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Biomedical subjects

L S Ul'ianinskiĭ

Publications and source records attributed to L S Ul'ianinskiĭ.

At least 19 recordsLinked to original sources
PubMed1995

[Physiological approaches to enhancing cardiac resistance in emotional stress].

The role of parasympathic effects, graded motor activity, positive emotions, and delta-sleep peptide in enhancing the resistance of cardiac performance in experimental emotional stress was studied in chronic rabbit experiments. The prevalence of parasympathic effects was demonstrated to increase cardiac electric stability and to prevent the elevation of catecholamine levels and the development of myocardial structural damages during stress. A moderate motor activity was found to lead to the session of ventricular extrasystole occurring in stress due to decreases in the myocardial levels of epinephrine with its high levels remaining in blood. Ventricular extrasystole also disappeared after activation of the positive emotional centers of the hypothalamus and after administration of delta-sleep peptide normalizing the electrical stability of the heart in emotional stress.

Animals↗
PubMed1994

[Emotional stress and extracardiac regulation].

Chronic experiments in rabbits and rats revealed that, when sympathetic influences on the heart prevail during emotional stress, reduce the heart electric stability, induce disorders in the heart rhythm and lead to arterial hypertension. Prevailing of parasympathetic influences, on the contrary, augments the heart electric stability, interferes with an increase in the catecholamines content and prevents structural lesions in the myocardium. Arterial hypertension is absent, at that. The vagal nerves seem to exert an adaptational-trophic and defensive effects on the heart in emotional stress.

Adaptation, Physiological↗
PubMed1991

[Sympathetic regulation of heart rhythm under the effect of delta sleep peptide and its deficiency].

In acute experiments on 16 rabbits we've studied effects of delta-sleep peptide and its deficiency on the irritation of the stellate ganglion. It has been revealed, that peptide injection (60 nM/kg) produces lowered positive chronotropic effect and elongated response development during irritation of this ganglion. Administration of antiserum to delta-sleep peptide (T = 1:3000) causes opposite effect: enhances sympathetic response during irritation of the stellate ganglion. Thus, delta-sleep peptide promoted lowered sympathetic influences on the heart.

Animals↗
PubMed1990

[The role of delta-sleep-inducing peptide in the normalization of cardiac electric stability in experimental emotional stress].

In chronic experiments on rabbits, a delta-sleeping inducing peptide was tested for effects on the cardiac electric stability and onset of ventricular premature beats during experimental emotional stress. The peptide in a dose of 60 nm/kg was found to normalize the thresholds of ventricular fibrillation and its predictors and to decrease or abolish spontaneous ventricular premature beats occurring during the stress. This suggests that the delta-sleep-inducing peptide may be used to prevent cardiac arrhythmias during stresses.

Animals↗
PubMed1990

[Delta sleep-inducing peptide as a modulator of mediators acting on the heart].

Experiments on 51 isolated rabbit hearts have documented, that delta sleep-inducing peptide (6 X 10(-6) M/l) has a modulating effect on the mediators influencing the heart. This peptide enhances negative chronotropic effect of acetylcholine (1 X 10(-6) M/l) and decreases positive chronotropic effect of noradrenaline (1 X 10(-6) M/l). Such effect may be one of mechanisms of changes in the extracardiac regulation on the heart influenced by this peptide.

Acetylcholine↗
PubMed1988

[Hemodynamics in emotional responses and in emotional stress].

Negative emotional states induced with electrical stimulation of ventro-medial hypothalamus (VMH) or with behavioral conflicts were followed by vascular pressor responses tending to sum up. Positive emotional states were followed mainly by pressor-depressor vascular responses in animals. Obvious disorders of cardio-vascular functions occurred in experimental-emotional stress, vascular responses to the VMH stimulation being mostly of the pressor character. Changes in vascular tone were shown to play a major part in disturbances of the AP regulation in the immobilization stress, a progressing fall in the AP due to a sharp decrease in total peripheral resistance being the main reason of the animals' death. The resistance of cardio-vascular functions against emotional stress seems to be determined mainly by genetic mechanisms.

Adaptation, Physiological↗
PubMed1987

[Parasympathetic regulation of cardiac rhythm in delta sleep-inducing peptide deficiency].

The effect of delta-sleep peptide (DSP) deficiency on the parasympathetic regulation of the heart rate was studied on 35 rabbits. It was established that the injection of an-serum (titer-1:2000-1:3000) leads to the attenuation of parasympathetic influences: heart rate increase in freely behaving animals and a decrease in negative chronotropic effect with direct vagus irritation. Antiserum, like DSP, administration causes practically no damage of the myocardial ultrastructure.

Animals↗
PubMed1986

[Mechanisms of the development of the terminal state in experimental emotional stress].

The development of ventricular fibrillation associated with experimental emotional stress was studied in chronic rabbit experiments. Changes in myocardial-fibre action potentials, thresholds for ventricular fibrillation and its precursors, blood and myocardial catecholamine levels and heart-muscle ultrastructure were examined. Emotional stress was shown to increase, via sympathoadrenal activation, functional and structural heterogeneity of the myocardium, leading, alongside other causes, to arrhythmias and death from ventricular fibrillation. Moderately prevailing parasympathetic effects on the heart during stress exposure contribute to the elevation of fibrillation and fibrillation precursor thresholds and prevent catecholamine rise and myocardial structural damage.

Action Potentials↗
PubMed1986

[Effect of the delta-sleep peptide on parasympathetic regulation of the cardiac rhythm].

Effect of delta-sleep peptide (60 nM/kg) on the parasympathetic regulation of cardiac activity has been studied in the experiments on rabbits. It has been established that intravenous administration of this peptide to voluntary-behaving animals results in heart rate reduction by an average of 16%, that can be eliminated by atropine. Delta-sleep peptide has been demonstrated to intensify negative chronotropic effect in the case of directly irritated wandering nerve. The data obtained explain a protective effect of delta-sleep peptide on the heart under emotional stress.

Animals↗
PubMed1985

[Hemodynamic changes in immobilization stress].

In chronic experiments on 75 Wistar, August and randombred rats hemodynamic changes were examined during 30-hour immobilization stress. The ECG was recorded and arterial blood pressure measured. The basic hemodynamic characteristics were determined with the help of the previously implanted ultrasonic blood flow probes. Analysis of hemodynamic changes in animals resistant, adapted and prone to stress demonstrated that changes in the total peripheral resistance play the leading role in the disturbance of the arterial blood pressure control. It was established that a progressive lowering of arterial blood pressure resulting from the abruptly reduced total peripheral resistance is the main and the most frequent cause of death of animals exposed to immobilization stress. At the same time the cardiac hemodynamic component may play an essential role in the mechanism of death. This component may include either progressive bradycardia or a combination of an ischemic myocardial damage and reduced total peripheral resistance.

Adaptation, Physiological↗
PubMed1981

[Effect of motor activity on the development of arrhythmia in experimental emotional stress].

Studies on monkeys and rabbits have shown that the experimental emotional stress can produce various disorders of cardiac rhythm: sinus tachycardia, atrial fibrillation, ventricular extrasystoles and paroxysmal ventricular tachysystoles. In these conditions the adrenaline content in the blood and myocardium is increased 3-4 times, the noradrenaline level is raised in the blood and decreased in the myocardium. Moderate motor activity leads to a relative decrease of adrenaline in the myocardium and arrest of cardiac arrhythmias. Marked motor activity on the contrary leads to an increase of the adrenaline and noradrenaline level in the myocardium and to the development of disorders of cardiac rhythm even up to ventricular fibrillation.

Animals↗
PubMed1981

[Effect of reserpine on the ultrastructure and electrical instability of the heart].

The time course of ultrastructural and electrophysiological disorders and their role in sudden death of ventricular fibrillation at various intervals of desympathization caused by reserpine administration were studied. Early in the effect of reserpine (up to 30 min), glycogen granules were found to accumulate in the sarcoplasm of cardiomyocytes. At later intervals (1-24 hours), along with glycogen accumulation destructive lesions of organoids were observed in the form of myofibrillar recontraction, destruction of mitochondria, degeneration of sarcolemma. These changes are morphologic reflections of metabolic disorders developing in the myocardium under conditions of acute desympathization of the patient, and may be one of the causes of increased vulnerability of the heart in fibrillation.

Animals↗
PubMed1979

[Change in the thresholds of development of ventricular arrhythmias after stimulation of negative emotiogenic hypothalamic centers].

The dynamics of changes in the thresholds of the origin of ventricular extrasystole, paroxysmal ventricular tachysystole and ventricular fibrillation in long-term stimulation of the ventromedial hypothalamic nucleus were studied in experiments on rabbits. It was found that myocardial resistance to the development of arrhythmias depended on the manifestation of the sympathetico-parasympathic interaction on the heart. In predominance of parasympathetic effects on the heart during hypothalamic stimulation, the threshold of the origin of arrhythmia increased by 40% for ventricular extrasystole, by 38% for paroxysmal ventricular tachysystole and by more than 36% for ventricular fibrillation. In predominance of sympathetic effects during stimulation of negative emotiogenic hypothalamic centers, the threshold of arrhythmia origin decreased by 45% for ventricular extrasystole, by 32% for paroxysmal ventricular tachysystole and by 24% for ventricular fibrillation.

Animals↗
PubMed1978

[Optimal parameters for electrical auricular defibrillation].

In acute experiments on dogs the chest was opened and auricular flutter and fibrillation were induced. Current, energy and charge thresholds which eliminated this arrhythmia by the monopolar direct impulse of 1--15 ms duration were determined. The current and energy values that evoked the auricular defibrillation during direct application of the electrodes to them were minimal when the impulses of 8 ms were used: 113 +/- 13.7 mA and 10.4 +/- 2.6 mWs in elimination of the flutter, and 275 +/- 18.2 mA and 62.3 +/- +/- 9.0 mWsec in elimination of the fibrillation. The current that restored the nomotopic rhythm during direct auricular defibrillation was 50 times less than that determined during the transthoracic auricular defibrillation in dogs. The efficacy of direct auricular defibrillation indicated the necessity of the elaboration of an adequate method for its application in clinical practice.

Animals↗
PubMed1978

[Cardiac arrhythmias of hypothalamic origin].

It was established in chronic rabbit experiments that periodical prolonged electric stimulation of the hypothalamic ventrolateral nucleus may induce, besides tachycardia and ventricular extrasystole, episodes of cardiac fibrillation and sudden death from ventricular fibrillation. The development of cardiac fibrillation is associated with increased content of catecholamines in the blood and myocardium. It was also found that the energy-producing activity of the mitochondria and active ion transportation were impaired in the myocardium, the intracellular content of potassium and sodium was changed, and the ultrastructure of the heart muscle was markedly altered. It was shown that the predominance of parasympathetic effects over sympathetic was one of the factors determining the resistance of the heart to the development of cardiac fibrillation of hypothalamic origin.

Animals↗