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O V Baziliuk

Publications and source records attributed to O V Baziliuk.

At least 19 recordsLinked to original sources
PubMed2005

[Age-related characteristics of contractile vascular reactions and the content of oxygen free radicals and nitric oxide metabolites in BALB/c mice in conditions of alienation zone].

Peculiarities of changes of the endothelium-dependent and endothelium-independent vascular reactions of relaxation, and the content of oxygen free radicals and stable metabolites of nitric oxide (NO) were studied in the aorta preparations of BALB/c mice of the two age groups (6 and 18 months), which were born and lived in the Chernobyl alienation zone. The results obtained showed no endothelium-dependent reactions of aortal smooth muscles relaxation to acetylcholine and only partially impaired endothelium-independent reactions to sodium nitroprusside in animals of both age groups. There was a significant decrease in the content of high-molecular nitrosothiols (HMNT) in old animals, which may signify a depletion of NO depot in the aorta. A decrease of HMNT levels induced an increase of the shares of anion nitrite and low-molecular nitrosothiols (LMNT) in the total amount of endogenous donors of NO in the aorta of old animals. Exposure of old animals to low doses of radiation resulted in an over 3-fold increase of LMNT. In old mice the levels of oxygen active forms, superoxide and hydroxyl radicals increase, while the level of H2O2 remained unchanged.

Aging↗
PubMed2004

[Inhibitors of arginase pathway in L-arginine metabolism as a new class of antihypertensive drugs: action of urea on oxidative and nonoxidative metabolism of L-arginine and vascular tone in chronic hypertension].

It has been studied an action of chronic urea introduction (40 mg/kg, 14 and 28 days) as arginase inhibitor on nonoxidative (arginase activity, urea, polyamines content) and oxidative (NOS activity, nitrite- and nitrate-anion content) metabolism of L-arginine in aorta, heart, plasma and erythrocytes of SHR. It has been shown that urea is an inhibitor of not arginase only, but also ornitinedecarboxilase (ODK) reactions, limiting L-arginine consumption for urea and polyamines synthesis and thus facilitating its utilization for nitric oxide synthesis by NOS. These exogenous effects of urea are not accompanied by amelioration of tissue ischaemization within cardiovascular system. It has been shown that exogenous urea down regulate blood pressure without any normalization of endothelim-dependent reactions of smooth muscle cells on acetylcholine in SHR.

Animals↗
PubMed2002

[Endothelium-dependent contractile reactions of vascular smooth muscles and content of oxygen free radicals in aging rats].

Endothelium-dependent and endothelium-independent reactions of vascular smooth muscles were studied in isolated preparations of thoracic part of aorta and portal vein of rats of two age groups--6.8 mo. (control) and 24-26 mo. (old animals). In old rats the disturbances occurred primarily in endothelium-dependent vascular reactions. This age-related dysfunction of endothelium resulted in inhibition of NO-dependent regulation of vascular tone. Age-related changes in the state of plasmic membranes of erythrocytes were established using a method of acid hemolysis. Age-related changes in the levels of active forms of oxygen (.O2-, H2O2, .OH-) and nitrogen (NO2-, NO3-) were determined in the myocardium, aorta, blood plasma and erythrocytes of adult and old animals.

Aging↗
PubMed2001

[Inhibitors of arginase in the L-arginine metabolic pathway as a new class of antihypertensive drugs: effect of carbamide on lipid oxidative metabolism and on vessel tonus during arterial hypertension].

Have studied action of chronic urea--an arginase inhibitor--introduction (40 mg/kg, 28 days) on blood pressure, endothelium-dependent reactions of aorta smooth muscle cells (SMC) and nonenzymatic (contents of diene conjugates and H2O2) and enzymatic (contents of free arachidonic acid and vasoconstrictic eicosanoids LTC4 and TXA2) oxidizing lipid metabolism of heart, aorta, plasma and erythrocytes of spontaneously hypertensive rats. Have shown, that urea down regulate blood pressure without any normalization of endothelium-dependent reactions of SMC of aorta and down regulate both enzymatic and nonenzymatic oxidizing lipid metabolism. Down regulation of two alternative (by cyclooxygenase and by lipoxygenase) enzymatic pathways of free arachidonic acid oxidizing metabolism by urea can be one of mechanisms of its antihypertensive action. The possibility of urea use at hypertension and various pathophysiological conditions are discussed.

Animals↗
PubMed2000

[The nitric oxide system in a chronic deficiency of mesostriatal dopamine: the action of nitroglycerin].

Unilateral chronic deficiency in dopamine was induced by injection of the neurotoxin 6-hydroxydopamine into the mesostriatum of male Wistar rats (n = 15). The content of the nitric oxide metabolite--NO2- was three time less than in controls in the neostriatum on the operated side only, whereas, in the heart, aorta and plasma it was reduced by 1.9, 1.7 and 3.2 times, respectively. Four hours after subcutaneous injection of nitroglycerin (10 mg/kg, n = 4), a significant 6 fold increase in NO2- content in the neostriatum in the operated hemisphere and 2 fold increase on the in the intact side was observed. In heart, aorta and plasma NO2- content increased 2, 9, 3 times, respectively. The same dose of nitroglycerin given to intact rats (n = 4) had less effect on NO2- content: a 2 fold increase in heart, aorta and plasma only. Activity of NO-synthase (NOS) in animals with dopamine deficiency was reduced 2.7 fold in the neostriatum of the operated hemisphere and by 1.8 time on the intact side, in heart and aorta--by 1.8 and 3 time, respectively. Injection of nitroglycerin increased activity of NOS in the neostriatum of the operated hemisphere 2 fold and on the intact side 3 time; in heart (11 time) and aorta (1.3 time) after 4 hours. Similarly subcutaneous nitroglycerin injection restored the reduced endothelium-dependent vasodilator responses characteristic of the rats with mesostriatal dopamine deficiency. Thus the amplitude of acetylcholine-induced smooth muscles relaxation of the aorta increased by more than 70%. In these animals the injection of nitroglycerin also exerted a normalizing effect on the characteristic apomorphine-induced behaviour asymmetry (rotatory movements). On week after the injection of nitroglycerin the rotatory behaviour was reduced by 20.7% of control rotations. We show that nitroglycerin, a NO-donor, is a useful drug. It correct the abnormalities in the metabolic pathways on NO synthesis in a variety of tissues, endothelium-derived vascular responses and also the behaviour abnormalities induced by unilateral mesostriatal lesions. Our experimental animals are thought to be a model of human hemi-Parkinsonism. Thus nitroglycerin might be of use in Parkinson's disease.

Animals↗
PubMed2000

[Disorders of endothelium-dependent vascular reactions and of the arginase and NO-synthase pathways of L-arginine metabolism in arterial hypertension].

In normotensive rats (NTR) and spontaneously hypertensive rats (SHR) with high (subgroup 1) and low (subgroup 2) level of the systemic arterial pressure (SAP) we studied an activity of arginase and nitric oxide synthase (NOS) in different tissues, and the content of their metabolites: urea and nitrit anion (NO2-). In isolated preparations of a thoracic aorta we recorded endothelium-dependent (ED) dilator reactions on acetylcholine (Ach). It has been found that in heart, aorta, plasma and erythrocytes of rats (subgroup 2) both the activity of arginase and content of urea increase remarkably. In heart, the activity of arginase reaches 27.96 +/- 5.92 nmol.min-1.mg-1 of protein, in aorta 4.74 +/- 0.99 nmol.min-1.mg-1 of protein (as compared with NTR 1.32 +/- 0.12 nmol.min-1.mg-1 of protein and 1.12 +/- 0.07 nmol.min-1.mg-1 of protein, accordingly). Content of urea in heart reaches 679.5 +/- 121.19 nmol.mg-1 of protein, in aorta 350.6 +/- 63.6 nmol.mg-1 of protein (in NTR it was 36.8 +/- 5.3 nmol.mg-1 of protein and 43.02 +/- +/- 9.55 nmol.min-1.mg-1 of protein, accordingly). It was followed with a decrease in the NOS activity and heterogeneous changes in NO2- content in the tissues under exploration. For example, the activity of NOS in heart and aorta decreased to 0.018 +/- 0.005 nmol.min-1.mg-1 of protein, in aorta 0.183 +/- 0.037 nmol.min-1.mg-1 of protein, accordingly, as compared to 0.093 +/- 0.014 nmol.min-1.mg-1 of protein and 0.41 +/- 0.07 nmol.min-1.mg-1 of protein in NTR. Content of NO2- in aorta decreased by 0.79 +/- 0.06 nmol.mg-1 of protein, but in heart it increased to 0.63 +/- +/- 0.13 nmol.mg-1 of protein, (in NTR it was 2.15 +/- 0.18 nmol.mg-1 of protein and 0264 +/- 0.04 nmol.min-1.mg-1 of protein, accordingly). In rats, subgroup 2, ED dilator responses of the smooth muscle (SM) of the thoracic aorta were inhibited by Ach (10(-6) mol). Their amplitude reduced by almost twice, and a latency for their response became 4 times as much. All the changes in the biochemical parametres in heart, aorta, plasma and erythrocytes, and changes in contractile activity of vascular SM proved to be also characteristic for rats in subgroup 1, but they were less expressed quantitatively. Thus, for the first time we have studied an activity of two alternative pathways for the metabolism of L-arginine on the model of arterial hypertension. The data obtained evidence that at hypertension non-oxidative (arginase) pathway of L-arginine metabolism is activated, while the oxidative pathway (NOS) is inhibited. Changes in the balance between them are followed with an essential inhibition of ED vasodilator responses. All this give us the prove to think of the origin for the arterial pressure increase to be both genetically and quantitatively determined damages in the biochemical homeostasis and dependent on it endothelial regulation of vascular tone.

Acetylcholine↗
PubMed1999

[The nitrous oxide system under conditions of chronic cerebral dopamine deficiency and hypoxia].

Acute experiments were conducted on adult Wistar rats two months after unilateral microinjection of the 6-hydroxydopamine into the medial forebrain bundle. This led to a greater than 90% decrease of dopamine, fell by 70% of the content of the stable metabolite of nitric oxide-nitrite anion and by up to 80% of nitric oxide synthase activity in the lesioned neostriatum. Nitric oxide synthase activity fell by 30% in the heart, by 60% in the aorta, while nitrite anion decreased in the heart and aorta, in blood plasma and erythrocytes by 45%, 40%, 70%, 30% compared with controls rats, respectively. Lesioned rats also showed changes in the pattern of responses of the smooth muscle of the aorta predominantly to endothelium-dependent (acetylcholine), rather than to endothelium-independent (nitroprusside) vasoreactivity. The amplitude of acetylcholine-induced relaxation of aortic smooth muscle decreased 4-fold, the rate of this response decreased 5-fold and the latent period increased 4-fold. Exposure of lesioned rats, controls rats to moderate hypoxia for 30 min resulted in a rise of nitrite anion content in all tissues; it increased 2-fold in erythrocytes of lesioned rats vs controls rats, in the lesioned and unlesioned neostriatum hypoxia restored the values to controls, while in the heart, aorta and plasma the levels were also increased but did not reach control values. Hypoxia also led to a rise of nitric oxide synthase activity in both lesioned rats and controls rats. However, compared to normoxia, the levels increased over 2 times in the lesioned neostriatum and in the heart, whereas in controls the increase was less that 2-fold. Hypoxia resulted in partial normalization of the functional deficit in endothelium-dependent dilatory responses of aortic smooth muscle. We conclude that the disturbances in nitric oxide system induced by mesostriatal dopaminergic lesions in animals may have relevance to Parkinson's disease. The improvement with ambient hypoxia in quantitative and functional aspects of the disturbances in nitric oxide system may also have relevance in the management of the disease.

Animals↗
PubMed1997

[The role of the endothelium and of biologically active substances of endothelial origin in regulating blood circulation and cardiac activity].

The role of endothelium and its biologically active derivatives in the central and local control of circulation is under consideration. Molecular and cellular mechanisms of the activation of the endothelium-dependent responses of different functional significance are being discussed, as well as the state of endothelial responses in the development and compensation of pathological processes in the cardiovascular system.

Animals↗
PubMed1989

[Cellular mechanisms of transitory smooth muscle contraction of the coronary arteries during hypoxia: role of intracellular Ca2+].

In experiments on isolated porcine and canine coronary artery rings it was shown that vascular smooth muscle (VSM) during hypoxia (decreasing bath PO2 with 147 to 20-15 mm Hg) response to biphasic constriction-dilation reaction. Transient hypoxic contractions (THC) of VSM preserved completely in Ca2+-free solution and partially (up 50-60%) in the presence of Ca2+-channel blockers, but abolished by procaine. THC of VSM skinned by saponin significantly depressed at depletion of Ca2+-store sarcoplasmic reticulum (SR) by caffeine nd abolished after SR destruction. THC is not linked with Na+-K+-ATPase inhibition because it preserved (or increased) at ouabain treatment. THC significantly depressed under selective glycolysis blockade by monoiodoacetic acid and pyruvate and also after inositol-1 monophosphatase inhibition by lithium (the phase of hypoxic relaxation of VSM was augmented in this condition). Our results indicate that transient contraction of coronary arteries under hypoxia may be mediated mainly by release of Ca2+ from SR and linked obviously with production of inositol-1,4,5-trisphosphate. The participation of glycolysis in this process is unknown.

Animals↗
PubMed1989

[Endothelial modulation of arterial smooth muscle reactions to biological amines and electrical stimulation].

The effects of 5-hydroxytryptamine (5-HT), noradrenaline (NA), acetylcholine (Ach), ATP and electrical stimulation (ES) were studied in isolated porcine epicardial coronary artery and the rat thoracic aorta preparations. A dose-dependent contraction of vascular smooth muscle (VSM) segments with endothelium in response to biological amines (10(-7)-10(-5) M) and ES (2-16 Hz, 20 msec, 50 V) was demonstrated. Removal of the endothelium abolished the dilatory effect of the ATP (10(-5) M), Ach (10(-7) M), but potentiated the constrictor responses of the VSM to 5-HT, NA, ES. The results corroborate the hypothesis that the endothelium-derived relaxing factor, first, promotes the effect of vasodilators and, second, limits the vasoconstrictory effect to endogenous neurohumoral stimuli and plays a major role in the protection against a vasospasm.

Animals↗
PubMed1988

[Mechanisms of endothelium-dependent transient contraction of coronary artery smooth muscles during hypo-oxygenation].

The effect of endothelium on hypo-oxygenation--induced reactions of preactivated smooth muscle (SM) of the canine and porcine large coronary arteries, was studied. Decreased oxygenation of Krebs--bicarbonate solution (PO2-26.6-19.9 gPa) resulted in biphasic changes in the preparation with intact endothelium: a considerable relaxation was preceded by transient contractions. After removal of the endothelium a transient increase of tension was reduced or absent. Blockade of prostaglandins, leukotrienes and free radicals did not affect hypo-oxygenation-induced contraction of the VSM. The data suggest that endothelium can modulate the response of the coronary arteries SM to decrease in oxygen tension. Endothelium-dependent transient contraction during hypo-oxygenation is mediated through the increase of cGMP production.

Animals↗
PubMed1988

[Magnesium ions and contractile activity of vascular smooth muscle cells in hypoxia].

In isolated smooth muscle of the rat portal vein removal of Mg2+ from perfusate induced rapid enhancement of frequency and amplitude of spontaneous contractions and decreased inhibiting effect of hypoxia on the smooth muscle contractile activity. Concomitant elevation of extracellular Ca2+ has no additional protective effect on the smooth muscle in hypoxia. Ten-fold lowering of Mg2+ content in buffer solution resulted in a significant rise in the tension of the smooth muscle activated by Ca2+. The data obtained suggest that protective effect of Mg2+-free solution on vascular smooth muscle in hypoxia may be mediated not only through increases intracellular Ca2+ concentration but also due to rising sensitivity of the smooth muscle cells contractile protein to Ca2+.

Animals↗
PubMed1986

[Role of the endothelium in the development of the contractile reactions of vascular smooth muscle during decreased oxygenation].

Noradrenaline-preactivated vascular smooth muscles (VSM) of the rat thoracic aorta showed two-phase reactions in response to decreased oxygenation: significant relaxation was preceded by transient constriction. When the endothelium was removed only VSM relaxation phase was retained, with no constriction observed. The data obtained suggest an endothelium-dependent nature of VSM constriction reaction to hypoxia, in contrast to endothelium-independent VSM relaxation. Intracellular calcium is also assumed to play an essential role in the formation of endothelium-dependent constriction VSM reaction to hypoxia.

Acetylcholine↗
PubMed1981

[Changes in sympathetic activity in the renal and splenic nerves upon stimulation of bulbar nuclei during hypoxic hypoxia].

Microinjections of acetylcholine into the cat ventral reticular nucleus and nucleus of tractus solitarii in acute hypoxic hypoxia induce much lesser changes of efferent activity in renal and splenic nerves than in normoxia. Stimulation of the ventral reticular nucleus in hypoxia induces more obvious shifts of the efferent nerve activity than stimulation of the tractus solitarius nucleus. Bulbar reflex influences on cat's renal vascular bed are much more reduced in hypoxia than on the splenic one.

Acetylcholine↗
PubMed1981

[Effect of restricted oxygenation of vascular smooth muscles on the contractile effects of direct electrical and mechanical stimulation].

Contractility reactions of the smooth muscles of the rat portal vein and the umbilical vein of man to direct electrical stimulation and rapid stretch were examined under different PO2 levels in perfusate. It was shown that during perfusion of vascular preparations with oxygenated Krebs solution, the active myogenic responses to rapid stretch and contractility reactions to electrical stimulation are well pronounced and dependent on the stimulation intensity. The decrease in perfusate PO2 is accompanied by a considerably less increment of the amplitude of spontaneous contractions and tonic tension of the smooth muscles in response to direct mechanical and electrical stimulation, respectively. The data obtained allow a suggestion that physiological variation of the PO2 level may influence the reactivity and myogenic activity of the vascular smooth muscles and that this mechanism may participate in the local blood flow control and correction of central neurogenic effects.

Animals↗