Glad · The American journal of physiology 1997 · Controlled animal physiological experiment · n=?

Importance of vagus nerves in duodenal acid neutralization in anesthetized pigs.

Cited 13 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Animal experimental study

PubMed 9038889 · doi:10.1152/ajpgi.1997.272.1.G154 · record verified 2026-08-29

What was done

In anesthetized pigs subjected to splanchnicotomy, researchers applied electrical vagal stimulation (10 ms, 15 mA, 12 Hz, with additional tests varying duration from 3 to 10 ms and amplitude from 3 to 50 mA) with or without atropine (2.0 mg/kg). They simultaneously measured bicarbonate secretion from the pancreas, liver, and duodenal mucosa, assayed portal plasma secretin and vasoactive intestinal peptide levels, and evaluated biliary [14C]mannitol clearance.

What was found

After splanchnicotomy, electrical vagal stimulation significantly increased pancreatic bicarbonate secretion from 0 to 4.17 mmol/h, hepatic bicarbonate secretion from 0.16 to 0.22 mmol/h, and duodenal mucosal bicarbonate secretion from 0.17 to 0.31 mmol/h. Pancreaticobiliary secretion was atropine-resistant, whereas duodenal mucosal secretion was diminished by atropine. Portal plasma vasoactive intestinal peptide increased from 14 to 29 pM with no change in secretin. Varying stimulation duration and amplitude caused no further secretory changes, and biliary [14C]mannitol clearance was found to be an unreliable marker for canalicular bile secretion.

Why it matters

This study delineates organ-specific contributions to vagally mediated duodenal acid neutralization, demonstrating that pancreatic bicarbonate provides the primary protective response through combined cholinergic and noncholinergic mechanisms, supported by duodenal mucosal secretion, while hepatic bicarbonate output is negligible.

Limits

The study was conducted in anesthetized pigs, limiting direct extrapolation to conscious human physiology. The number of animals used was not stated in the abstract. Biliary [14C]mannitol clearance failed as a valid canalicular secretion marker, precluding reliable measurement of canalicular bile flow.

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