Investigation of Pathogenetic Mechanisms of Experimental Cerebral Hemorrhagic Insult in Rats

Nana Tsanava, Vladimer Bakhutashvili

Department of Neurology, Tbilisi State Medical University, Georgia

Have been studied oxidative metabolism and NO synthesis in rats during experimental hemorrhagic insult of the brain using the noninvasive photochemical and Electronic Paramagnetic Resonance (EPR) Methods. It is stated, that generators of oxygen active forms (ubisemiquinons, xanthinoxidase, Fe2+ and Mn2+ ions), excess amount of NO, and complexes of NO with heme- and nonheme iron are produced in cerebral cortex. Mitochondrial FeS containing proteins and cytochromes are nitrozilized; therefore mitochondrial electron transport and oxidative phosphorylation are suppressed. Presence of EPR signals of FeSNO and HbNO complexes pointing on nitrosilation of mitochondrial heme and nonheme iron containing proteins by free NO, make favorable conditions for apoptosis. In adjacent cells of the brain, that were not directly exposed to illumination, developed disorders are the same albeit of lesser intensity and delayed in development.

Keywords:  hemorrhagic insult, nitric oxide, oxygen reactive forms, EPR spectrum, brain, oxidative metabolism