Weidenbach H, Printz H, Göke B, Koop I, Schafmayer A, Adler G
Dept. of Internal Medicine, Philipps University, Marburg, Federal Republic of Germany.
Res Exp Med (Berl). 1989;189(3):221-8. doi: 10.1007/BF01852170.
In the present study the effect of atropine on feedback regulation of pancreatic function was investigated in male rats. Orogastric tube feeding of a single dose of the protease inhibitor camostate (100 mg) caused a 6-fold increase in plasma CCK. This was accompanied by a 50% decrease in pancreatic enzyme content for up to 6 h. The effect of i.v. infusion of atropine (100 micrograms.kg-1.h-1) was studied 60 and 180 min after camostate feeding. Atropine completely abolished the decrease in enzyme content 180 min after camostate feeding. The stimulated CCK plasma levels were significantly lowered by the infusion of atropine 60 min, but not 180 min, after feeding of camostate. It is discussed that a cholinergic pathway mediates CCK release in the early phase of feedback regulation of pancreatic function.
在本研究中，对雄性大鼠进行实验，以探究阿托品对胰腺功能反馈调节的影响。经口胃管单次给予蛋白酶抑制剂卡莫司他（100毫克）后，血浆胆囊收缩素（CCK）水平增加了6倍。同时，胰腺酶含量在长达6小时内降低了50%。在给予卡莫司他60分钟和180分钟后，研究静脉输注阿托品（100微克·千克⁻¹·小时⁻¹）的效果。在给予卡莫司他180分钟后，阿托品完全消除了酶含量的降低。在给予卡莫司他60分钟后，输注阿托品可使受刺激的CCK血浆水平显著降低，但在180分钟后则无此效果。讨论认为，胆碱能途径在胰腺功能反馈调节的早期阶段介导CCK的释放。
