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One of the most important pathological consequences of renal ischemia/reperfusion (I/R) is kidney malfunctioning. I/R leads to oxidative stress, which affects not only nephron cells but also cells of the vascular wall, especially endothelium, resulting in its damage. Assessment of endothelial damage, its role in pathological changes in organ functioning, and approaches to normalization of endothelial and renal functions are vital problems that need to be resolved. The goal of this study was to examine functional and morphological impairments occurring in the endothelium of renal vessels after I/R and to explore the possibility of alleviation of the severity of these changes using mitochondria-targeted antioxidant 10-(6'-plastoquinonyl)decylrhodamine 19 (SkQR1). Here we demonstrate that 40-min ischemia with 10-min reperfusion results in a profound change in the structure of endothelial cells mitochondria, accompanied by vasoconstriction of renal blood vessels, reduced renal blood flow, and increased number of endothelial cells circulating in the blood. Permeability of the kidney vascular wall increased 48 h after I/R. Injection of SkQR1 improves recovery of renal blood flow and reduces vascular resistance of the kidney in the first minutes of reperfusion; it also reduces the severity of renal insufficiency and normalizes permeability of renal endothelium 48 h after I/R. In in vitro experiments, SkQR1 provided protection of endothelial cells from death provoked by oxygen-glucose deprivation. On the other hand, an inhibitor of NO-synthases, L-nitroarginine, abolished the positive effects of SkQR1 on hemodynamics and protection from renal failure. Thus, dysfunction and death of endothelial cells play an important role in the development of reperfusion injury of renal tissues. Our results indicate that the major pathogenic factors in the endothelial damage are oxidative stress and mitochondrial damage within endothelial cells, while mitochondria-targeted antioxidants could be an effective tool for the protection of tissue from negative effects of ischemia.

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In experiments on rats using high frequency ultrasonic measurement technique and selective M4-cholinoreceptor antagonist tropicamide it was shown that i/v injection of the cholinolitic block agent in large doses exceeding of its selective threshold (1 mg/kg) causes pronounced inhibition of the cardiovascular system in rats. Severe transitory hypotension and bradycardia are developed, general vascular resistance, minute cardiac output, are decreased. The block of M4-cholinoreceptors with smaller doses of tropicamide (0.1-0.001 mg/kg) causes transitory dose-depended effect on hemodynamic--system blood pressure and vascular resistance, pulse, minute cardiac output, as soon as velocity of aortic blood flow, strike cardiac output are increased on the contrary. The following decrease the dose of the high selective M4-cholinolitic antagonist (0.0001 mg/kg) reveals that its negative chronotropic effect are not detected practically but tropicamide vessel action (decrease of system blood pressure and vascular resistance) are preserved distinctly. The obtained data are discussed in aspect of the possible involvement of M4-muscarinic receptor subtype in acetylcholine-induced vasoconstriction in rats.

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We studied changes in breathing pattern in nembutal-anaesthetized mongrel rats after administration of euphylline against the background of preliminary treatment with lithium hydroxybutyrate. Two types of external respiration responses to euphylline were observed; they depended on the initial blood pressure in systemic circulation and on its drop after euphylline administration. Thus, the reaction of the respiratory system to adenosine receptors blockade against the background of hydroxybutyrate pretreatment was associated with not only the effect of euphylline, but also the state of brain hemodynamics. The effects of euphylline on chemosensitive contour of the respiratory system regulation were also investigated. It was found that euphylline did not abolish desensitization of respiratory system to hypercapnia, but smoothed the response to hypoxia under conditions of GABA(b)-receptor activation.

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The present study is aimed toward a comparative real-time analysis of organ-specific characteristics of the liver, kidney and brain blood supply in the dynamics of acute massive hemorrhage in rats with different resistance to circulatory hypoxia. The survival time of experimental animals after the arrest of bleeding was used as a criterion of their resistance to acute blood loss. The rats with high resistance (HR) to hypoxia had the survival time not less than 3 h, while the rats with low resistance (LR) to hypoxia lived not more than 1.5 h. A marked decrease in arterial organ blood flow velocity and tissue perfusion of the liver, kidney and brain in LR and HR rats was observed at the end of acute massive hemorrhage in ultrasonic and Doppler flowmetry. In the post-hemorrhagic period the organ hemodynamics and microcirculation showed a tendency to a further decrease in LR rats. In HR animals the blood flow velocities in hepatic, renal and common carotid arteries were temporarily restored to 115-120, 85-90 and 60-65%, respectively, following the bleeding arrest. In the compensated phase of the post-hemorrhagic period the brain blood flow was maintained at this new post-hemorrhagic level due to autoregulatory changes in the carotid resistance. Such a response of brain blood vessels of HR rats is considered to be an adaptive response which protects the brain from autoreperfusion- and reoxygenation-induced injuries under conditions of posthemorrhagic autorestoration of tissue circulation.

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To date the hindlimb suspension model utilizing rats has a wide application to simulate weightlessness. In our previous study we have examined the cardiovascular responses in the tail suspension model using the radiolabeled microspheres technique. We have reported increases of cardiac output (CO) and decreases of total peripheral vascular resistance (TPVR) after 24 hours of head-down tilt (HDT). However, there is no comparison of arterial and venous systems parameters with blood flow changes in organs and tissues. Apart from the preliminary HDT training influence on these parameters is unknown. Thus we aimed to evaluate the role of HDT training in central circulation responses, venous tone and regional blood flow.

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