A comparative analysis of heart rate variability (HRV) indices after injection of the acetylcholinesterase inhibitor (AChE) physostigmine (¾ LD50) and the T-type calcium channel blocker (T-VDCC) Ni2+ (ED100) into animals was performed in experiments on 3-day-old newborn rats. Both drugs cause phenomenologically similar pathological heart rhythm with significant bradycardia complexes (PHRBC). Analysis of HRV indices showed that the disturbance of heart rhythm regulation mechanisms in NiCl2 poisoning of rats and in cholinoreactive structure activation caused by AChE inhibition develop according to a similar pattern. In both cases there is a decrease in the total power of the spectrum and the absolute power values of the LF (predominantly sympathetic) and HF (parasympathetic influences) bands. Significant decrease in the level of nerve influences leads to the fact that the dominant role in the regulation of heart rhythm begins to play neurohumoral factors (VLF-band). It was found that under conditions of premedication with H- or M-cholinolytics, when rats do not develop cardiac rhythm disturbances, the initial decrease in the severity of neurohumoral and subsequent increase in sympathetic and, to a lesser extent, parasympathetic influences is common. In this case, vagosympathetic balance is not decisive. In case the influence of neurohumoral factors increases after premedication, then later there is a decrease in the proportion of nerve influences and the occurrence of PHRBC. The obtained data suggest that in newborn rats both direct blockade of T-VDCC and changes in ICaT current mediated through M3-subtype muscarinic cholinoreceptors lead to disruption of pacing and development of PHRBC.
