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Biomedical subjects

N A Mazur

Publications and source records attributed to N A Mazur.

At least 19 recordsLinked to original sources
PubMed1992

[Effect of captopril on myocardial ischemia, intracardiac hemodynamics and regional left-ventricular contractility in patients with stenocardia].

Technetium-99m pertechnetate equilibrium ventriculography was used to evaluate the effects of captopril in a single dose of 50 mg on the changes in ST segment depression during the identical bicycle ergometer exercise, as well as on systemic and regional hemodynamic parameters in 10 patients (mean age 52 years) with Functional Classes II-III exercise-induced angina pectoris. During exercise performed 45 and 90 minutes after captopril, ST segment depression decreased by 30 +/- 0 (p less than 0.05), and 32 +/- 10% (p less than 0.02), respectively as compared to baseline ST segment displacement. Following 90 minutes after the drug administration, end-systolic volume reduced both at rest and during exercise, resting stroke volume increased from 71 +/- 4 to 76 +/- 4 ml (p less than 0.01), whereas exercise stroke volume rose from 69 +/- 3 to 74 +/- 3 ml (p less than 0.03); with the drug, ejection fraction showed a 5% increase (p less than 0.02) at rest and a 4% increase (p less than 0.02) on exercise. Thus, captopril had a beneficial effect on the hemodynamics and reduced myocardial ischemia in patients with exercise induced angina.

Adult↗
PubMed1992

[The dynamics of the concentration of atrial natriuretic factor depending on changes in the arterial pressure level in patients with arterial hypertension].

The purpose of the study was to explore the dynamics of the concentration of atrial natriuretic hormone (ANH) in response to changes in arterial pressure including those induced by hypertonic crisis, 7-day hypotensive monotherapy with the drugs having different action mode, and the acute test with the basic hypotensive drugs. 75 patients suffering from arterial hypertension were entered into the study. Measurements of the concentration of ANH in blood plasma were performed by radioimmunoassay with the aid of the kits manufactured by the Amersham Company (Great Britain). The activity of renin and aldosterone was determined by radioimmunoassay according to the standard technique. A strong positive correlation was revealed between the concentration of ANH and the level of both systolic and diastolic AP. A significant rise of the concentration of ANH elicited by hypertonic crisis reflects the growth of the tension of the depressor mechanisms by which AP is regulated. The lack of significant changes in the level of ANH during the acute pharmacological tests and effective continuous treatment with the hypotensive drugs attests to the existence of the complex mechanisms that regulate ANH secretion, determined not only by the level of AP.

Aldosterone↗
PubMed1992

[The efficacy of combinations of anti-arrhythmia preparations in patients with the paroxysmal form of atrial fibrillation].

The efficacy of allapinin, ethacizine, ritmilen, kinilentin, obsidan and finoptin given alone and in different combinations was studied in 44 patients with paroxysmal atrial fibrillation provoked by transesophageal pacing. The use of the combinations of the drugs belonging to the first group as well of those of the first group combined with the drugs belonging to the 2nd-4th group permitted one to significantly enhance the treatment efficacy, to reduce drug doses in a lot of patients and, therefore, to minimize the rate of side effects. The data obtained promoted the choosing of the therapy algorithm to prevent paroxysms of atrial fibrillation. While designing the algorithm, account was taken of the rate of paroxysms and of the initial sinus rhythm as was of the results of estimating the comparative efficacy of the drugs under study.

Adult↗
PubMed1992

[Vasodilators and the catecholamine content of the blood plasma in patients with the moderate form of hypertension].

Vasodilators (verapamil, nifedipine, and prazosin) versus hypothiazide and clofelin were studied for their effects on resting and exercise blood levels of catecholamines in 58 patients with moderate arterial hypertension. Clofelin decreased norepinephrine levels, whereas hypothiazide increased it at rest and during exercise test. The most marked effect on norepinephrine levels was produced by nifedipine, then prazosin, particularly in patients with initially enhanced total peripheral vascular resistance. Verapamil failed to substantially affect norepinephrine levels. Due to the fact that the elevated levels of norepinephrine may have a negative action, it is suggested that antiadrenergic agents should be supplemented to a long-term therapy with nifedipine or prazosin.

Adult↗
PubMed1992

[Natriuretic hormone and blood pressure in patients with arterial hypertension].

The examination comprised 58 patients with essential hypertension and 17 with nephrogenic arterial hypertension. An analysis of the baseline levels of natural natriuretic factor in patients with essential and nephrogenic hypertension revealed no intergroup differences (55.3 +/- 3.0 and 45.7 +/- 5.2 ng/ml, respectively). The concentration of natural natriuretic factor was significantly higher in even patients with mild arterial hypertension than in healthy persons (28.4 +/- 4.7 and 17.4 +/- 2.9 ng/ml). There was a direct correlation between the level of natural natriuretic factor and blood pressure and left ventricular myocardial hypertrophy. There were higher positive correlations between the levels of natural natriuretic factor and those of hormones of the renin-angiotensin-aldosterone system and catecholamines in patients having a diastolic pressure of greater than 115 mm Hg. A significant increase in natural natriuretic factor levels (92.1 +/- 11.8 ng/ml) was found in the presence of hypertensive crisis.

Adult↗
PubMed1991

[Anti-anginal effects of calcium antagonists and intra-cardiac hemodynamics].

The intracardiac hemodynamics was studied in 33 patients with exertional angina pectoris undergoing an acute drug test with verapamil (n-15) and nifedipine (n-18) by using radionuclide ventriculography both at rest and during exercise. All the patients were divided into 2 groups by the increase in exercise duration with the two drugs: 1) those who exhibited a marked antianginal effect and 2) those without it. At rest, the calcium antagonists enhanced ejection fraction in the two groups. Exercise ejection fraction also increased, but in a subgroup of patients who displayed no higher exercise tolerance with verapamil. Verapamil and nifedipine in Group 1 patients resulted in lower left ventricular end diastolic volume. It is suggested that the antianginal effect of calcium antagonists is to a certain degree associated with decreased afterload, as manifested by diminished left ventricular end systolic volume.

Adult↗
PubMed1991

[Comparative effectiveness of class I anti-arrhythmia drugs and the algorithms of their selection in patients with ventricular arrhythmia].

The efficacy of 7 well-known Class I antiarrhythmic agents were retrospectively and by+crossover compared in 2 groups of patients treated in hospital in different years for ventricular arrhythmias. Class IC agents proved to be the most potent in the two groups of patients. The following algorithm is proposed to choose Class I agents: if quinidine or mexiletine is beneficial in the same patients, the other drugs will be also effective. If disopyramide fails to be beneficial, allapinin , ethacizine , propaphenon will be the most effective. When allapinin produces effects, ethacizine and propaphenon show their highest potency, but when each of them fails, a combination of antiarrhythmic agents should be used.

Adolescent↗
PubMed1990

[Calcium antagonists and the regional contractility of the left ventricle in stenocardia patients].

The overall and regional left ventricular ejection fraction (EF) was assessed by rest-exercise equilibrium radionuclide ventriculography in 33 patients (mean age 52.3 +/- 10.3 years) given a single dose of calcium-channel blockers (CCB). Of these, 18 patients were administered 20 mg of nifedipine and 15 patients received 80 mg of verapamil. According to the antianginal effects (AE) of nifedipine and verapamil at exercise all the patients were divided into 4 groups: 9 were on nifedipine, 10 on verapamil with AE (groups I and 3), 9 were on nifedipine, 5 on verapamil without AE (groups 2 and 4). After administration of a single dose of nifedipine and verapamil the overall rest EF increased in group I from 55.5 +/- 6.1 to 65.0 +/- 7.7%, in group 3, from 59.8 +/- 4.8 to 67.4 +/- 5.4%, in group 2, from 55.5 +/- 9.8 to 60.9 +/- 9.9%, and in group 4, from 54.8 +/- 5.4 to 59.6 +/- 4.5%. The exercise EF increased only in patients with AE of CCB (from 51.5 +/- 4.2 to 64.6 +/- 7.9%, group 1) and from 54.8 +/- 6.2 to 61.1 +/- 5.7%, group 4). In patients with AE of CCB (groups 1 and 3), the baseline values of the regional EF before drug administration decreased from rest to exercise in ischemic segments and that decrease ranged from 9 to 17%, while in patients of groups 2 and 4, from 1 to 8%. After administration of CCB insignificant improvement of the regional rest-exercise EF was recorded in groups 1 and 3 in the formerly ischemic segments.

Adult↗
PubMed1990

[Effect of cordarone on the cellular adrenergic systems].

Cordarone was examined for its effects on alpha- and beta-adrenergic receptors and adenylate cyclase (AC) of some tissues. Cordarone was shown to suppress the binding of [3H]-clonidine with alpha 2-receptors of the rabbit brain (Ki = 4 microM) and that of [3H]-prazosin with alpha 1-receptors of the rat liver (Ki = 22 microK), but not to displace [3H]-dihydroalprenolol from rabbit cardiac and pulmonary beta 1-receptors and from beta 2-receptors of rat reticulocytes and human lungs. Cordarone failed to affect the activity of rabbit heart and lung AC, as well as that of thrombocytes and human lungs, but showed a 80% inhibition of the activating effect of isoproterenol on reticulocyte AC. It was suggested that the effect of cordarone on reticulocytes was not mediated by beta-receptors and was tissue specific and dependent on the characteristics of AC regulation in these cells. Cordarone's antiadrenergic effect found in vitro may be one of the causes of its coronary dilating and antiarrhythmic effects.

Adenylyl Cyclase Inhibitors↗
PubMed1990

[Effects of cordarone on Ca2+-dependent cellular systems].

Cordarone was studied for effects on the pharmacological receptors of myocardial potential-dependent Ca channels, on the receptor-dependent increase in platelet Ca2+ content, on muscarinic cholinergic receptors of the M1- and M2-type, and on calmodulin regulation of cAMP phosphodiesterase (PDE). Without showing selectivity, cordarone is able to interact both with M1-, and M2-muscarinic choline receptors with Ki = 5.3-5.6 microM. Cordarone was found to displace [3H]-nitrendipine with Ki = 1.25 microM and [3H]-desmethoxyverapamil with Ki = 1 microM. The pattern of ligand displacement suggests that the interaction of cordarone with these receptors has no competition. Cordarone was demonstrated to affect neither PDE activity nor its activation with calmodulin. Cordarone suppressed a platelet activation factor-induced increase in intracellular Ca2+ levels in the thrombocytes. Thus, cordarone is capable of affecting Ca2(+)-dependent processes at Ca2+ entry across the potential-dependent Ca channels and influencing the receptor-dependent platelet Ca2+ mobilization and muscarinic cholinergic regulation. The above effects may underlie antiarrhythmic action and determine vascular dilating and anti-fibrillating properties of cordarone.

3',5'-Cyclic-AMP Phosphodiesterases↗