title: Inhibitory effects of octreotide on luminal cholecystokinin-releasing factor, plasma cholecystokinin, and pancreatic secretion in conscious rats.
abstract: BACKGROUND
  Luminal cholecystokinin-releasing factor (LCRF), purified from rat intestinal secretions, is an intraluminal regulator of cholecystokinin (CCK) secretion during bile and pancreatic juice diversion.
  
  
  OBJECTIVE
  Because the LCRF content was not influenced by intravenous administration of atropine or somatostatin, the inhibitory effect of a potent somatostatin analog octreotide on LCRF content, the plasma CCK level, and pancreatic secretion was examined.
  
  
  METHODS
  Rats were prepared with bile and pancreatic cannulae and two duodenal cannulae and with an external jugular vein cannula. After 1.5-hour basal collection, bile and pancreatic juice was diverted for 2 hours, during which octreotide was infused intravenously or into the duodenal lumen. The changes in pancreatic secretion were recorded for 2 hours, and the plasma CCK level and LCRF content 2 hours after the treatment were measured.
  
  
  RESULTS
  Bile and pancreatic juice diversion significantly increased pancreatic secretion and plasma CCK and LCRF levels. Intravenous infusion of octreotide (0.2 and 0.5 nmol/kg/hour) inhibited all parameters. Intraduodenal infusion of a lower dose of octreotide (33 nmol/kg/hour) inhibited pancreatic secretion, but did not inhibit CCK release or LCRF content. The higher doses (100 and 300 nmol/kg/hour) inhibited all parameters.
  
  
  CONCLUSIONS
  Intravenous and intraduodenal administrations of octreotide inhibited CCK release and LCRF content and pancreatic secretion induced by bile and pancreatic juice diversion.
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: Masao
authors.initials: M
authors.lastname: Masuda
authors.forename: Setsuko
authors.initials: S
authors.lastname: Kanai
authors.forename: Minoru
authors.initials: M
authors.lastname: Ohta
authors.forename: Shinji
authors.initials: S
authors.lastname: Suzuki
authors.forename: Kayoko
authors.initials: K
authors.lastname: Tateishi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000818:Animals; D001646:Bile / Q000737:chemistry / Q000502:physiology; D002766:Cholecystokinin / Q000097:blood*; D004386:Duodenum / Q000187:drug effects; D005765:Gastrointestinal Agents / Q000008:administration & dosage / Q000494:pharmacology*; D006133:Growth Substances / Q000032:analysis* / Q000097:blood; D007262:Infusions, Intravenous; D036341:Intercellular Signaling Peptides and Proteins; D007421:Intestine, Small / Q000737:chemistry / Q000187:drug effects; D008297:Male; D015282:Octreotide / Q000008:administration & dosage / Q000032:analysis / Q000494:pharmacology*; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism*; D010189:Pancreatic Juice / Q000737:chemistry / Q000502:physiology; D011506:Proteins / Q000378:metabolism; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D014359:Trypsin Inhibitor, Kazal Pancreatic
chemical_list: D005765:Gastrointestinal Agents; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins; C504705:Spink1 protein, rat; D014359:Trypsin Inhibitor, Kazal Pancreatic; D002766:Cholecystokinin; D015282:Octreotide