Remodeling of ventricular repolarization in experimental right ventricular hypertrophy.

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. Vulnerability to ventricular arrhythmias was measured as the threshold dose of aconitine required to produce sustained ventricular tachycardia. Histological examination of the heart ventricles was performed. Activation-recovery intervals (ARIs) and ARI dispersions were used as indices of durations and heterogeneity of repolarization respectively to assess ventricular repolarization. RESULTS AND CONCLUSIONS: The development of compensated RVH was characterized by the dramatic prolongation of repolarization against the less expressed increase in repolarization heterogeneity, whereas the dramatic increase in repolarization heterogeneity against the less expressed but inhomogeneous prolongation of repolarization occurred in the progression of compensated RVH to heart failure. These changes increased vulnerability of the failing heart but not the compensated heart to aconitine-induced ventricular arrhythmias.

[Changes of repolarization properties of the right ventricle in hypertensive left ventricular hypertrophy].

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. In hypertensive rats relative LV mass was 26% greater than in control rats, while relative mass of RV was similar in both groups. Length of activation recovery intervals in hypertension was 1.7 times greater than in control group on both LV and RV surfaces. Dispersion of activation recovery intervals did not differ significantly between groups. Thus in LV hypertrophy in rats caused by renovascular hypertension electrical remodeling of myocardium occurs not only in left but also in right ventricle.

[Structure of the cardiac systole in mammals and birds].

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. The functioning of the left ventricle in male rats is more strained than in female rats. One fundamental factor determining a more strained functioning of the left ventricle in birds in comparison with mammals is the heart rate. The relative weight and activation pattern of the left ventricular myocardium govern the contractile function of the left ventricle to a lesser extent.

[A cardiac electric field on the body surface in rats with left ventricular hypertrophy caused by experimental renovascular hypertension].

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. The shifting trajectory of the positive and negative areas and their extremal ranges on the body surface does not change during the ventricular activity in rats with left ventricular hypertrophy of the heart as compared to the initial normotensive state.

Method of experimental constriction of renal artery for modeling of renovascular hypertension in rats.

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.

Contractile and electrical functions of rat heart during left ventricular hypertrophy.

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.