The purpose of the given work is to study an efficiency of different inhibitors of NO-synthase under conditions of experimental cerebral ischemia by their capability to limit reactions of oxidative and nitrosative stress.
It has been established that neurotoxic NO effect depends on definite enzyme of NO-synthase. Analysis of the obtained data shows a limited role of neuronal isoform in conditions of experimental impairment of blood circulation. The most relevant target for pharmacological regulation of NO-dependent mechanisms of neurodestruction is iNOS because of the fact that its activity begins to increase in 12 hours after ischemia development and its action is realized during next several days.