Kuvshinoff B W, Brodish R J, Fink A S, McFadden D W
Department of Surgery, Cincinnati Department of Veterans Affairs Medical Center, Ohio 45220.
J Surg Res. 1994 May;56(5):397-401. doi: 10.1006/jsre.1994.1063.
Although vagal cholinergic stimulation is the predominant regulatory mechanism governing the release of pancreatic polypeptide (PP), recent studies suggest that cholecystokinin (CCK) is also an important mediator. The present study examined the role of cholinergic neural pathways in the PP response to exogenous CCK-8 using a selectively denervated canine pancreas model. Chronic denervated pancreatic preparations were created in five dogs, while five dogs underwent sham laparotomy as controls. On study days, the fasted animals were infused intravenous CCK-8 (40 or 400 pmole/kg/hr) for 60 min both with and without atropine (20 micrograms/kg/hr). Plasma was collected at 20-min intervals and PP levels were determined by radioimmunoassay. CCK-8 elicited a dose-dependent increase in circulating PP in dogs with a neurally intact pancreas. Atropine and pancreatic denervation eliminated the PP response to CCK-8 at 40 pmole/kg/hr (P < 0.01) and inhibited the PP response to CCK-8 at 400 pmole/kg/hr (P < 0.05). The high dose of CCK-8 still elicited a small PP response in the denervated dogs (P < 0.05), which was subsequently abolished by the addition of atropine. These findings suggest that extrapancreatic cholinergic nerves are essential components of CCK-stimulated PP release, and that intrapancreatic cholinergic activity may play a limited role.
尽管迷走神经胆碱能刺激是调节胰腺多肽（PP）释放的主要机制，但最近的研究表明，胆囊收缩素（CCK）也是一种重要的介质。本研究使用选择性去神经支配的犬胰腺模型，研究了胆碱能神经通路在PP对外源性CCK-8反应中的作用。在五只犬身上制备了慢性去神经支配的胰腺标本，同时五只犬接受假剖腹手术作为对照。在研究日，禁食的动物在有和没有阿托品（20微克/千克/小时）的情况下，静脉输注CCK-8（40或400皮摩尔/千克/小时）60分钟。每隔20分钟采集血浆，并用放射免疫分析法测定PP水平。CCK-8在胰腺神经完整的犬中引起循环PP的剂量依赖性增加。阿托品和胰腺去神经支配消除了犬对40皮摩尔/千克/小时CCK-8的PP反应（P<0.01），并抑制了犬对400皮摩尔/千克/小时CCK-8的PP反应（P<0.05）。高剂量的CCK-8在去神经支配的犬中仍引起小的PP反应（P<0.05），随后加入阿托品后该反应被消除。这些发现表明，胰腺外胆碱能神经是CCK刺激PP释放的重要组成部分，而胰腺内胆碱能活性可能起有限的作用。
