Kataoka K
Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
Gastroenterol Jpn. 1988 Jun;23(3):292-8. doi: 10.1007/BF02779473.
The effect of atropine on the feedback regulatory mechanism of pancreatic enzyme secretion exerted by intraluminal trypsin was investigated in conscious rats. Intravenous atropine infusion (50 micrograms/kg/h) suppressed pancreatic enzyme secretion to the same extent in both the presence and the absence of pancreatic juice in the intestine. However, with or without atropine infusion, pancreatic secretory rate was higher throughout diversion of pancreatic juice than during intraduodenal return of the juice. Atropine also inhibited the stimulatory response to intraduodenal trypsin inhibitor and intravenous caerulein. The atropine-induced inhibitory effect was not significantly different between the two experimental conditions. Regardless of atropine administration, both trypsin inhibitor and caerulein caused a significant increase in pancreatic secretion. The results suggest that cholinergic mechanisms have little influence on the feedback regulation. Cholinergic mechanisms may play an important role in maintaining the physiologically basal secretion because the basal secretion is atropine-sensitive.
在清醒大鼠中研究了阿托品对肠腔内胰蛋白酶所发挥的胰腺酶分泌反馈调节机制的影响。静脉输注阿托品(50微克/千克/小时)在肠内存在和不存在胰液的情况下,均将胰腺酶分泌抑制至相同程度。然而,无论是否输注阿托品,在整个胰液转流期间胰腺分泌速率均高于胰液十二指肠内回输期间。阿托品还抑制对十二指肠内胰蛋白酶抑制剂和静脉注射蛙皮素的刺激反应。在两种实验条件下,阿托品诱导的抑制作用无显著差异。无论是否给予阿托品,胰蛋白酶抑制剂和蛙皮素均引起胰腺分泌显著增加。结果表明胆碱能机制对反馈调节影响很小。胆碱能机制可能在维持生理性基础分泌中起重要作用,因为基础分泌对阿托品敏感。