CENTRAL ACTIVATION OF THE SYMPATHETICO-ADRENAL SYSTEM BY HYPOXIA AND HYPERCAPNIA

Abstract

SUMMARY In rabbits under urethane anaesthesia sympathetico-adrenal vasoconstrictor activity was monitored by the reduction of oxygen tension (measured polarographically with needle electrodes) in the testis and lactating mammary gland, and by the inhibitory effect on milk ejection. Electrical stimulation of the dorsal, lateral and posterior hypothalamus evoked a sympathetic response in these organs, characterized by a rapid nervous effect and secondary humoral effect which outlasted the stimulus, resembled the response to intravenous adrenaline, and was abolished by removal of both adrenal glands. Hypoxia produced by making the animals inhale nitrous oxide or nitrogen for 15–30 sec. and hypercapnia induced by inhalation of a mixture of 80% CO2 and 20% O2 for 5–15 sec. both induced a sympathetic discharge similar to that resulting from hypothalamic stimulation. Hypercapnia was a notably more potent stimulus than hypoxia. The effects were reversibly blocked by thoraco-lumbar spinal anaesthesia. Placement of discrete bilateral lesions in the septum, hippocampus and medial thalamus did not impair the sympathetic activation elicited by hypercapnia. Hypothalamic lesions, on the other hand, often reduced and occasionally prevented the central sympathetic discharge. The possible role of the hypothalamus in cardiovascular regulation is discussed in the light of these findings.