ON THE CONTROL OF VENTRICULAR FIBRILLATION DURING HYPOTHERMIA.
LUND UNIV (SWEDEN) DEPT OF ANATOMY
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Preliminary results are presented of studies on the possible role of adrenergic mechanisms in the production of ventricular fibrillation during hypothermia. The pattern of adrenergic innervation in the heart ventricles was investigated by means of a histochemical fluorescence method. In the hibernating animal studied hedgehog few - if any - adrenergic nerves were found in the ventricular muscle tissue, whereas the blood-vessels were supplied by a system of adrenergic nerve terminals. This contrasts with the cat ventricles, in which adrenergic nerves enclose both the muscle fibres and the vessels. One group of cats were pretreated with segontin N--3-phenyl-propyl-2-1, 1-diphenyl-propyl-3-amine, which causes a severe depletion of noradrenaline from the adrenergic nerves to the heart miscle, whereas noradrenaline more or less remains in the nerves to the heart vessels. The animals were then cooled to a rectal temperature of 17.8 - 17.2C and re-warmed to 24C. None of these animals developed ventricular fibrillation. The same number of control cats died in ventricular fibrillation at 22 to 19C rectal temperature. Blockage of the adrenergic beta-receptor with INPEA N-isopropyl-p-nitrophenylethanolamine prevented ventricular fibrillation in cats cooled to 17.2 - 17C rectal temperature. These animals were returned to normothermia and kept for long-term survival. Author
- Medicine and Medical Research
- Stress Physiology