Abstract
Hibernators are resistant to ventricular fibrillation (VF) induced by hypothermia. This is in contrast to non-hibernating mammals which develop circulatory arrest, usually VF, in the temperature region 15–20°C. The hedgehog which is a hibernator showed resistance to VF also when VF-evoking procedures other than hypothermia were used, such as local application of aconitine on the epicardium, administration of 0·55 M CaCl2 to isolated hearts perfused with a potassium-free modified Tyrode solution, injection of procaine HCl into isolated hearts perfused with a modified Tyrode solution after previous adrenaline administration, and ligation of the left descending coronary artery. Electrical stimulation in the vulnerable period produced VF in some but not in all the hedgehogs but a greater current was necessary than in guinea-pigs, all of which developed VF. Factors of possible importance to explain this difference in VF resistance are the QT duration which is short in hibernators, adrenergic innervation (ventricular muscle fibres in hibernators lack sympathetic innervation), metabolic factors (different temperature activity curves in hibernators compared to nonhibernating mammals) and ultrastructure (less skeletin filament in the conduction system of the hedgehog heart).

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