Aging Impairs Afferent Nerve Function in Rat Intestine

Reduction of Mesenteric Hyperemia Induced by Intraduodenal Capsaicin and Acid

Kyoji Seno, Kan Lam, Joseph Leung, Felix W. Leung

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The high incidence of peptic ulcer disease despite decreased acid secretion in the elderly suggests an impairment of mucosal defense mechanism with aging. Stimulation of the intestinal mucosal afferent nerves by intraduodenal application of capsaicin or hydrochloric acid (HCI) increases superior mesenteric artery (SMA) blood flow and protects the duodenal mucosa against deep damage. We tested the hypothesis that the intestinal hyperemia induced by intraduodenal capsaicin or HCI is significantly reduced in older (12 months) rats compared with younger (2 months) rats. Mesenteric blood flow was measured by pulsed Doppler flowmetry in anesthetized rats with the flow probe around the SMA. Two milliliters per kilogram of 160 μM capsaicin or 0.1 N HCI administered intraduodenally increased SMA blood flow significantly in both age groups. The peak response in SMA blood flow, however, was significantly smaller in the older rats than in the younger rats. These observations support the hypothesis that impairment of afferent nerve function occurs with aging in the rat intestine.

Original languageEnglish (US)
Pages (from-to)346-351
Number of pages6
JournalDigestive Diseases and Sciences
Volume41
Issue number2
StatePublished - 1996

Fingerprint

Capsaicin
Hyperemia
Intestines
Superior Mesenteric Artery
Acids
Hydrochloric Acid
Rheology
Peptic Ulcer
Mucous Membrane
Age Groups
Incidence

Keywords

  • Afferent nerve
  • Aging
  • Blood flow
  • Intestine

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Aging Impairs Afferent Nerve Function in Rat Intestine : Reduction of Mesenteric Hyperemia Induced by Intraduodenal Capsaicin and Acid. / Seno, Kyoji; Lam, Kan; Leung, Joseph; Leung, Felix W.

In: Digestive Diseases and Sciences, Vol. 41, No. 2, 1996, p. 346-351.

Research output: Contribution to journalArticle

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