Miyasaka K, Suzuki S, Kanai S, Masuda M, Funakoshi A
Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Japan.
Pancreas. 1999 Oct;19(3):217-23. doi: 10.1097/00006676-199910000-00001.
Whether cholecystokinin (CCK) has a direct action on duct cells and the role of CCK-A receptor in bicarbonate secretion were examined by comparing the results obtained from OLETF (CCK-A receptor-deficient rats) and control (LETO) rats. Rats were prepared with cannulae for draining bile and pancreatic juice separately, with two duodenal cannulae and an external jugular vein cannula. The experiments were conducted without anesthesia. The responses of bicarbonate secretion to intravenous infusion of CCK, acetyl-beta-methylcholine (Ach), and 2-deoxy-D-glucose (2DG), and to intraduodenal infusion of HCl and a liquid meal were examined. To examine the synergistic effect between CCK and secretin, the effect of CCK during a background secretin infusion was examined in LETO rats. CCK did not stimulate bicarbonate secretion in either strain, nor in LETO rats with secretin infusion. When gastric acid secretion was prevented by administration of omeprazole, Ach did not increase bicarbonate secretion, but 2DG did in both strains. Intraduodenal infusion of HCI and a liquid meal significantly increased bicarbonate secretion in both strains; however, the responses were much less in OLETF than LETO rats. In conclusion, intravenous injection of CCK did not stimulate bicarbonate secretion, and the lack of CCK-A receptor decreased bicarbonate secretion in response to luminal stimulants.
通过比较OLETF（CCK-A受体缺陷大鼠）和对照（LETO）大鼠的实验结果，研究了胆囊收缩素（CCK）对胆管细胞是否有直接作用以及CCK-A受体在碳酸氢盐分泌中的作用。分别为大鼠制备用于引流胆汁和胰液的插管、两个十二指肠插管以及一个颈外静脉插管。实验在无麻醉状态下进行。检测了碳酸氢盐分泌对静脉注射CCK、乙酰-β-甲基胆碱（Ach）和2-脱氧-D-葡萄糖（2DG）以及十二指肠内注射HCl和流食的反应。为了检测CCK和促胰液素之间的协同作用，在LETO大鼠中检测了在背景促胰液素输注期间CCK的作用。CCK在两种品系的大鼠中均未刺激碳酸氢盐分泌，在输注促胰液素的LETO大鼠中也未刺激分泌。当通过给予奥美拉唑抑制胃酸分泌时，Ach在两种品系的大鼠中均未增加碳酸氢盐分泌，但2DG能增加分泌。十二指肠内注射HCl和流食在两种品系的大鼠中均显著增加了碳酸氢盐分泌；然而，OLETF大鼠的反应比LETO大鼠小得多。总之，静脉注射CCK不会刺激碳酸氢盐分泌，并且CCK-A受体的缺失会降低对腔内刺激物的碳酸氢盐分泌反应。
