title: Importance of vagus nerves in duodenal acid neutralization in anesthetized pigs.
abstract: During the cephalic phase of gastric acid secretion, vagally mediated synchronous stimulation of bicarbonate provides protection against the acid. The purpose of this study was to determine simultaneously the effect of electrical vagal stimulation (EVS) on pancreatic, hepatic, and duodenal mucosal bicarbonate secretion, thereby estimating their relative importance in vagally induced duodenal acid neutralization. Splanchnicotomy increased vagally induced pancreaticobiliary bicarbonate secretion, whereas duodenal mucosal bicarbonate secretion was unchanged. After splanchnicotomy, EVS (10 ms, 15 mA, 12 Hz) significantly increased pancreatic bicarbonate secretion (0-4.17 mmol/h), hepatic bicarbonate secretion (0.16 to 0.22 mmol/h), and duodenal mucosal bicarbonate secretion (0.17 to 0.31 mmol/h). Pancreaticobiliary bicarbonate secretion was atropine resistant, whereas vagally induced duodenal mucosal bicarbonate secretion was diminished by atropine (2.0 mg/kg). After splanchnicotomy, EVS (10 ms, 15 mA, 12 Hz) had no effect on portal plasma concentration of secretin, whereas vasoactive intestinal peptide was increased (14-29 pM). EVS at 12 Hz with varying duration (3 or 10 ms) and amplitude (3-50 mA) had no further effect on the bicarbonate secretion from the three organs. In addition, biliary [14C]mannitol clearance was shown not to be a reliable marker of canalicular bile secretion in pigs. These results suggest that in the anesthetized pig 1) vagal stimulation is only of minor importance to hepatic bicarbonate secretion; 2) vagal stimulation activates pancreatic bicarbonate secretion through both cholinergic muscarinic and noncholinergic transmission; and 3) vagal stimulation induces duodenal mucosal bicarbonate secretion mainly through cholinergic muscarinic transmission. In conclusion, these results suggest that only pancreatic and duodenal bicarbonate production play a role in vagally induced duodenal acid neutralization.
authors.affiliation: Department of Medical Gastroenterology, Odense University Hospital, Denmark.
authors.forename: H
authors.initials: H
authors.lastname: Glad
authors.forename: P
authors.initials: P
authors.lastname: Svendsen
authors.forename: O
authors.initials: O
authors.lastname: Olsen
authors.forename: O B
authors.initials: OB
authors.lastname: Schaffalitzky de Muckadell
mesh_terms: D000136:Acid-Base Equilibrium; D000143:Acids / Q000378:metabolism*; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001646:Bile / Q000378:metabolism; D001647:Bile Acids and Salts / Q000378:metabolism; D002320:Cardiovascular Physiological Phenomena; D004386:Duodenum / Q000378:metabolism*; D004558:Electric Stimulation; D005260:Female; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008353:Mannitol / Q000378:metabolism; D010179:Pancreas / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D012633:Secretin / Q000097:blood; D013552:Swine; D014630:Vagus Nerve / Q000502:physiology*; D014660:Vasoactive Intestinal Peptide / Q000097:blood
chemical_list: D000143:Acids; D001639:Bicarbonates; D001647:Bile Acids and Salts; D011506:Proteins; D012633:Secretin; D014660:Vasoactive Intestinal Peptide; D008353:Mannitol