The effect of NO synthase inhibition on blood oxygen-carrying function during hyperthermia in rats

Hyperthermia is known to be accompanied by considerable worsening of body oxygen delivery. Nitric oxide (NO) is a messenger that contributes to the regulation of oxygen transport (vasodilation, formation of nitrosohemoglobin, erythrocyte deformability), but also has cytotoxic effects (when abundantly generated by inducible NO synthase and through a formation of peroxynitrite). The effects of NO synthesis inhibition on the blood oxygen transport (hemoglobin-oxygen affinity and erythrocyte deformability) were investigated in rats with hyperthermia. The most considerable changes in blood oxygen transport indices and the most pronounced hypoxia were observed in rats that received the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) i.p. Its administration before heating significantly impaired body oxygen delivery, with a shift of the oxyhemoglobin dissociation curves rightwards and lowering of erythrocyte deformability. The changes in the blood oxygen transport in animals receiving L-arginine and L-NAME to prevent NO synthase inhibition were similar to those in rats treated with isotonic NaCl before heating.