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本工作采用制备有Thomas胰瘘和胃瘘的狗作慢性麻醉实验,观察迷走冲动对酸化十二指肠引起胰液分泌的作用。结果如下:(1)在酸化十二指肠的背景下,迷走冲动加强胰蛋白质和碳酸氢盐的排出量,其效果超过单独迷走冲动和酸化十二指肠所产生效应之和。(2)在酸化十二指肠引起胰分泌效应停止的短时间内,迷走冲动引起的胰分泌的潜伏期缩短,蛋白质和碳酸氢盐排出量增多。(3)阻断迷走冲动或注阿托品后,酸化肠引起胰分泌的效应明显降低。(4)用利多卡因麻痹肠粘膜后,酸化肠的效应也明显降低。上述结果提示:酸化十二指肠引起胰液分泌的机制中,有迷走冲动和局部神经的参与,迷走冲动和内源性促胰酶素与促胰液素共同作用靶器官时,有相互加强作用,而这两种激素又有“易化”迷走冲动的作用,一旦迷走冲动被阻断,这两种激素的作用即明显下降。
In this work, dogs with Thomas pancreatic fistula and gastric fistula were used for chronic anesthesia experiments to observe the effect of vagus impulse on pancreatic secretion induced by acidified duodenum. The results are as follows: (1) In the context of acidified duodenum, vagal impulses enhance the release of trypsin and bicarbonate, which outperforms the sum of the effects of solitary vagal impulses and acidified duodenum. (2) In the short period of time after acidification of the duodenum causes pancreatic secretion, the latency of pancreatic secretion induced by vagal impulse is shortened, and the amount of protein and bicarbonate released is increased. (3) block the vagus of impulse or injection of atropine, acidification of the intestine caused by pancreatic secretion was significantly reduced. (4) With lidocaine paralytic intestinal mucosa, the effect of acidification of the intestine was significantly reduced. The results suggest that: acidification of the mechanism of pancreatic secretion caused by the duodenum, vagal impulse and local nerve involvement, vagal impulse and endogenous pancreatic hormone and secretin together target organs, there is mutual reinforcement, And these two hormones have “easy to” vagal effect, once the vagus impulse is blocked, the role of these two hormones decreased significantly.