[Hibernation--nature's model of resistance to ventricular fibrillation].

During hibernation, animals lower their body temperature to a few degrees above 0 degree C. This means that when entering and emerging from hibernation their body temperature passes through the critical level of +20 degrees C, a temperature region at which non-hibernating mammals develop circulatory arrest, usually due to ventricular fibrillation (VF). The hibernator heart is resistant to VF, not only that caused by hypothermia, but also VF as induced by local application of aconitine on the epicardium, and also by other factors which ordinarily cause VF in non-hibernators. Several mechanisms may explain the resistance to VF observed in the hibernator heart. The factors of greatest importance seem to be contrasting patterns of adrenergic innervation, divergent physico-chemical properties with a lower solidification point of lipids in the hibernator, distinct enzyme temperature activity curves seen in the hibernator, and differences in the handling of intracellular calcium, resulting in protection against calcium overload in the hibernator heart as compared with the non-hibernator heart.