Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 494, Issue 2-3, Pages 241-249Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2004.04.048
Keywords
intestinal ischemia/reperfusion; lung inflammation; neutrophil accumulation; adult respiratory distress syndrome; vascular permeability; NO; (nitric oxide)
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We investigated the effect of two inhibitors of nitric oxide (NO) synthesis, N-w-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, on lung inflammation caused by intestinal ischemia/reperfusion in rats. Relative to the sham-operated rats, intestinal ischemia/reperfusion (ischemia: 45 min; reperfusion: 30 min, 2 and 4 h) induced neutrophil recruitment (increased myeloperoxidase activity) and increased microvascular permeability (Evans blue dye extravasation) in the lungs and increased tumor necrosis factor (TNF) levels in the serum (L-929 cytotoxicity assay). L-NAME given before the ischemia exacerbated neutrophil accumulation, plasma extravasation, serum TNF and caused death of the animals, which was prevented by concomitant injection of L-arginine. Lung and systemic effects of intestinal ischemia/reperfusion were not modified when L-NAME was given just before reperfusion. Treatment with aminoguanidine inhibited plasma extravasation without affecting the other parameters evaluated. Dexamethasone reduced all the parameters. Our results indicate that during intestinal ischemia/reperfusion both constitutive and inducible NO synthases are called to exert a differential modulatory effect on lung inflammation and that maintenance of adequate levels of NO during ischemia is essential for the animals survival. (C) 2004 Elsevier B.V. All rights reserved.
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