The purpose of the given research is to study the efficiency of different inhibitors of NO-synthase in conditions of experimental cerebral ischemia by their capability to limit reactions of oxidative and nitrosative stress. In the given study a non-selective NOS inhibitor - N-nitro-L-arginine; a highly selective inhibitor of neuronal NOS - N-propyl-L-arginine and a highly selective competitive inhibitor of inducible NOS - (S)-methylurea were used. Cerebral circulation impairment was simulated by means of double-sided occlusion of common carotid arteries. 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 12 hours after ischemia development and its action is implemented during several following days.