In vivo microcirculation of a scald burn and the progression of postburn dermal ischemia.
The homozygous hairless mouse ear provides a reproducible model for the study of the microcirculatory changes of the burn wound during and following a scald burn injury. This model has allowed us to correlate the dynamic changes of the microcirculation to progressive zones of injury, which show an approximate tenfold increase in the area of complete capillary occlusion during the first 48 hours after injury. Platelet thromboembolism appears to be the major factor causing this progression of postburn dermal ischemia. Edema (increased skin water content) was greatest in the burned ear at 6 hours after the burn (20 percent greater than control values); edema of the unburned, contralateral ear was significant at 2 hours after the burn (9 percent greater than control values).
D000818:Animals; D001163:Arteriovenous Anastomosis / Q000503:physiopathology; D002056:Burns / Q000503:physiopathology*; D002196:Capillaries / Q000033:anatomy & histology / Q000503:physiopathology*; D004423:Ear / Q000033:anatomy & histology / Q000098:blood supply; D007511:Ischemia / Q000209:etiology*; D051379:Mice; D008819:Mice, Nude; D008833:Microcirculation; D008954:Models, Biological; D012867:Skin / Q000033:anatomy & histology / Q000098:blood supply*; D013923:Thromboembolism / Q000150:complications / Q000209:etiology