Why the study?
To evaluate the effect of Ni2+, a T-type calcium channel and Na+/Ca2+ exchanger blocker, on cardiac and respiratory rhythm parameters across early postnatal development in newborn rats.
Blockade of T-type calcium channels and Na+/Ca2+ exchanger by Ni2+ induces age-dependent arrhythmogenic and respiratory disorders in newborn rats.
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Ni2+-induced age-dependent arrhythmias in neonatal rats; leaves open translational relevance to human infant rhythms.
The effect of Ni2+, a T-type low-threshold calcium channel (T-VDCC) and Na+/Ca2+ exchanger (NCX) blocker, on cardiac and respiratory rhythm parameters was studied in newborn rats aged 3–16 days (P3–16). A distinct age dependence of the intensity of the arrhythmogenic effect evoked by calcium channel blockade was found. In 3-day-old rats injected with NiCl2 at a dose of 109 mg/kg (ED100), a transient atypical heart rhythm, representing the alternating periods of moderate bradycardia with a pathologically slow (up to 20–60 bpm) heart rhythm, occurs in 100% of animals. In parallel, a pronounced respiratory system dysfunction with burst breathing develops. This symptom complex occurs in 75% of 10–14-day-old rats and is completely absent in 15–16-day-old animals. Phenomenologically similar heart rhythm disorders are observed in newborn rats after NiCl2 injection, during poisoning with acetylcholinesterase inhibitors, and upon activation of the central N-cholinergic structures. The obtained data suggest that in the early period of rat postnatal ontogenesis, impaired mechanisms of calcium metabolism may play a certain role in the development of arrhythmogenic disorders.
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Кузнецов et al. (2022) studied this question.
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