Aim. To estimate in a 12-month study mortality and frequency of recurrent cardiovascular events, dynamics of neurological deficit and endothelial dysfunction in patients with the first-time ischemic stroke treated with simvastatin 40 mg/day in acute period of the disease. Materials and methods. The efficacy of high-dose simvastatin (40 mg/day) therapy initiated in acute stage of ischemic stroke was evaluated in 12-month comparative randomized study. Patients of the first group (n=97) received standard stroke therapy, and patients of the second group (n=86) also received standard treatment and simvastatin additionally. Combined endpoint (cardiovascular death + recurrent cardiovascular events + necessity of readmission), dynamics of neurological status and endothelial function were considered. Results. Primary combined endpoint was achieved in 66 cases in the first group (68.04%) and in 47 (54.65%) in the second one (p=0.043). Neurological status evaluated by National Institutes of Health Stroke Scale (NIHSS), Mini-Mental State Examination (MMSE) scale, and Scandinavian scales had a faster positive dynamics in patients receiving simvastatin. The same patients revealed more intense and quick decrease in desquamated plasma endotheliocytes. Conclusion. Simvastatin 40 mg/day prescribed along with neuroprotective and antihypertensive treatment in acute stage of ischemic stroke leads to lowering of recurrent cardiovascular events number, positive dynamics of neurological status, regression of endothelial dysfunction reflected by significant decrease in number of circulating desquamated endotheliocytes.

Complex impairment of peripheral blood flow in CHF including restricted microcirculation, attenuated regulatory mechanisms and impaired hemorheological properties caused the reduced oxygen utilization contributing to symptoms and advance of heart failure.

In consequence of limitation of capillary dilatation reserve the role of erythrocyte membrane elasticity and their microrheological properties is very important for the tissue perfusion. The drugs that enter blood flow could be as signaling molecules and their action can lead to alteration of red blood cell aggregation and whole cell deformability. Therefore the subject of this study was to estimate the effect of some antitumor chemotherapy drugs on red blood cell aggregation (RBCA) and deformability (RBCD). It was found that an exposure of red blood cells (RBCs) to cisplatin and epoetin alfa led to significant positive changes in the RBC microrheological properties. It was shown that cisplatin could activate tyrosine protein kinase (TPK). Preincubation of RBCs with the inhibitor of EGF-R and Src kinase lavendustin A was accompanied by a significant decrease of the cisplatin effect. It was found RBC aggregation rise after cell incubation with 5-fluorouracil. This effect was removed with Ca2+ chelation with EGTA and also with pentoxifylline. The drug for the targeted antitumor therapy sunitinib raised RBCA markedly. Whereas RBC deformability index was altered only slightly. The combination of two chemicals: sunitinib and cisplatin led to an elimination of proaggregative effect of sunitinib. Examination of the effects of some antitumor drugs on red blood cell microrheological properties has enabled us to suggest that the observed changes in red cell aggregation and deformability may be partly related to the effects of tyrosine protein kinase activation. It is accompanied by the alteration of red blood cell microrheology and the blood transport efficacy.

The review discusses published data on the effect of hydrogen sulfide on the functioning of the cardiovascular system. Hydrogen sulfide has become the third gas molecule, along with NO and CO, which was classified as gasotransmitters – signaling molecules, a unique feature of which is their ability to easily penetrate the cell membrane due to their good solubility in lipids. Signal transduction with the participation of gasotransmitters significantly differs from classical concepts – there is no need for either special membrane receptors or transport systems, gasotransmitters realize their effect practically in the zone of their biosynthesis, which makes such regulation fast and accurate. In the cardiovascular system, hydrogen sulfide has shown a pronounced cardioprotective effect, especially pronounced in conditions of hypertension and myocardial ischemia. Along with NO, hydrogen sulfide is the most important regulator of vascular tone, while it affects both the properties of the endothelium and regulates the contractility of vascular smooth muscle cells. The role of H2 S in the pathogenesis of arterial hypertension and the therapeutic potential of this gasotransmitter and its derivatives in arterial hypertension treatment both in animal models and in clinical studies have been demonstrated. Experimental data confirming the participation of hydrogen sulfide in the processes of angiogenesis and in the pathogenesis of atherosclerosis were published. For the cardiovascular system, the main function of which is the oxygen supply to organs and tissues, the ability of this gasotransmitter to influence the blood system and act as an oxygen sensor seems to be important. Hydrogen sulfide affects the functional properties of platelets, thrombus stability and microvascular thrombolysis; there is experimental evidence of the effect of H2S on the microrheological properties of erythrocytes and the process of erythrogenesis. And although the mechanisms of the effect of hydrogen sulfide have not yet been sufficiently studied, there is evidence that all gasotransmitters are in close interaction and their joint action gives a synergistic effect.

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