NEUROCHEMICAL STATUS OF NITRIC OXIDE IN THE SETTINGS OF THE NORM, ISHEMIC EVENT OF CENTRAL NERVOUS SYSTEM, AND...

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.