Alterations of intestinal motor responsiveness in a model of mild mesenteric ischemia/reperfusion in rats

Vigilio Ballabeni1, Elisabetta Barocelli, Simona Bertoni

  • 1Dipartimento di Scienze Farmacologiche, Biologiche e Chimiche Applicate, Università degli Studi di Parma, Parco Area delle Scienze 27/A, 43100 Parma, Italy.

Life Sciences
|August 15, 2002
PubMed

Insights

Mild mesenteric ischemia followed by 24-hour reperfusion significantly alters intestinal motor function in rats. This study reveals key changes in motility linked to reduced nitric oxide and eicosanoid availability.

Area of Science:

  • Gastroenterology
  • Physiology
  • Surgical Research

Background:

  • Intestinal motor dysfunction can arise after ischemic events.
  • Understanding the mechanisms of post-ischemic gut motility is crucial for clinical management.

Purpose of the Study:

  • To investigate alterations in intestinal motor responsiveness following mild mesenteric ischemia/reperfusion.
  • To identify the specific time course and molecular mediators involved in these functional changes.

Main Methods:

  • Isolated rat ileum from sham-operated and ischemia/reperfused groups (0, 24, 72 hours).
  • Pharmacological (acetylcholine, indomethacin) and electrical field stimulation were used to assess motor responses.
  • Involvement of nitric oxide synthase (NOS) and proteolytic enzymes was examined using specific inhibitors.

Main Results:

  • A 24-hour reperfusion period significantly suppressed acetylcholine-induced contractions and indomethacin-induced relaxation.
  • A nitric oxide-dependent relaxant response to field stimulation was diminished at 24 hours post-reperfusion.
  • This diminished response was sensitive to NOS inhibition and alpha-chymotrypsin but not iNOS inhibition.

Conclusions:

  • Mild mesenteric ischemia/reperfusion in rats induces reversible changes in enteric motility.
  • These motility alterations are associated with decreased availability of eicosanoids, nitric oxide, and neuropeptides.
  • The findings highlight the role of nitric oxide pathways in post-ischemic intestinal dysfunction.

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