[Physiological approaches to enhancing cardiac resistance in emotional stress]. / Fiziologicheskie podkhody k povysheniiu ustoichivosti serdechnoi deiatel'nosti pri émotsional'nom stresse.

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.

[Emotional stress and extracardiac regulation]. / Emotsional'nyi stress i ékstrakardial'naia reguliatsiia.

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.

[Sympathetic regulation of heart rhythm under the effect of delta sleep peptide and its deficiency]. / Simpaticheskaia reguliatsiia serdechnogo ritma pri deistvii peptida del'ta-sna i ego defitsite v organizme.

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.

[Delta sleep-inducing peptide as a modulator of mediators acting on the heart]. / Peptid del'ta-sna kak moduliator deistviia mediatorov na serdtse.

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.

[Delta-sleep peptide as a modulator of cardiac activity: theoretical recommendations for practice]. / Peptid del'ta-sna kak moduliator serdechnoi deiatel'nosti: teoreticheskie rekomendatsii dlia praktiki.

In acute and chronic animal (rabbits, rats) experiments it has been shown that delta-sleep producing peptide (DSPP) exerts a noticeable effect on the cardiac function and regulation. DSPP at a dose of 60 nm/kg can prolong the effects of vagus and inhibit those of sympathetic nerves on the cardiac function and, consequently, can influence the function of choline- and adrenergic transmitters. DSPP blocks pressor vascular reactions in response to direct electrical stimulation of ventromedian hypothalamus and thus increases the survival of animals exposed to an acute emotional stress. DSPP normalizes the electrical stability of the heart and produces an antiarrhythmic effect on ventricular ectopic beats that occur in response to emotional stresses. In view of this, DSPP can be recommended for clinical trials as a drug preventing cardiac arrhythmias in stressful situations.

[The role of delta-sleep-inducing peptide in the normalization of cardiac electric stability in experimental emotional stress]. / Rol' peptida delta-sna v normalizatsii elektricheskoi stabil'nosti serdtsa pri éksperimental'nom émotsional'nom stresse.

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.

[Hemodynamics in emotional responses and in emotional stress]. / Gemodinamika pri émotsional'nykh reaktsiiakh i émotsional'nom stresse.

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.

[Parasympathetic regulation of cardiac rhythm in delta sleep-inducing peptide deficiency]. / Parasimpaticheskaia reguliatsiia serdechnogo ritma v usloviiakh defitsita peptida del'ta-sna v organizme.

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.

[Mechanisms of the development of the terminal state in experimental emotional stress]. / O mekhanizmakh razvitiia terminal'nogo sostoianiia pri eksperimental'nom emotsional'nom stresse.

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.

[Effect of the delta-sleep peptide on parasympathetic regulation of the cardiac rhythm]. / Vliianie peptida del'ta-sna na parasimpaticheskuiu reguliatsiiu serdechnogo ritma.

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.

[Hemodynamic changes in immobilization stress]. / Izmeneniia gemodinamiki pri immobilizatsionnom stresse.

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.

[Effect of motor activity on the development of arrhythmia in experimental emotional stress]. / Vliianie dvigatel'noi aktivnosti na vozniknovlenie serdechnykh aritmii pri eksperimental'nom émotsional'nom stresse.

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.

[Effect of reserpine on the ultrastructure and electrical instability of the heart]. / Vliianie rezerpina na ul'trastrukturu i élektricheskuiu nestabil'nost' serdtsa.

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.

[Change in the thresholds of development of ventricular arrhythmias after stimulation of negative emotiogenic hypothalamic centers]. / Izmenenie porogov vozniknoveniia zheludochkovykh aritmii pri razdrazhenii otritsatel'nykh émotsiogennykh tsentrov gipotalamusa.

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.

[Optimal parameters for electrical auricular defibrillation]. / Optimal'nye parametry élektricheskoi defibrilliatsii predserdii.

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.