Bulbar and Suprabulbar Control of the Cardiovascular Autonomic Effects during Arterial Hypoxia in the Rabbit
The autonomic effects on heart rate, portal, renal, cutaneous and muscle blood flows were studied during approximately constant severe arterial hypoxia in unanesthetized sham-operated, thalamic and pontine rabbits, 3 hours after operations conducted under halothane anesthesia. Neural and adrenal effects were estimated by comparing the responses of different groups of animals: (a) with all neural effectors intact, (b) after adrenalectomy, (c) after selective and (d) after complete pharmacological block of neural effector mechanisms. In pontine animals hypoxia greatly increased cardiac sympathetic activity and seemed to evoke a greater release of adrenal catecholamine (epinephrine) than in other preparations, but caused significant neural peripheral sympathetic constrictor effects in only the portal bed. In thalamic animals, hypoxia caused reflex bradycardia, striking neural constrictor effects in the portal, renal and muscle beds, and cutaneous dilatation. There was little evidence of an increase in epinephrine secretion. It is suggested that there is an inhibitory pathway between diencephalon and bulb that limits the release of epinephrine. Sham-operated animals exposed to hypoxia secreted epinephrine which played an important role in the total reflex response; this group had similar cardioinhibitory and cutaneous effects to thalamic animals, but a more rapid onset of portal and renal constriction and a marked increase in muscle blood flow. The sympathetic responses of the different preparations resulted in different rates of metabolic H+ ion production.
- adrenal catecholamines
- diencephalic and pontomedullary circulatory centers
- arterial chemoreceptors
- portal, renal, muscle, skin blood flow
- Received October 27, 1969.
- © 1970 American Heart Association, Inc.