Contrasting cholinergic dependence of pancreatic and gallbladder responses to cholecystokinin.
Contrasting cholinergic dependence of pancreatic and gallbladder responses to cholecystokinin.
复制标题
对比胰腺和胆囊对胆囊收缩素反应的胆碱能依赖性。
DOI：
10.1152/ajpgi.1986.250.5.g665
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
H. Debas
中科院分区：
文献类型：
--
作者：
K. M. Strah;T. Pappas;R. Melendez;H. Debas
胆囊收缩素（CCK）的胆碱能受体已在肠神经系统的神经元上发现，包括胆囊的神经元。为了确定CCK作用对胰腺和胆囊中毒碱胆碱能受体的依赖程度是否存在差异，我们分别给11只胰腺犬和7只胆道瘘管犬增加剂量静脉注射CCK-8 （15-250 ng X kg-1 X h-1）或十二指肠内注射油酸钠（0.1-9 mmol/h），并给予和不给予阿托品预处理。胰腺蛋白对CCK-8的反应是剂量依赖性的，在最高剂量时达到448 +/- 76 mg/15 min的最大值。阿托品预处理对最低剂量的反应无显著性降低，但对其他剂量的反应无影响，最高剂量CCK的反应为473 +/- 82 mg/15 min。相比之下，通过胆瘘胆红素输出量测量的胆囊收缩对阿托品的抑制非常敏感。16、32、62.5、125和250 ng X kg-1 X h-1的胆红素反应分别为14 +/- 5、18 +/- 5、28 +/- 5、36 +/- 6和52 +/- 12 mg/h，不含阿托品和0 +/- 0、6 +/- 2、7 +/- 2、18 +/- 4和18 +/- 4 mg/h。同样，胰腺对油酸钠输注的反应比胆囊反应更不容易受到阿托品的抑制。在胰腺蛋白分泌方面，只有最低剂量的油酸钠才会被阿托品显著抑制。（摘要删节250字）
Cholinergic receptors for cholecystokinin (CCK) have been identified on neurons of the enteric nervous system, including those of the gallbladder. To determine whether any differences exist in the extent to which CCK action depends on muscarinic cholinergic receptors in the pancreas and gallbladder, 11 dogs with pancreatic and 7 dogs with biliary fistulas were given increasing doses of intravenous CCK-8 (15-250 ng X kg-1 X h-1) or intraduodenal sodium oleate (0.1-9 mmol/h) with and without atropine pretreatment. Pancreatic protein response to CCK-8 was dose dependent, reaching a maximal of 448 +/- 76 mg/15 min at the highest dose. Atropine pretreatment caused nonsignificant reduction in the response to the lowest dose but had no effect on the responses to the other doses, with the response to the highest dose of CCK being 473 +/- 82 mg/15 min. In contrast, gallbladder contraction as measured by bile fistula bilirubin output was very sensitive to inhibition by atropine. Bilirubin responses to 16, 32, 62.5, 125, and 250 ng X kg-1 X h-1 were 14 +/- 5, 18 +/- 5, 28 +/- 5, 36 +/- 6, and 52 +/- 12 mg/h, respectively, without atropine and 0 +/- 0, 6 +/- 2, 7 +/- 2, 18 +/- 4, and 18 +/- 4 mg/h with atropine pretreatment. Similarly, pancreatic responses to sodium oleate infusion were less susceptible to inhibition by atropine than were the gallbladder responses. With respect to pancreatic protein secretion, the response to only the lowest dose of sodium oleate was significantly inhibited by atropine.(ABSTRACT TRUNCATED AT 250 WORDS)