation in inflammation. II. Autoradiographic studies in x-irradiated leukopenic rats after thermal injury to the skin.
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 C, 20 seconds) 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 control 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. The results indicate that infiltration by monocytes is not a necessary stimulus for endothelial proliferation of new vessel growth in sites of nonimmunologic acute inflammation.
mesh_terms: D000818:Animals; D002056:Burns / Q000473:pathology*; D004247:DNA / Q000096:biosynthesis; D004727:Endothelium / Q000378:metabolism / Q000473:pathology*; D005260:Female; D007249:Inflammation / Q000473:pathology*; D007970:Leukopenia / Q000473:pathology*; D008833:Microcirculation / Q000473:pathology*; D009000:Monocytes / Q000473:pathology; D009504:Neutrophils / Q000473:pathology; D051381:Rats; D012867:Skin / Q000098:blood supply
chemical_list: D004247:DNA