Publications by authors named "Krandycheva V"

Background: To understand electrophysiological mechanisms that underlie the progression of compensated right ventricular hypertrophy (RVH) to heart failure, the purpose of the study was to evaluate remodeling of ventricular repolarization in connection with hemodynamic abnormalities and vulnerability of the heart ventricles to arrhythmias in RVH rats with pulmonary arterial hypertension (PAH) and heart failure.

Methods: PAH followed by heart failure was induced by monocrotaline in adult female Wistar rats. Unipolar epicardial electrograms and cardiac hemodynamic parameters were recorded in situ.

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Isoproterenol in high doses induces infarction-like myocardial damage and structural and functional remodelling of the ventricular myocardium. The purpose of the present study was to investigate ventricular repolarization in a rat model of isoproterenol-induced heart failure. Isoproterenol was administered twice to female Wistar rats (170 mg/kg, s.

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Anthracycline chemotherapy produces cardiac repolarization abnormalities and arrhythmias because of cardiac toxicity of drugs. Ventricular arrhythmogenesis is attributable to increase in repolarization heterogeneity that is characterized by spatial dispersion of repolarization. The purpose of this work was to study the delayed effects of doxorubicin, the most frequently used anthracycline, on repolarization heterogeneity of the ventricular epicardium.

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Doxorubicin, one of the most effective anticancer drugs, is characterized by severe cardiotoxic effects, which induce cardiac remodeling and congestive heart failure. The aim of the study was to evaluate remodeling of ventricular repolarization heterogeneity in chronic doxorubicin cardiotoxicity in rats. Doxorubicin cardiotoxicity was produced by six equal intraperitoneal injections of the drug in a cumulative dose of 15 mg/kg in a 2-week period.

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Repolarization properties of left ventricular (LV) myocardium change during its hypertrophy of various genesis. Aim of this work was to study repolarization of epicardial surface of the right ventricle (RV) in experimental model of LV hypertrophy caused by renovascular hypertension in rats. We registered 32 unipolar electrograms on the surface of cardiac ventricles and calculated duration of activation recovery intervals for assessment of repolarization.

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Background And Objective: Alterations in the recovery sequence of hypertrophied myocardium favour the development of cardiac arrhythmias. The aim of the present study was to investigate apex-to-base and interventricular heterogeneities in the duration of epicardial ventricular repolarization in rats with renovascular hypertension.

Method: Renovascular hypertension was induced in six Wistar rats by constricting the left renal artery for one month.

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The comparative analysis of the contractile function of the heart left ventricle in four species of homoeothermic tetrapods (chicken, quail, rat, sheep) who differ in their spatio-temporal pattern of ventricular excitation, heart rate, and heart weight was performed. The analysis of cardiac cycle structure was performed on the basis of synchronous recording of ECG, phonocardiogram, and apex cardiogram. Indices of myocardial contractility of the left ventricle calculated on the basis of the analysis of the cardiac dynamics indicate disadvantageous contractile function of the left ventricle in rodents and non-flying birds in comparison with sheep.

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The aim of this study was to investigate body surface potential distribution during the P wave in Wistar rats. We performed body surface potential mapping by means of a 64-channel synchronous electrocardiotopography. The positive area covered the caudal part of the thorax, and the negative one covered the cranial part of the thorax.

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The dynamics of potential distribution of cardiac electric field on the body surface was studied in renovascular hypertensive rats (Goldblatt type) during the ventricular activity. Three inversions of the mutual location of positive and negative areas of the cardiac electric field on the body surface were found in normotensive and hypertensive rats during the QRS-T period. Left ventricular hypertrophy of the heart in rats caused by renovascular hypertension results in changes of temporal and amplitude characteristics of the body surface potential distribution during the initial and terminal ventricular activity.

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The present study is the first attempt to examine the effect of left ventricular hypertrophy (LVH) on the excitation pattern of the ventricular epicardium in experimental hypertensive rats. The left renal artery was clipped in Wistar rats (n = 8; 6-8 months old; weight, 174-295 g) to produce two-kidney one-clip (2K1C) hypertension. After 4 weeks, blood pressure was measured, and epicardial potential mapping was performed under sinus rhythm from 64 unipolar electrodes regularly distributed over the ventricular epicardium.

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We propose a method of constriction of the renal artery consisting in pulling of a loop of isolated artery into a thin plastic tube with calibrated inner diameter. This method can be used in experiments with constriction of other small blood vessels to diminish the local blood flow.

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Left ventricular hypertrophy of the hearts in Wistar rats caused by renovascular hypertension prolongs depolarization of epicardial surface of the ventricles and increases the duration of excitation phase in the left ventricular epicardium. Sex-related differences in changes of myocardial contractility were revealed during hypertrophy of the left ventricle caused by renovascular hypertension.

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