title: Stimulatory effect of ethanol on pancreatic secretion in conscious rats requires CCK-A receptor.
abstract: OBJECTIVE
  Although many studies have investigated the acute effect of ethanol on the rat pancreas, the effect of intravenous injection of ethanol on pancreatic secretion has been controversial. The purposes of this study were to examine whether intraduodenal and intravenous administration of ethanol stimulates pancreatic secretion in Wistar rats. To elucidate the mechanism, we examined whether ethanol influences pancreatic secretion in CCK-A receptor-deficient rats.
  
  
  METHODS
  Rats were prepared with cannulae for draining bile and pancreatic juice separately. The experiments were conducted in unanesthetized rats. Different concentrations of ethanol solutions were infused at the rate of 1.5 mL/h into the duodenum, and half concentrations of the respective ethanol solutions were prepared and infused into the duodenum at a rate of 3 mL/h. Then we determined the pancreatic responses to simultaneous administration of a liquid meal with ethanol. Moreover, the effect of intravenous infusion of ethanol on pancreatic secretion was examined. Finally, the effect of intraduodenal and intravenous infusion of ethanol was determined in CCK-A receptor-deficient rats.
  
  
  RESULTS
  Intraduodenal infusion of ethanol significantly increased pancreatic secretion, and these responses depended on the amount of ethanol instilled into the lumen, except for 3% ethanol solution, which did not affect pancreatic secretion. Simultaneous administration of a liquid meal with ethanol augmented pancreatic response in rats treated with the higher 2 ethanol concentrations (33% and 66%). Intravenous administration of ethanol slightly but significantly increased pancreatic secretion. However, no stimulation was observed in CCK-A receptor-deficient rats regardless of ethanol administration route.
  
  
  CONCLUSIONS
  Both intraduodenal and intravenous administration of ethanol stimulated pancreatic secretion, and this stimulation required CCK-A receptor.
authors.affiliation: Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. miyasaka@tmig.or.jp
authors.forename: Kyoko
authors.initials: K
authors.lastname: Miyasaka
authors.forename: Setsuko
authors.initials: S
authors.lastname: Kanai
authors.forename: Minoru
authors.initials: M
authors.lastname: Ohta
authors.forename: Akihiro
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000818:Animals; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology*; D003243:Consciousness; D004305:Dose-Response Relationship, Drug; D004386:Duodenum; D004435:Eating; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D007262:Infusions, Intravenous; D008297:Male; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism*; D010189:Pancreatic Juice / Q000378:metabolism; D051381:Rats; D020334:Rats, Inbred OLETF; D017208:Rats, Wistar; D043886:Receptor, Cholecystokinin A / Q000235:genetics / Q000378:metabolism*
chemical_list: D002492:Central Nervous System Depressants; D043886:Receptor, Cholecystokinin A; D000431:Ethanol