The degree of oxidative stress in the rat brain during ischemia and reperfusion in conditions of correction of the L-arginine-NO system.

The aim of the present work was to evaluate oxidative stress in the brains of rats during ischemia/reperfusion in conditions of correction of the L-arginine-NO system. Experiments on 128 rats with brain ischemia/perfusion in conditions of modulation of the L-arginine-NO system were used to study changes in the concentrations of (a) lipid peroxidation products, i.e., diene conjugates, malonic dialdehyde, and Schiff bases, and (b) antioxidant protection factors, i.e., retinol, alpha-tocopherol, and SH-groups. Administration of L-arginine and NO synthase inhibitors, i.e., the non-selective inhibitor N(omega)-nitro-L-arginine methyl ester, the selective neuronal NO synthase inhibitor 7-nitroindasole, and the selective inhibitor of inducible NO synthase S-methylisothiourea, established that oxidative stress in rats with brain ischemia/perfusion is NO-dependent. NO formed by the various isoforms of NO synthase had different roles: hyperactivation of neuronal NO synthase was responsible for oxidative stress in both periods of brain ischemia/reperfusion, while increased inducible NO synthase activity was responsible in the late period.