Jo Y H, Lee Y L, Lee K Y, Chang T M, Chey W Y
Genesee Hospital, University of Rochester School of Medicine and Dentistry, New York 14607.
Am J Physiol. 1992 Jul;263(1 Pt 1):G12-6. doi: 10.1152/ajpgi.1992.263.1.G12.
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)
在本研究中，我们研究了阿托品对十二指肠内给予油酸钠或外源性胆囊收缩素（CCK）所刺激的胰腺分泌的影响。在4只制备了胃和十二指肠托马斯插管的狗中，收集胰液以测量其体积、碳酸氢盐和蛋白质输出量，并采集外周静脉血样本用于放射免疫测定促胰液素和CCK。胰液的体积、碳酸氢盐和蛋白质输出量对油酸钠（1 - 4 mmol/h）呈剂量依赖性显著增加。胰腺分泌的增加与血浆CCK和促胰液素的增加平行。静脉注射阿托品完全抑制了油酸钠刺激的胰腺分泌和CCK释放，而促胰液素的释放未受影响。外源性CCK八肽（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只狗中，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释放以及体积和碳酸氢盐的胰腺分泌，除了蛋白质分泌受到显著抑制。先前已表明，生理剂量的阿托品可显著抑制促胰液素刺激的胰腺碳酸氢盐分泌。因此，我们得出结论，阿托品对油酸钠刺激的胰腺外分泌的抑制作用是通过抑制CCK释放和抑制促胰液素对外分泌胰腺的作用介导的。（摘要截断于250字）
