半胱胺诱发大鼠十二指肠溃疡过程中十二指肠防御机能的变化

CHANGES IN DUODENAL DEFENSIVE FUNCTIONS DURING DUODENAL ULCERATION INDUCED BY CYSTEAMINE

本工作观察到在半胱胺(400mg/kg×2,po)诱发大鼠十二指肠溃疡过程中,十二指肠近端pH明显降低,十二指肠壁结合粘液量减少,而十二指肠纽织DNA合成速率出现暂时性升高。这些结果提示:溃疡的生成可能与十二指肠酸化以及粘液-HCO_3^-盐屏障作用的降低有关,而与十二指肠组织修复能力的大小似无明显关系。但致溃疡剂量的半胱胺(250mg/kg,sc)并不增加shay大鼠的胃总酸排出量。因此,半胱胺导致十二指肠酸化的主要原因似不是由于其酸负荷的增加,而可能由于十二指肠对酸处置能力的降低。

The present work indicated that during duodenal ulceration induced by cysteamine(400 mg/kg×2, po), the pH of proximal duodenum decreased markedly; the content of binding mucus decreased; while DNA synthetic rate of duodenal tissue did not reduce but increased transiently. These results suggest that the duodenal acidification and decrease in mucus-HCO3- barrier function may contribute to the pathogenesis of ulceration. Since the gastric total acid output observed on Shay rats treated with cysteamine remained unchanged or reduced, the acidification in duodenum seems not to be a result of increase in acid load to the duodenum, but may be that of reduction in acid disposal ability of the duodenum.