Miller T A, Watson L C, Rayford P L, Thompson J C
World J Surg. 1977 Jan;1(1):93-7. doi: 10.1007/BF01654742.
The inhibitory effect of glucagon on pancreatic exocrine secretion induced by endogenously released secretin was studied in 4 dogs with chronic pancreatic fistulas and open gastric fistulas. After a constant level of pancreatic secretion was established by intraduodenal hydrochloric acid perfusion (9 mEq/hr), glucagon (30 microng/kg-hr) was administered intravenously for 1 hr. Compared to a separate control study in which dogs received intraduodenal HC1 alone, glucagon caused a significant decrease in both pancreatic volume flow and bicarbonate output. Glucagon had no effect on pancreatic protein secretion, and circulating levels of endogenously released secretin remained unchanged. It is concluded that the inhibitory effect of glucagon on pancreatic secretion is not mediated through inhibition of secretin release. The chemical homology between glucagon and secretin suggests that glucagon may mediate its inhibitory action by competing with secretin at the level of the pancreatic receptor site.
在4只患有慢性胰瘘和开放性胃瘘的狗身上，研究了胰高血糖素对内源性释放的促胰液素诱导的胰腺外分泌的抑制作用。通过十二指肠内灌注盐酸（9毫当量/小时）使胰腺分泌达到恒定水平后，静脉注射胰高血糖素（30微克/千克·小时），持续1小时。与单独给予十二指肠内盐酸的对照研究相比，胰高血糖素使胰腺体积流量和碳酸氢盐输出量均显著降低。胰高血糖素对胰腺蛋白质分泌没有影响，内源性释放的促胰液素的循环水平保持不变。得出的结论是，胰高血糖素对胰腺分泌的抑制作用不是通过抑制促胰液素释放来介导的。胰高血糖素和促胰液素之间的化学同源性表明，胰高血糖素可能通过在胰腺受体部位与促胰液素竞争来介导其抑制作用。
