Hachiya A, Bessho M
First Department of Internal Medicine, Toho University School of Medicine, Tokyo, Japan.
Am J Physiol. 1994 Jun;266(6 Pt 1):G1011-6. doi: 10.1152/ajpgi.1994.266.6.G1011.
The relationship of gastric mucosal hemodynamics, energy metabolism, and acid to antral histological lesion incidence following hemorrhage and retransfusion was investigated in rats. Decrease of mucosal blood flow and of the index of mucosal oxygen saturation (ISO2) during hemorrhage were slightly greater in the corpus than in the antrum. ATP content and redox ratio in the corpus were decreased by shock; however, these hardly changed in the antrum. The index of tissue hemoglobin concentration (IHb) recovered to above the prehemorrhage value only in the antrum after retransfusion. Histological lesion incidence in the antral mucosa was more markedly increased by acid instillation and/or retransfusion than in the corpus. From these results, it was concluded that the decrease of blood flow is related as an underlying factor to induction of ischemic damage in the antral mucosa and that intraluminal acid and/or postischemic hyperemia play a causative role in the development of histologic lesions in the antral mucosa during shock and retransfusion in the rat stomach.
研究了大鼠出血和再输血后胃黏膜血流动力学、能量代谢以及胃酸与胃窦组织学损伤发生率之间的关系。出血期间胃体部黏膜血流量和黏膜氧饱和度指数（ISO2）的下降略大于胃窦部。休克导致胃体部ATP含量和氧化还原比降低；然而，胃窦部的这些指标几乎没有变化。再输血后，仅胃窦部的组织血红蛋白浓度指数（IHb）恢复到出血前水平以上。与胃体部相比，胃窦黏膜的组织学损伤发生率因滴注酸和/或再输血而增加得更为明显。从这些结果可以得出结论，血流量的减少是胃窦黏膜缺血性损伤诱导的潜在相关因素，管腔内酸和/或缺血后充血在大鼠胃休克和再输血期间胃窦黏膜组织学损伤的发展中起致病作用。
