THE EFFECTS OF BLOOD FLOW AND ANOXIA ON SPINAL CARDIOVASCULAR CENTERS

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Abstract
Direct recordings of the tonic activity in the inferior cardiac nerve were used as an index to the activity in the sympathetic outflow to the cardiovascular system of the cat. A rise in thoracic blood pressure inhibited this tonic activity even though all possible sources of reflex inhibition were eliminated. In an acute deafferent spinal prepn. in which the upper thoracic cord had been isolated from all other nerve influences including its own dorsal roots, some residual tonic activity was found. This tonic activity becomes minimal under conditions of optimal lung ventilation and is greatly stimulated by asphyxiation. The asphyxial stimulation can not be reproduced by hypercapnia in the presence of adequate O2, but is caused by anoxia which has a marked stimulatory action on the isolated spinal cardiovascular centers. It is shown that a rise in blood pressure inhibits sympathetic activity in the deafferent spinal prepn. by increasing the blood flow and hence the O2 supply to the spinal centers. In the normal animal, the buffer reflexes are undoubtedly dominant to any direct action of anoxia on spinal cardiovascular centers, but it is suggested that the local O2 tension may play a subsidiary role in determining the general excitatory state of these centers.

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