Blood oxygen-carrying function during the oxidative stress induced by lipopolysaccharide with a modification of the L-arginine-NO pathway.

PURPOSE Our aim was to study the blood oxygen-carrying function during the oxidative stress with a modification of the L-arginine-NO pathway. MATERIAL AND METHODS Oxidative stress was induced by intravenous administration of Escherichia coli lipopolysaccharide (LPS) to rabbits. To modify the L-arginine-NO pathway, animals were administered with NG-nitro-L-arginine methyl ester intravenously 60 min after the LPS. Mixed venous blood was sampled for evaluation of blood oxygen transport before and at 120 and 240 min after the LPS administration; tissue samples (heart, lung, liver, kidney and muscle) were also prepared. The following parameters were measured hemoglobin-oxygen affinity, concentrations of conjugated dienes, Schiff bases, alpha-tocopherol and activity of catalase. RESULTS During the NO synthase inhibition the oxidative stress was characterized by a shift of hemoglobin oxygen dissociation curve rightwards, more prominent activation of lipid peroxidation and decreased tissue levels of antioxidant defense factors. CONCLUSIONS The inhibition of NO generation induces a shift of prooxidant-antioxidant balance--obviously, not only due its potentially high levels and reactivity with the various target molecules (with a development of oxidative stress), but also because of the lower contribution of other factors including the hemoglobin-oxygen affinity change into the body antioxidant potential.