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Am J Physiol Gastrointest Liver Physiol 282: G647-G655, 2002;
0193-1857/02 $5.00
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Vol. 282, Issue 4, G647-G655, April 2002

Endothelin receptor blockers reduce I/R-induced intestinal mucosal injury: role of blood flow

Berna K. Oktar1, M. Ali Gülpinar1, Ayhan Bozkurt1, Salah Ghandour1, ule Çetinel2, Hadi Moini3, Berrak Ç. Yegen1, Serpil Bilsel3, D. Neil Granger4, and Hizir Kurtel1

Departments of 1 Physiology, 2 Histology, and 3 Biochemistry, Marmara University School of Medicine, 81326 Haydarpasa, İstanbul, Turkey; and 4 Department of Molecular and Cellular Physiology, Louisiana State University, Health Sciences Center, Shreveport, Louisiana 71130

The aim of the present study was to assess the role of endothelin (ET) in ischemia-reperfusion (I/R)-induced mucosal injury. Mucosal permeability (51Cr-EDTA clearance) and tissue myeloperoxidase (MPO) activity were significantly increased after 30 min of ischemia followed by 30 min of reperfusion. The I/R-induced increases in mucosal permeability and polymorphonuclear leukocyte (PMN) infiltration were significantly attenuated by pretreatments with ETA (BQ-485) and/or ETB (BQ-788) receptor antagonists. Monoclonal antibody (MAb) directed against intercellular adhesion molecule-1 (ICAM-1; MAb 1A29) and superoxide dismutase (SOD) pretreatments significantly attenuated the increased mucosal permeability and PMN infiltration in a similar manner as with ET receptor antagonists. Superior mesenteric artery blood flow was significantly reduced during the reperfusion period. Both ET receptor antagonists caused a significant rise in blood flow compared with an untreated I/R group. In conclusion, our data suggest that ETA and/or ETB receptors, ICAM-1, and superoxide play an important role in I/R-induced mucosal dysfunction and PMN infiltration. Furthermore, ET is involved in the pathogenesis of postreperfusion-induced damage and beneficial effects of ET receptor antagonism are related to an improvement of disturbed blood flow during the reperfusion period.

mucosal permeability; mucosal injury; BQ-485; BQ-788; superoxide dismutase


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