Microcirculatory dysfunction during intestinal ischemia-reperfusion

Research output: Contribution to journalReview article

21 Citations (Scopus)

Abstract

Oxido-reductive stress is a crucial factor of the tissue response during ischemia-reoxygenation injuries. Reperfusion affects primarily the microvasculature in a manner consistent with an acute inflammatory reaction. In this respect, the salient data suggest an important connection between endothelial cell-derived humoral mediators and the perivascular mast cell system. Increased endothelin-1 and decreased nitric oxide formation, mast cell degranulation and leukocyte accumulation coexist in gastrointestinal ischemia-reperfusion syndromes too. Constitutively produced nitric oxide inhibits, while increasingly formed endothelin-1 significantly enhances the degranulation of the intestinal mast cells. The endothelin-A receptor-dependent mast cell degranulation per se plays a secondary role in reperfusion-induced structural injury, but contributes significantly to leukocyte recruitment into the reperfused intestinal mucosa. It is conceivable therefore, that the nitric oxide - endothelin-1 - mast cell cycle is involved in the mechanism of ischemia-reperfusion-induced endothelial cell-leukocyte interactions, where mast cells act to amplify the process of leukocyte sequestration. The alteration in the balance between endothelial cell-derived proadhesive vasoconstrictor and antiadhesive vasodilator factors exerts a significant influence on the mucosal integrity, and the antagonism of endothelin-A receptor activation in this setting tips the equilibrium toward tissue salvage.

Original languageEnglish
Pages (from-to)263-279
Number of pages17
JournalActa physiologica Hungarica
Volume90
Issue number4
DOIs
Publication statusPublished - Dec 1 2003

Keywords

  • Endothelin-1
  • Ischemia-reperfusion
  • Mast cell
  • Microcirculation
  • Nitric oxide

ASJC Scopus subject areas

  • Physiology (medical)

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