The hibernator heart--nature's model of resistance to ventricular fibrillation

During hibernation the animals decrease their body temperature down to a few degrees above 0 degree C. This means that when entering into and arousing from hibernation their body temperature passes the critical level of 20 degrees C, a temperature region where nonhibernating mammals develop circulatory arrest, usually ventricular fibrillation (VF). We found in other experiments that the hibernator heart is resistant to VF, not only induced by hypothermia, but also when induced by local application of aconitine on the epicardium, addition of 0.55 molar CaCl2 to isolated hearts perfused with a potassium free Tyrode solution, addition of procaine to isolated hearts perfused with Tyrode solution after previous administration of adrenaline, ligation of the proximal part of the left anterior descending coronary artery, and electrical stimulation in the vulnerable phase of the heart cycle. Several mechanisms are at work to explain this resistance to VF of the hibernator heart when compared to the nonhibernator heart. The factors of greatest importance seem to be the different adrenergic innervation pattern, different physico-chemical properties with a lower melting point of the lipids in the hibernator, different enzyme temperature activity curves in the hibernator and a different handling of intracellular calcium resulting in a protection against calcium overload in the hibernator heart, when compared with the nonhibernator heart.