Duodenal lipid inhibits gastric acid secretion by vagal, capsaicin- sensitive afferent pathways in rats

Kevin C K Lloyd, H. H. Holzer, T. T. Zittel, Helen E Raybould

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume264
Issue number4 27-4
StatePublished - 1993
Externally publishedYes

Fingerprint

Afferent Pathways
Capsaicin
Gastric Acid
Lipids
Acids
Reflex
Peptones
Vagus Nerve
Perfusion
Gastric Fistula
Neural Pathways
Spinal Nerves
Sympathetic Ganglia
Neurotoxins
Duodenum
Ganglia
Abdomen
Fats
Therapeutics

Keywords

  • awake rat
  • enterogastrone
  • intestinal phase regulation
  • primary vagal afferent

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

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abstract = "Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8{\%} peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20{\%}) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81{\%} during 5{\%} lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.",
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AU - Lloyd, Kevin C K

AU - Holzer, H. H.

AU - Zittel, T. T.

AU - Raybould, Helen E

PY - 1993

Y1 - 1993

N2 - Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.

AB - Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.

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KW - primary vagal afferent

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