Despite numerous studies cardiovascular diseases are among the leading causes of death and disability. Thus, researches’ objectives focused at understanding the pathogenesis and development of preventive measures are obviously shifted toward endothelial dysfunction and the cytokine role in developing atherosclerotic vascular lesions. The use of HMG-Co-A reductase inhibitors of simvastatin, atorvastatin, rosuvastatin and nanoparticulative rosuvastatin against the background of simulating endotoxin-induced pathology by introducing 603 Staphylococcus aureus strain leads to the development of dose-response endothelioprotective action, manifested itself in normalization of QED, prevention of increased adrenoreactivity and exhaustion of myocardial reserve, and normalization of biochemical markers of inflammation (C-reactive protein) and proinflammatory cytokine level. However, the positive dynamics of NO end-products and expression of eNOS were revealed.

Many recent studies have confirmed the effect of NO and that its relative signaling pathway is important for preconditioning of the cardioprotective effect. Mitochondria as a target for the cardioprotective effects of nitric oxide in ischemia-reperfusion injury is considered to be the ultimate goal of cardioprotection. During preconditioning, signaling is initiated from the sarcolemmal membrane and then spread into the cytoplasm via many series of enzymes, including nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC), and protein kinase G (PKG). As a result, the signal is transmitted into the mitochondria, where the cardioprotective effect occurs. It is now well established that mitochondria act to protect the heart against ischemia-reperfusion injury via the opening of the mitochondrial ATP-sensitive K+ channel and the inhibition of mitochondrial permeability transition. This knowledge may be useful in developing novel strategies for clinical cardioprotection from ischemia-reperfusion injury.

The article is about possibilities of correction L-NAME indused deficiency of the nitric oxide by arginase inhibitor L-norvaline. Nitrous oxide is the basic vasodilatative agent in an organism. L-arginine is the basic sourse of nitrous oxide. Arginase enzyme of urea cycle, wich catalized metamorphosis of L-arginine in an ornithine. Oppression of activity of this enzyme by arginase inhibitors increases nitrous oxide production.

At the laboratory of the Cardiofarmacology Scientific Research Institute of Ecological medicine endothelioprotective, cardioprotective activity of inhibitor of 3-gidroksi-3-metilglutaril-CoA reductase simvastatin and its combinations with L-arginin and resveratrol were investigated in experiments on rats. The received results have shown the presence of expressed endothelioprotective effects, amplifying with additional introduction of L-arginin and resveratrol at simvastatin The most expressed correction of endothelial dysfunction is observed in application of simvastatin in a combination with L-arginin. Warm loading tests have revealed more expressed cardioprotective activity of simvastatin, in comparison with its combinations with L-arginin and resveratrol.