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Biomedical subjects

V M Pokrovskiĭ

Publications and source records attributed to V M Pokrovskiĭ.

At least 19 recordsLinked to original sources
PubMed1999

[The role of different mechanisms of cholinergic regulation in controlled bradycardia evoked by vagal stimulation].

In experiments on anesthetised cats we investigated functional significance of different cholinergic mechanisms regulating the magnitude of vagal chronotropic effect components, inhibitory tonic and synchronizing. It was established that inhibitory tonic vagal component is determined by intensity of acetylcholine hydrolysis and total amount of excited cardiac M-cholinoreceptors. The magnitude of synchronizing vagal component depended on subtypes of cholinoreceptors selectively excited by acetylcholine released from vagal terminals. In particular, the blockade of M1- or M3-cholinoreceptors potentiated the synchronizing vagal component, whereas the blockade of M2-cholinoreceptors inhibited it.

Acetylcholine↗
PubMed1999

[The dynamics of the chronotropic effect of a single vagal stimulus in cats under the action of met-enkephalin and neurotensin].

Following a burst of pulses applied to the vagus nerve with progressively incremental delay after the P wave of the ECG, the narrow zone of the cardiac cycle was identified where even a small shift of the vagal burst position evoked an abrupt alteration of the chronotropic effect magnitude. Met-enkephalin potentiated the phase-dependent vagal chronotropic effect, whereas neurotensin moved its limits toward the initial part of the P-P interval.

Animals↗
PubMed1999

[Types of the peptide modulation of the vagus nerve effect on the heart rhythm].

In anaesthetised cats, effects of 24 regulatory peptides upon inhibitory tonic and synchronizing components of vagal chronotropic action, were studied. The findings allowed to divide the peptidergic vagotropic activity into three types: (1) a selective action upon inhibitory tonic vagal effect; (2) a selective modulation of synchronizing vagal effect; (3) opposite changes in the vagal chronotropic effect components. The peptides seem to be able to modulate both the vagal bradycardia and the functional structure of parasympathetic chronotropic effect.

Animals↗
PubMed1997

[Paradoxical vagal effects on the cardiac rhythm in cats].

In anaesthetised cats, an increase in the vagal burst rate resulted in a paradoxical decrease of vagal bradycardia. This seems to be due to a shift of the vagal stimulus position towards early phase of cardiac cycle. The mechanism of this paradoxical effect depends on the magnitude of vagal chronotropic effect upon the time of vagal stimulus delivery within cardiac cycle.

Animals↗
PubMed1997

[The connection between the structure and activity of enkephalins in the realization of their cardiotropic effects in cats].

In experiments on anesthetized cats the ability of natural enkephalins to affect baseline heart rate, the magnitude of vagal chronotropic effect and its components, inhibitory tonic and synchronizing, was compared with activity of synthetic analogs and short fragments of enkephalins. Substitutions of met-enkephalin structure in second and fifth positions did not modify its cardiac activity. When Tyr1 was removed the peptide lost ability to affect baseline heart rate and the magnitude of synchronizing vagal component, but modulatory influence on inhibitory tonic vagal effect still persisted. The conclusion has been made that various parts of amino acid chain of met-enkephalin have different significance in realization of cardiac effects evoked by this peptide.

Amino Acid Sequence↗
PubMed1996

[A comparative evaluation of the cardiotropic effects of neurotensin and adrenaline in cats].

I.v. neurotensin induced acceleration of the heart rate which was prevented by with beta-adrenoreceptor blocker in anesthetised cats. Both neurotensin and adrenaline potentiated the vagal chronotropic effect and its tonic component. The synchronizing vagal component was inhibited by adrenaline. The findings suggest that the adrenergic link is involved in implementation of the cardiac effect exerted by neurotensin.

Adrenergic beta-Antagonists↗