In order to investigate the role of NO in hypoxic tissue damage in newborns, we studied the effect of the systemic administration of a inhibitor of NO synthase, NG-nitro-L-arginine (L-NNA), and the precursor for the synthesis of NO, L-arginine (L-ARG), on brain, heart, lung, liver, kidney, intestine, and skeletal muscle tissues. Four groups of 1-d-old Wistar rat pups(5-6g) were used: control, hypoxia alone, hypoxia and L-ARG or L-NNA groups. 100 mg/kg L-ARG or 2 mg/kg L-NNA were administered as a bolus intraperitoneally 1.5 h before the hypoxia. Hypoxia was induced by breathing of a mixture of 8% oxygen and 92% nitrogen for three hours. Then pups were allowed to inhale normal atmospheric air for 30 minutes. The rats were decapitated at the end of the reoxygenation period. The tissues were taken and frozen immediately. Lipid peroxidation levels measured as Thiobarbituricacid-reacting substances (TBARS) nmol/g wet tissue are summarized below: Table

Table 1 No caption available.

Hypoxia increased lipid peroxidation in all tissues except muscle; this increase was reversed by L-ARG and L-NNA in brain, heart, lung, liver, and kidney. Histopathological changes in intestines were epithelial separation and hyperemia in hypoxic and L-NNA groups, which was not observed in control and L-ARG groups. Pulmonary hemorrhage was observed only in hypoxic group. In muscles, irregular muscle fibers with indefinite cell borders were seen in hypoxic and L-ARG groups. These data suggest that NO acts both as a destructive and a protective agent in the pathogenesis of hypoxia-reoxygenation injuries in brain, heart, lung, liver, and kidney tissues. NO has an important protective role in the intestines against hypoxia whereas it has destructive effect in the hypoxic skeletal muscles.