Gastric mucosal lesions after burn injury: relationship to H+ back-diffusion and the microcirculation.
Rats were subjected to a 30% body surface area full-thickness burn. Two hours after injury, 93% of animals had gastric mucosal erosions. At 5 hours this increased to 100%, but at 24 and 72 hours, lesions were fewer and less severe. Histologic study suggested that lesions noted at 24 and 72 hours represented erosions formed earlier. No mucosal abnormalities were noted in control rats. A causal relationship between mucosal ischemia and the development of erosions is suggested by the presence of A-V shunts at 2 and 5 hours only. Significant increases in H+ back-diffusion and protein leakage into the gastric lumen at 2 and 5 hours also implicated changed mucosal permeability in the etiology of erosions. The return of H+ back-diffusion to control values at 24 and 72 hours, when lesions were still present, appears to contradict the theory that permeability changes are secondary to erosion formation.
D000818:Animals; D002056:Burns / Q000150:complications* / Q000503:physiopathology; D004058:Diffusion; D005753:Gastric Mucosa / Q000098:blood supply; D006859:Hydrogen / Q000378:metabolism; D008297:Male; D008833:Microcirculation; D051381:Rats; D013276:Stomach Ulcer / Q000209:etiology*; D013997:Time Factors
D006859:Hydrogen