论文部分内容阅读
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。
This work observed in the cysteamine (400mg / kg × 2, po) induced duodenal ulcer in rats, the proximal duodenal pH was significantly reduced, duodenal wall mucus decreased, and ten A transient increase in the rate of DNA synthesis in the duodenum was observed. These results suggest that the formation of ulcer may be related to the duodenal acidification and the decrease of mucus-HCO 3 3- salt barrier function, but not to the size of duodenal tissue repair ability. However, an ulcer dose of cysteamine (250 mg / kg, sc) did not increase total gastric acid output in shay rats. Thus, the primary reason cysteamine leads to duodenal acidification does not appear to be due to an increase in its acid load, which may be due to a decrease in duodenum acid handling capacity.