Publications by authors named "Uchitel I"

Optimal duration of dual antiplatelet therapy (DAPT) after stent implantation is uncertain. Some patients have an extended risk of thrombotic complications including that of very late stent thrombosis after cessation of recommended course of DAPT (6-12 months). On the other hand, there is a real risk of bleeding on DAPT.

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A covalent bienzyme superoxide dismutase-chondroitin sulfate-catalase conjugate (SOD-CHS-CAT) demonstrated the dose-dependent inhibitory action on induced aggregation of platelets in the presence of hydrogen peroxide. Antioxidant activity of SOD-CHS-CAT appeared at much lower doses than for other CAT derivatives. We detected the antiaggregation effect of SOD-CHS-CAT for platelet aggregation induced by ADP, serotonin, TRAP (with their different mechanism of action).

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Effects of H(2)O(2) on platelet aggregation were estimated in vitro in the presence and absence of inductors (ADP, serotonin, TRAP) and native and modified catalase. Dose-dependent effect of H(2)O(2) (50 μM or more) was investigated in a pathophysiological concentration of 300 μM inducing platelet aggregation. H(2)O(2) modulated aggregation induced by ADP, serotonin, and TRAP significantly increasing the initial platelet aggregation followed by disaggregation, which was always more pronounced than in control.

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Bienzyme conjugate was obtained by the covalent connection of superoxide dismutase with catalase through endothelial glycocalyx glycosaminoglycan - chondroitin sulfate (SOD-CHS-CAT). This SOD-CHS-CAT conjugate has vasoprotective activity in respect to platelet interactions, tonus of the ring arterial fragment of a rat blood vessel, as well as normalization of hemodynamic parameters in rats and rabbits in conditions of oxidative stress caused by the administration of hydrogen peroxide. The SOD-CHS-CAT conjugate had antiplatelet potential due to its antiaggregation action manifested through the combination of enzyme activities and an acquired supramolecular structure.

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We studied morphological characteristics of platelets and parameters of platelet aggregation in patients with dilation cardiomyopathy. Augmented aggregatory activity of platelets was found in 76% of patients. In blood of majority of patients we found circulating leukocyte-platelet aggregates.

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Aim: To evaluate platelet activity changes in patients with coronary artery disease (CAD) treated with aspirin, clopidogrel and combination of these drugs; to estimate the rate of resistance of CAD patients to antiplatelet treatment.

Material And Methods: 199 patients with stable CAD were included in the study. Of them, 83 were given aspirin, 46 received clopidogrel, 34--double antiplatelet therapy (both aspirin and clopidogrel).

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In some patients with stable and unstable angina pectoris and in some donors without clinical manifestations of cardiovascular diseases and other pathologies, spontaneous platelet aggregation was completely suppressed by glycoprotein IIb-IIIa antagonists blocking the interaction of this glycoprotein with fibrinogen. Antibodies inhibiting binding of glycoprotein Ib with von Willebrand factor had no effect on the level and rate of spontaneous platelet aggregation. In the donor group, the level of spontaneous aggregation was almost 1.

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Aim: To study morphological features and functional activity of platelets, their relations with the level of inflammation markers in coronary heart disease (CHD) patients with depression.

Material And Methods: The study group consisted of 33 CHD patients with stable effort angina (NY-HA FC I-III), 14 had depression, 19 were free of depression. Sixteen healthy volunteers comprised the control group.

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Human arterial tissue was shown to have renin-like activity. For its determination the authors propose methodological approaches. The optimum pH of renin activity in the vascular wall was found to be 5.

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The results of examination and treatment by surgery of 103 patients with vasorenal hypertension are analysed. Retromboses and restenoses of the reconstructed renal arteries and grafts and uncorrected hyperaldosteronism were the most frequent causes of the poor results. Adequate reconstruction of the renal arteries leads to correction of hyperaldosteronism in patients with normal or high activity of plasma renin.

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The captopril test was used to make a differential diagnosis of various types of primary aldosteronism. After captopril, there was no change in the activity of the renin-angiotensin-aldosterone system only in the group of patients with aldosterone-producing adenomas in a histological variant of "adenoma and atrophy". The findings suggest that aldosterone secretion regulation is autonomic in the adenoma unassociated with the function of the renin-angiotensin-aldosterone system only in the case of isolated adenoma with a histological variant of adenoma and atrophy.

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Unilateral adrenalectomy was performed in 32 patients with primary hyperaldosteronism due to tumour of the adrenal gland and with arterial hypertension (AH) of various degree of severity. Stable normalization of AH occurred in 14 patients and in 18 its course improved. The results of a retrospective analysis of a hypotensive effect, the morphological picture of the removed adrenal and the findings of clinico-biochemical and instrumental study made it possible to establish preoperatively the diagnostic criteria for the identification of two tumorous forms of primary hyperaldosteronism: aldosterone-producing adenoma proper and the tumorous form of adrenocortical hyperplasia.

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Components of the renin-angiotensin system (plasma renin activity, total and inactive renin, angiotensinogen and angiotensin II) were examined in 90 patients with labile and stable essential hypertension before and after functional and pharmacologic tests. New data have been obtained on intrasystemic regulatory mechanisms of the pressor renin-angiotensin systems. Different patterns of plasma active and inactive renin variations in response to salt loading are demonstrated in patients with different "renin" variants of essential hypertension.

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Captopril effects were studied in 27 patients with second-stage essential hypertension following administration of a single 25 mg oral dose of the drug. Blood pressure (BP), blood angiotensin-1-converting enzyme (ACE) activity, active (APR) and inactive (IPR) plasma renin levels were measured every 30 minutes for 3 hours. Before and near the end of the acute test, urinary kallikrein and catecholamine excretions were measured, and systemic and regional hemodynamic changes assessed.

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The total renin activity (TRP) and inactive renin levels (IR) in the blood plasma were examined with the help of cryo- and trypsin activation in 9 normal subjects, in 40 patients with essential hypertension and in 18 patients with primary aldosteronism (PA). The cryoactivation method was shown to detect 40-80% of IR determined by the method of trypsin activation. Both methods revealed analogous ratios of the two renin forms in its total production in the presence of essential hypertension (in different "renin" subgroups) and arterial hypertension secondary to PA and may be used as the methods of choice when examining essential hypertension patients with the normal and subnormal plasma renin activity.

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The authors studied the effect of adrenocorticotropic hormone (ACTH), potassium and plasma renin activity on blood aldosterone in normal subjects as well as in patients with essential hypertension (of a labile and stable course) and hyperaldosteronism (primary and idiopathic). It was demonstrated that in normal subjects and patients with labile essential hypertension, the secretion of aldosterone was simultaneously stimulated by the renin-angiotensin system (RAS) and the hypothalamus-adenopituitary. The RAS dominated in normal conditions whereas in labile hypertension the hypothalamus-adenopituitary system was predominant.

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Two forms of renin (active-APR and inactive-IPR) and its total production were studied in relation to the daily excretion of kallikrein in patients with essential hypertension of the labile and the stable stage at rest and following the stimulation by an hour's walk and the intravenous infusion of prostaglandin E (PGE). The results showed inverse correlations of APR and IPR in the total production of renin in hypertensive patients in different "renin" subgroups, and an inverse correlation between the level of IPR and the 24-hour excretion of kallikrein in the basal conditions and following an hour's walk. PGE infusion elevated APR and decreased IPR levels, leaving the total production of renin unchanged.

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Renin-aldosterone function was studied in 23 patients with low-renin essential hypertension (LREH) under resting and stimulated conditions. Patients were selected on the basis of differential diagnostic tests of renin-angiotensin stimulation and inhibition as well as roentgeno-radiologic findings in order to rule out adrenal lesions. The results were compared with those of patients with primary aldosteronism and with essential hypertension where renin activity can be stimulated under similar sodium balance conditions.

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Levels of PGE2, PGF2 alpha and renin activity were measured in renal venous blood of 29 patients with essential hypertension (EH), 23 patients with renovascular hypertension (RVH) and 10 patients with unilateral pyelonephritis and high arterial hypertension. The pattern of change in renal venous PG content was found to be related to the type of renal lesion: the level of PGE2 was lowered and PGF2 alpha/PGF2 ratio increased in the blood outflow from the kidneys of EH patients and from ischemized kidneys of RVH patients as compared to similar parameters in the outflow from contralateral kidneys of patients with RVH and pyelonephritis. Venous levels of both PGs were the highest in pyelonephritis-affected kidneys.

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