Key result
The hibernator heart is resistant to ventricular fibrillation during severe hypothermia due to differences in adrenergic innervation, lipid composition, enzyme activity, and calcium handling.
The natural resistance of hibernating animals to ventricular fibrillation during extreme hypothermia provides a unique biological model for understanding arrhythmia prevention mechanisms.
Hibernator models highlight VF resistance mechanisms; leaves open translation to human hypothermia management.
During hibernation animals decrease their body temperature down to a few degrees above 0 degrees C. This means that when entering into and arousing from hibernation their body temperature passes through the critical level of 20 degrees C, a temperature region where nonhibernating mammals develop circulatory arrest, usually ventricular fibrillation (VF). The hibernator heart is resistant to VF, not only induced by hypothermia, but also when induced by local application of aconitine on the epicardium, and other ways of inducing VF in nonhibernators. Several mechanisms may explain this resistance to VF of the hibernator heart. The factors of greatest importance seem to be the different adrenergic innervation pattern, the different physico-chemical properties with a lower melting point of the lipids in the hibernator, the different enzyme temperature activity curves in the hibernator and the different handling of intracellular calcium, which results in protection against calcium overload in the hibernator heart, when compared with the nonhibernator heart.
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B. Johansson (1996) conducted a review in Ventricular fibrillation during hypothermia. Hibernation physiology vs. Nonhibernating mammals was evaluated on Resistance to ventricular fibrillation. The hibernator heart is resistant to ventricular fibrillation during severe hypothermia due to differences in adrenergic innervation, lipid composition, enzyme activity, and calcium handling.
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