Kuvshinoff B W, Demar A R, James L, McFadden D W, Fink A S
Department of Surgery, University of Cincinnati Medical Center, Ohio 45267.
Pancreas. 1993 Sep;8(5):609-14. doi: 10.1097/00006676-199309000-00013.
To study the influence of extrapancreatic nerves and intrapancreatic cholinergic activity on the pancreatic response to secretin, six dogs underwent extrapancreatic denervation and creation of pancreatic fistulae. A second group of six dogs had pancreatic fistulae created without pancreatic denervation. The pancreatic exocrine response to graded doses of secretin (16-500 ng/kg/h) was determined, both alone and during a background infusion of cholecystokinin-octapeptide (CCK8, 50 ng/kg/h). All studies were replicated during administration of atropine (10 micrograms/kg/h). Secretin-induced bicarbonate output was significantly inhibited by atropine in both the innervated and denervated groups. Combined secretin and CCK8 elicited a dose-dependent increase in bicarbonate output and a sustained increase in protein output in both groups, regardless of atropine. In addition, potentiation of secretin-induced bicarbonate output by CCK8 was observed despite both extrinsic pancreatic denervation and administration of atropine. We conclude that endogenous intrapancreatic cholinergic activity influences the pancreatic response to secretin. Potentiation of secretin-induced bicarbonate output by CCK, however, is not dependent on neural mediation.
为研究胰腺外神经和胰腺内胆碱能活性对胰腺对促胰液素反应的影响，六只犬接受了胰腺外去神经支配并建立了胰瘘。第二组六只犬未进行胰腺去神经支配而建立了胰瘘。测定了单独给予不同剂量促胰液素（16 - 500 ng/kg/h）时以及在背景输注八肽胆囊收缩素（CCK8，50 ng/kg/h）期间胰腺的外分泌反应。所有研究均在给予阿托品（10微克/千克/小时）期间重复进行。在有神经支配和去神经支配的两组中，阿托品均显著抑制促胰液素诱导的碳酸氢盐分泌。无论是否使用阿托品，联合给予促胰液素和CCK8均使两组的碳酸氢盐分泌呈剂量依赖性增加，蛋白质分泌持续增加。此外，尽管进行了胰腺外去神经支配并给予了阿托品，但仍观察到CCK8对促胰液素诱导的碳酸氢盐分泌有增强作用。我们得出结论，内源性胰腺内胆碱能活性影响胰腺对促胰液素的反应。然而，CCK对促胰液素诱导的碳酸氢盐分泌的增强作用不依赖于神经介导。
