Circulatory control in hypoxia by the sympathetic nerves and adrenal medulla
- 1 May 1966
- journal article
- research article
- Published by Wiley in The Journal of Physiology
- Vol. 184 (2) , 272-290
- https://doi.org/10.1113/jphysiol.1966.sp007915
Abstract
The effects of severe arterial and primary tissue (carbon monoxide) hypoxia on cardiac output, arterial and right atrial pressures, heart rate and ventilation, were studied in unanaesthetized normal rabbits, and in animals subjected to adrenalectomy+ ''sympathectomy'' (guanethidine), adrenalectomy+''sympathectomy'', and section of the carotid sinus and aortic nerves. In both arterial and primary tissue hypoxia the sympathetic nerves play a more Important part In the normal circulatory response than the adrenal medullary hormones. Provided one adrenergic effector pathway remains intact, animals with intact chemoreceptors and baroreceptors tolerate both types of hypoxia well. Circulatory control during both types of hypoxia by means of sympathetic nerves alone produces relatively more peripheral vasoconstriction than is observed during reflex control through increased adrenal catecholamine secretion. The occurrence of tonic sympathetic activity in animals with section of carotid sinus and aortic nerves permits maintenance of a high cardiac output during hypoxia but the arterial pressure is low and there is probably less selective distribution of blood flow to the periphery than in animals with normal reflex control. Absence of any adrenergic activity in adrenalectomized and ''sympathectomized'' animals results in a gradual fall in cardiac output during prolonged hypoxia, after an initial small rise. The results in guanethidine-treated animals suggest that the sympathetic discharge to the arterial chemoreceptors is a factor sustaining chemoreceptor discharge during prolonged arterial hypoxia.This publication has 5 references indexed in Scilit:
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