[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.

[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.