Kitajima M, Wolfe R R, Trelstad R L, Allsop J R, Burke J F
J Trauma. 1978 Sep;18(9):644-50.
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.
将大鼠的30%体表面积造成全层烧伤。受伤后两小时,93%的动物出现胃黏膜糜烂。5小时时,这一比例增至100%,但在24小时和72小时时,损伤数量减少且严重程度减轻。组织学研究表明,24小时和72小时观察到的损伤代表早期形成的糜烂。对照大鼠未发现黏膜异常。仅在2小时和5小时出现动静脉分流,提示黏膜缺血与糜烂形成之间存在因果关系。2小时和5小时时,H⁺反向扩散和蛋白质渗漏到胃腔中的显著增加也表明糜烂病因中黏膜通透性发生了改变。在24小时和72小时时,当损伤仍然存在时,H⁺反向扩散恢复到对照值,这似乎与通透性变化继发于糜烂形成的理论相矛盾。