Abstract

The analysis of heart rate variability in rats revealed that the blockade of vegetative ganglions (hexametonium, 7 mg/kg) increases heart rate frequency (HRF) by 12-16%, reduces the power of very low-frequency waves by 85% (p<0,001), low-frequency waves - by 60% (p < 0,05), high-frequency waves - by 40%. The blockade of M-cholinoreceptors (atropine, 1 mg/kg) increases the HRF by 30% (p < 0,001) and reduces the power of all waves of the heart rate variability by 96-98% (p < 0,001). The blockade of β-adrenoreceptors (anaprilinе, 2 mg/kg) reduces HRF by 25% (p < 0,001) and the power of very low-frequency waves by 70% ( p< 0,05). Against the background of the blockade of vegetative ganglions, the introduction of atropine reduces the power of the heart rate waves to a lesser extent, and the introduction of anapriline changes the HRF little, but potentiates the growth of the power of high-frequency waves. Thus, regulatory influences through cardiomyocytes M-cholinoreceptors are responsible for the formation of the power of all waves of the heart rate variability. The interaction of cholinergic mechanisms with signals coming through vegetative ganglions and β-adrenoreceptors determines the power of low-frequency waves. The activity of the vegetative ganglions affects the nature and severity of changes in heart rhythm when exposed to myocardial cholino- and adrenoreceptors.

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