Endothelial proliferation in inflammation. II. Autoradiographic studies in x-irradiated leukopenic rats after thermal injury to the skin.
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.
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
D004247:DNA