Mei M H
Department of Physiology, Dalian Medical College, PRC.
Sci China B. 1991 Jun;34(6):683-90.
Chronic experiments were made on eighteen dogs with Thomas pancreatic fistula and gastric fistula. Both in chronic and acute experiments the degenerated right cervical vagus nerve was stimulated by electrical shock and the endogenous secretin and CCK was released by means of duodenal acidification (D. A.). The exogenous secretin, atropine and lidocaine were infused to analyse the interrelationship of neurohormones in the pancreatic exocrine secretion. The results were as follows. In chronic experiments the pancreatic secretory latency was shorter and volume larger than that in acute experiments induced by D. A. The difference is very significant (P less than 0.001). Both vagotomy and atropine significantly inhibited pancreatic secretion induced by D. A. (P less than 0.01). Lidocaine infused into duodenum inhibited pancreatic secretion induced by D. A. as well. When vagal stimulation was combined with D. A., either simultaneously or successively, the pancreatic secretion was increased more than the additive sum obtained by separate action of vagal stimulation and D. A. or secretin. In view of the above-mentioned facts, the author suggests that vagal impulses combined with D. A. or secretin act on the pancreatic exocrine secretion, and that the interaction of nerve and hormones appear to be mutually potentiated.
对18只患有托马斯氏胰瘘和胃瘘的狗进行了慢性实验。在慢性和急性实验中,均通过电击刺激退化的右侧颈迷走神经,并通过十二指肠酸化(D.A.)释放内源性促胰液素和胆囊收缩素。输注外源性促胰液素、阿托品和利多卡因,以分析神经激素在胰腺外分泌中的相互关系。结果如下。在慢性实验中,胰腺分泌潜伏期比D.A.诱导的急性实验短,分泌量比急性实验大。差异非常显著(P<0.001)。迷走神经切断术和阿托品均显著抑制D.A.诱导的胰腺分泌(P<0.01)。向十二指肠内输注利多卡因也抑制D.A.诱导的胰腺分泌。当迷走神经刺激与D.A.同时或相继联合作用时,胰腺分泌增加量超过迷走神经刺激和D.A.或促胰液素单独作用时的相加总和。鉴于上述事实,作者认为迷走神经冲动与D.A.或促胰液素共同作用于胰腺外分泌,且神经与激素之间的相互作用似乎相互增强。