PubMed Health⌕ Search

Biomedical subjects

E Lepeschkin

Publications and source records attributed to E Lepeschkin.

8 recordsLinked to original sources
PubMed1978

The influence of atrial activity on ventricular capture by failing artificial pacemakers. I. Report of two new cases and review of the literature.

Atrial activity can influence the ability of a failing artificial pacemaker to excite the heart. An appropriately timed atrial beat may cause failure in excitation by pacemaker stimuli which are usually successful in ventricular capture. Conversely, stimuli which usually fail in excitation may be made to succeed by an appropriately timed atrial beat. Two case reports and a review of the literature are presented. Alternative mechanisms for this influence of atrial activity are electrotonic effects (Wedensky facilitation or inhibition) and mechanical effects (motion of the pacing catheter or ventricular myocardium). The authors consider the latter mechanism preferable.

Aged↗
PubMed1978

Response of cultured myocardial cells to countershock-type electric field stimulation.

Myocardial cells isolated from 8-day chick embryos were grown in monolayer culture under conditions that produce "standard embryonic" and "adult-type" cells. These cells were subjected to electric field stimulation that had a waveshape and intensities similar to those used in clinical electric countershock procedures. Photocell mechanograms obtained before, during, and after stimulation were correlated with simultaneously measured transmembrane potentials to determine the relationship between membrane polarization and arrhythmia production that occured after the stimulus. The results of these experiments demonstrate that a predictable sequence of mechanical responses occurs after stimuli ranging in intensity from 6 to 200 V/cm. This sequence, which closely resembles that observed in vivo after similar stimulation intensities, consists of a single response (activation), tachyarrhythmia, relaxed arrest followed by transient tachyarrhythmia, arrest with contracture, and cellular fibrillation. This diverse pattern of arrhythmias is associated with a prolonged depolarization of the cell membrane which increases with the intensity of the applied stimulus. It is probable that this depolarization is caused by a transient electromechanical deformation of the cell membrane during the shock. These findings contribute to a better understanding of the causes of the arrhythmias that appear after clinical and experimental electric countershock procedures.

Animals↗
PubMed1978

Effect of premature stimulation on fast and slow excitation channels in cultured myocardial cells.

Myocardial cells from chick embryos were cultured using a method which results in cell morphology and action potentials showing greater similarity to that of adult cells than to cells grown with standard methods of culture. The cells were paced by means of rectangular field stimuli (2 msec 2-5 times diastolic threshold). When the stimulus was given during the descending branch of the previous action potential, the action potential developed dissociation between a fast-rise component with short duration and a slow-rise component with longer duration. This dissociation was best in cells with an intermediate rate of rise of the spontaneous action potential and may be caused by different rates of reactivation of the slow and fast membrane excitation channels.

Action Potentials↗
PubMed1978

Local potential gradients as a unifying measure for thresholds of stimulation, standstill, tachyarrhythmia and fibrillation appearing after strong capacitor discharges.

The pattern of arrhythmias following capacitor discharges of increasing amplitude, which have been observed by the authors in cultured myocardial cells from chick embryos, was compared to the arrhythmia patterns caused by similar discharges in experimental animals and humans, as reported in the literature. While the absolute voltages and currents causing each type of arrhythmia showed great variation, the scatter decreased considerably when the stimulus level was recalculated on the basis of peak current density in myocardial tissue, and was reduced further when the peak potential gradient at the cell level was used as the common basis of comparison. The similarity in the arrhythmia patterns and in the voltage gradients at which they occur indicates that the mechanism of these arrhythmias may be similar in cultured cells and intact animals and humans.

Action Potentials↗
PubMed1976

Part I: abnormal patterns and physiological variations in magnetocardiograms.

Magnetocardiograms (MCGs) of six subjects with representative cardiac abnormalities and of one well-studied normal subject are compared with the 12-lead ECGs and VCGs of these subjects. The MCGs are recordings of the component of the magnetic vector which is normal to the skin, measured across the chest on a 5 cm X 5 am grid; an example is also presented of a sequence of instantaneous MCG maps. The heart abnormalities include myocardial infarction, angina pectoris, intraventricular conduction disturbances, and ventricular hypertrophy. The various MCG maps of the normal subject show MCG changes as a result of changes in body morphology (loss of weight), changes in the subject's position during recording, and changes as a result of exercise. They are presented as a basis for understanding some of the variability of MCG maps.

Angina Pectoris↗