Neurohormonal mechanism of pancreatic exocrine secretion stimulated by sodium oleate and L-tryptophan in dogs.
Neurohormonal mechanism of pancreatic exocrine secretion stimulated by sodium oleate and L-tryptophan in dogs.
复制标题
油酸钠和L-色氨酸刺激狗胰腺外分泌分泌的神经激素机制。
DOI：
10.1152/ajpgi.1992.263.1.g12
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Chey,WY
中科院分区：
文献类型：
--
作者：
Jo,YH;Lee,YL;Lee,KY;Chang,TM;Chey,WY
本研究观察了阿托品对十二指肠内注入油酸钠或外源性胆囊收缩素（CCK）刺激胰腺分泌的影响。在四只狗准备与胃和托马斯十二指肠插管，收集胰液的体积，碳酸氢盐和蛋白质输出量的测量，并获得外周静脉血样品的分泌素和CCK的放射免疫测定。体积，碳酸氢盐和蛋白质输出的胰液显着增加响应油酸钠（1-4 mmol/h）以剂量依赖性方式。胰腺分泌的增加与血浆CCK和促胰液素的增加相一致。静脉注射阿托品可完全抑制油酸钠刺激的胰腺分泌和胆囊收缩素的释放，而胰泌素的释放则不受影响。外源性八肽胆囊收缩素（CCK-8）在16、32和64微克（14、28和56 pmol）·kg-1·h-1时，以剂量依赖性方式显著增加胰腺分泌。阿托品仅部分抑制蛋白质输出，但不影响碳酸氢盐输出。在另外5只犬中，研究了阿托品对L-色氨酸刺激的胰腺分泌的影响。有趣的是，阿托品未能影响CCK释放和胰腺分泌量和碳酸氢盐，除了蛋白质分泌，这是显着抑制。以前研究表明，生理剂量的阿托品可显著抑制胰泌素刺激的胰腺碳酸氢盐分泌。因此，我们得出结论，阿托品抑制油酸钠刺激的胰腺外分泌是通过抑制CCK释放和抑制胰泌素对胰腺外分泌的作用介导的。（250字处删节）
In the present investigation, we have studied the effect of atropine on the pancreatic secretion stimulated by intraduodenal administration of either sodium oleate or exogenous cholecystokinin (CCK). In four dogs prepared with gastric and Thomas duodenal cannulas, pancreatic juice was collected for measurement of volume, bicarbonate, and protein output, and peripheral venous blood samples were obtained for radioimmunoassay of both secretin and CCK. Volume, bicarbonate, and protein output of the pancreatic juice increased significantly in response to sodium oleate (1-4 mmol/h) in a dose-dependent manner. The increase in pancreatic secretion paralleled the increments in both plasma CCK and secretin. Atropine given intravenously suppressed completely both pancreatic secretion and release of CCK stimulated by sodium oleate, whereas the release of secretin was not affected. Pancreatic secretion was significantly increased in a dose-dependent manner by exogenous CCK octapeptide (CCK-8) at 16, 32, and 64 micrograms (14, 28, and 56 pmol).kg-1.h-1. Atropine inhibited protein output only partially, but it did not influence bicarbonate output. In five additional dogs, the effect of atropine on L-tryptophan-stimulated pancreatic secretion was studied. Interestingly, atropine failed to influence the CCK release and pancreatic secretion of volume and bicarbonate, except for protein secretion, which was significantly inhibited. It was shown previously that atropine inhibited significantly the pancreatic secretion of bicarbonate stimulated by secretin in physiological doses. Thus we conclude that the inhibition by atropine of the pancreatic exocrine secretion stimulated by sodium oleate is mediated by both suppression of CCK release and inhibition of action of secretin on the exocrine pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)