Abstract

Hepatic ischemia (I) followed by reperfusion (R) results in mild to severe remote organ injury. Oxidative stress and nitric oxide (NO) seems to be involved in I/R injury. The aim was to investigate the effects of liver I/R on liver function and on lipid peroxidation, leukocyte infiltration and NO synthase (NOS) immunostaining in lung and kidney. 24 male Wistar rats were randomized into 3 groups: 1) sham, 2) 60 min of partial (70%) liver I and 2 h of global liver R, and 3) 60 min of partial (70%) liver I and 6 h of global liver R. The groups 2 and 3 presented a significant increase in plasma levels of alanine and aspartate aminotransferase and in tissue levels of malondialdehyde and myeloperoxidase. In the kidney, the positive endothelial NOS (eNOS) staining was significantly decreased in group 3 compared to 1 and the staining for inducible NOS (iNOS) and neuronal NOS (nNOS) did not differ among groups. In the lung, the staining for eNOS and iNOS did not present statistical differences among groups and no positive nNOS staining was observed in any group. These results suggest that partial liver I followed by global liver R induces liver, kidney and lung injuries characterized by neutrophil sequestration and oxidative stress increase. In addition, we can suppose that the reduction in NO formation via eNOS can be implicated in the moderate impairment of renal function, observed by others, 24 hours after liver I/R. Support: FAPESP; FAEPA.

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