Tomita H, Miyasaka K, Matsumoto M, Funakoshi A
Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology.
Nihon Shokakibyo Gakkai Zasshi. 1994 Mar;91(3):287-92.
The effects of bilateral truncal vagotomy on cholecystokinin (CCK) release and pancreatic hypersecretion produced by bile and pancreatic juice (BPJ) diversion were examined in conscious rats. In addition, the effect of exogenous administration of CCK-8 (100 pmol/kg/h) on pancreatic secretion were compared in rats with and without vagotomy. Rats were prepared with external bile and pancreatic juice fistulae and the experiment was conducted on the 4th postoperative day. Basal pancreatic secretion was not affected by vagotomy. CCK release produced by bile and pancreatic juice diversion was enhanced, whereas protein secretion in response to high plasma CCK was inhibited by vagotomy. Pancreatic secretion stimulated by intravenous infusion of 100 pmol/kg/h of CCK-8 was also inhibited by vagotomy. These results proposed that vagal nerve is mandatory for the full response of pancreatic exocrine secretion to circulating CCK.
在清醒大鼠中，研究了双侧迷走神经干切断术对胆汁和胰液转流（BPJ）引起的胆囊收缩素（CCK）释放及胰腺分泌亢进的影响。此外，比较了外源性给予CCK-8（100 pmol/kg/h）对迷走神经切断和未切断大鼠胰腺分泌的影响。给大鼠制备了体外胆汁和胰液瘘管，并在术后第4天进行实验。基础胰腺分泌不受迷走神经切断术的影响。胆汁和胰液转流引起的CCK释放增加，而迷走神经切断术抑制了对高血浆CCK的蛋白分泌反应。静脉输注100 pmol/kg/h的CCK-8刺激的胰腺分泌也受到迷走神经切断术的抑制。这些结果表明，迷走神经对于胰腺外分泌对循环CCK的充分反应是必需的。
