Brodish R J, Kuvshinoff B W, McFadden D W, Fink A S
Department of Surgery, University of Cincinnati School of Medicine, Ohio, USA.
Pancreas. 1995 May;10(4):401-6. doi: 10.1097/00006676-199505000-00013.
Although somatostatin is a potent inhibitor of pancreatic exocrine secretion in vivo, its mechanism of action remains unclear. The influence of extrapancreatic nerves and intrapancreatic cholinergic activity on somatostatin-induced inhibition of pancreatic exocrine secretion was studied in conscious dogs. Chronic pancreatic fistulae were created in six mongrel dogs, and a second group of six dogs also underwent complete pancreatic denervation. The pancreatic responses to graded doses of cholecystokinin (12.5-200 ng/kg/h) and bethanechol (57-916 micrograms/kg/h), both alone and during background infusion of somatostatin-14 (800 pm/kg/h), were determined in all dogs. The cholecystokinin dose-response with a somatostatin-14 background was then repeated with the addition of atropine (10 micrograms/kg/h). In both groups of animals, cholecystokinin elicited a dose-dependent increase in pancreatic protein secretion that was inhibited significantly by somatostatin-14. Regardless of the status of extrapancreatic nerves, atropine further inhibited cholecystokinin-induced protein secretion beyond that evoked by somatostatin-14. In both innervated and denervated animals, cholinergic stimulation with bethanechol elicited a dose-dependent increase in pancreatic protein secretion that was unaffected by somatostatin-14. We conclude that extrapancreatic nerves do not mediate the inhibitory effects of somatostatin-14. Somatostatin-14 appears to inhibit cholecystokinin-induced pancreatic secretion by an intrapancreatic cholinergic mechanism.
尽管生长抑素在体内是胰腺外分泌的强效抑制剂，但其作用机制仍不清楚。在清醒犬中研究了胰腺外神经和胰腺内胆碱能活性对生长抑素诱导的胰腺外分泌抑制的影响。给6只杂种犬制作了慢性胰瘘，另一组6只犬也进行了完全的胰腺去神经支配。测定了所有犬对分级剂量的胆囊收缩素（12.5 - 200 ng/kg/h）和氨甲酰甲胆碱（57 - 916 μg/kg/h）单独给药以及在背景输注生长抑素 - 14（800 pm/kg/h）期间的胰腺反应。然后在添加阿托品（10 μg/kg/h）的情况下重复进行有生长抑素 - 14背景的胆囊收缩素剂量反应实验。在两组动物中，胆囊收缩素引起胰腺蛋白质分泌呈剂量依赖性增加，这被生长抑素 - 14显著抑制。无论胰腺外神经的状态如何，阿托品进一步抑制胆囊收缩素诱导的蛋白质分泌，其抑制程度超过生长抑素 - 14所引起的抑制。在有神经支配和去神经支配的动物中，氨甲酰甲胆碱的胆碱能刺激引起胰腺蛋白质分泌呈剂量依赖性增加，这不受生长抑素 - 14的影响。我们得出结论，胰腺外神经不介导生长抑素 - 14的抑制作用。生长抑素 - 14似乎通过胰腺内胆碱能机制抑制胆囊收缩素诱导的胰腺分泌。
