Adaptations of the cardiovascular system in hibernating mammals.

Winter in temperate and high latitudes imposes severe challenges for animal survival, associated with low ambient temperature and limited food availability. In some mammalian species, these challenges are met by hibernation, a state characterized by marked reduction in core temperature and metabolic activity. Despite these extreme conditions, hibernating mammals preserve cardiac function and avoid life-threatening arrhythmias and vascular failure. This review summarizes the current evidence on cardiovascular adaptations supporting survival during torpor, focusing on cardiac electrophysiology, Ca2+ homeostasis, and regulation of vascular tone. The heart of a deep hibernator exhibits species-specific properties of ionic channels that maintain cardiac excitability and stable conduction at low temperatures. The resistance of Na+ current to cold-induced depolarization, coordinated modulation of Ca2+ and K+ currents, enhanced electrical coupling, and adaptive regulation of intracellular Ca2+ handling preserve myocardial excitability and protect it from cold-induced electrical instability and contractile dysfunction. At the vascular level, hibernation is associated with pronounced, organ-specific redistribution of blood flow. Increased vasoconstrictor responsiveness and attenuation of endothelial anticontractile mechanisms, along with structural remodeling and phenotypic switching of vascular smooth muscle cells, contribute to reduced perfusion in metabolically inactive tissues, whereas blood flow in vitally important organs is preserved. Although most available data were obtained from representatives of Sciuridae family, these findings highlight the fundamental principles of cardiovascular plasticity under extreme hypothermia and hypometabolism, with potential relevance to human cardiovascular pathophysiology.