H. Glad et al., IMPORTANCE OF VAGUS NERVES IN DUODENAL ACID NEUTRALIZATION IN ANESTHETIZED PIGS, American journal of physiology: Gastrointestinal and liver physiology, 35(1), 1997, pp. 154-160
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 e
ffect of electrical vagal stimulation (EVS) on pancreatic, hepatic, an
d duodenal mucosal bicarbonate secretion, thereby estimating their rel
ative importance in vagally induced duodenal acid neutralization. Spla
nchnicotomy increased vagally induced pancreaticobiliary bicarbonate s
ecretion, whereas duodenal mucosal bicarbonate secretion was unchanged
. After splanchnicotomy, EVS (10 ms, 15 mA, 12 Hz) significantly incre
ased pancreatic bicarbonate secretion (0-4.17 mmol/h), hepatic bicarbo
nate secretion (0.16 to 0.22 mmol/h), and duodenal mucosal bicarbonate
secretion (0.17 to 0.31 mmol/h). Pancreaticobiliary bicarbonate secre
tion was atropine resistant, whereas vagally induced duodenal mucosal
bicarbonate secretion was diminished by atropine (2.0 mg/kg). After sp
lanchnicotomy, EVS (10 ms, 15 mA, 12 Hz) had no effect on portal plasm
a 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 secr
etion from the three organs. In addition, biliary [C-14]mannitol clear
ance was shown not to be a reliable marker of canalicular bile secreti
on in pigs. These results suggest that in the anesthetized pig 1) vaga
l stimulation is only of minor importance to hepatic bicarbonate secre
tion; 2) vagal stimulation activates pancreatic bicarbonate secretion
through both cholinergic muscarinic and noncholinergic transmission; a
nd 3) vagal stimulation induces duodenal mucosal bicarbonate secretion
mainly through cholinergic muscarinic transmission. In conclusion, th
ese results suggest that only pancreatic and duodenal bicarbonate prod
uction play a role in vagally induced duodenal acid neutralization.