Fujimiya M, Kwok Y N
Department of Anatomy, Shiga University of Medical Science, Seta, Otsu, Japan.
Dig Dis Sci. 1997 Mar;42(3):634-9. doi: 10.1023/a:1018871731595.
The release of intestinal gastrin was examined using the isolated vascularly and luminally perfused rat duodenum. Results show that duodenal gastrin was released into both the intestinal lumen and circulation. The basal release of immunoreactive gastrin (IRG) into the lumen was 23.3 +/- 1.8 pg/min and that into the vasculature was 70.1 +/- 8.2 pg/min. The administration of 1 microM carbachol into the vascular perfusate resulted in a marked reduction of luminal release of IRG; however, vascular release of IRG was not affected. The carbachol-induced inhibition of luminal release of IRG was blocked by atropine but not by hexamethonium. These data suggest that only the luminal release of IRG from the rat duodenum, but not vascular release of IRG, is under the inhibitory control of the cholinergic muscarinic mechanism.
采用离体的经血管和管腔灌注的大鼠十二指肠来检测肠促胃液素的释放。结果显示,十二指肠促胃液素释放入肠腔和血液循环中。免疫反应性促胃液素(IRG)向肠腔内的基础释放量为23.3±1.8 pg/分钟,向血管系统的基础释放量为70.1±8.2 pg/分钟。向血管灌流液中加入1微摩尔的卡巴胆碱会导致IRG向肠腔的释放显著减少;然而,IRG向血管的释放不受影响。卡巴胆碱诱导的IRG向肠腔释放的抑制作用被阿托品阻断,但未被六甲铵阻断。这些数据表明,只有大鼠十二指肠中IRG向肠腔的释放,而非IRG向血管的释放,受胆碱能毒蕈碱机制的抑制性控制。