Carnosine, a specific constituent of excitable tissues of vertebrates, exhibits a significant antioxidant protecting effect on the brain damaged by ischemic-reperfusion injury when it was administered to the animals before ischemic episode. In this study, the therapeutic effect of carnosine was estimated on animals when this drug was administered intraperitoneally (100 mg/kg body weight) after ischemic episode induced by experimental global brain ischemia. Treatment of the animals with carnosine after ischemic episode under long-term (7-14 days) reperfusion demonstrated its pronounced protective effect on neurological symptoms and animal mortality. Carnosine also prevented higher lipid peroxidation of brain membrane structures and increased a resistance of neuronal membranes to the in vitro induced oxidation. Measurements of malonyl dialdehyde (MDA) in brain homogenates showed its increase in the after brain stroke animals and decreased MDA level in the after brain stroke animals treated with carnosine. We concluded that carnosine compensates deficit in antioxidant defense system of brain damaged by ischemic injury. The data presented demonstrate that carnosine is effective in protecting the brain in the post-ischemic period.

General idea of this comprehensive review is to summarize information about the role of nitric oxide in the human body-cardiovascular, respiratory, urgenital, gut, NO and immune system, however, NO signaling has a role also in musculoskeletal system, even in bones. NO in the past had been recognized as a molecule relevant to air pollution. In 1980 Furchgott and Zawadzki identified new messenger molecule within the endothelial cells with vasodilating potential and they named it endothelium derived relaxing factor (EDRF). Seven years later the role of NO as a relaxing factor was definitely proven. The fact of gas, being produced by cells, crossing membranes of neighboring cells and having a character of signal brought a brand new insight to the signaling physiology. The breakthrough in the NO history was in 1992, when it was assigned as "molecule of the year". Role of NO was defined mainly in the cardiovascular system, but as the research expanded, the ultimate function, and mechanism of action, dual effect of NO had been identified in all systems of human body. NO in low concentrations considerably regulates the physiological functions, but in high concentration may contribute to the pathogenetic process. Knowledge the physiology of NO signaling cascades could have clinical application, mainly considering therapeutic potential of NO donors, or antagonists of NO-synthases. This molecule has undoubtedly huge future potential.

Abstract. The competition between arginases and NO synthases (NOS) for their common substrate L-arginine can be important in the airways hyperreactivity. We investigated the effect of the simultaneous modulation of arginase and NOS activities in allergen-induced airways hyperreactivity. We analysed the response of tracheal and lung tissue smooth muscle to histamine or acetylcholine after administration N ω -nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG) and N ω -hydroxy-L-arginine (NOHA) in the combinations in in vitro conditions. The results show the decrease of ovalbumin-induced hyperreactivity after inhibition of arginase activity with NOHA. A supplementation of L-arginine caused favourable effect on the airway smooth muscle response. We found the airway reactivity decrease on the whole if we used the combination of NOS and arginase inhibitors. The inhibition of both types of enzymes caused more expressive effect in tracheal smooth muscles. We recorded the difference in the response to histamine or acetylcholine. The simultaneous inhibition of iNOS (with AG) and arginase (with NOHA) evoked the most expressive effect. Results show the importance of competition of both types enzymes -NOS and arginase for the balance of theirs activities in the control of airways bronchomotoric tone in the conditions of the airways hyperreactivity.

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The results confirm the possibility of NMDA receptors participation in the experimental airways hyperreactivity.