RECOVERY OF THE CEREBRAL CORTEX OF THE CAT FOLLOWING HYPOXIA

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Abstract
Healthy mature cats were exposed in an observation chamber to N2-air mixtures. When artificial respiration was begun at the point of respiratory failure ("survival" end point) only 6 deaths resulted from 300 hypoxia tests on 70 animals. The corrected mean survival time varied from 2.2 min. at zero cone, to 40 min. at 4.2% O2. At 45 to 5.0% O2 survival time rose to above 2 hrs. When the animals were exposed daily to the low O2 cone, adaptation of as high as 80% increase in survival time occurred. With weekly exposures, adaptation did not occur. During recovery, extensor responses preceded flexor in the same limb and lower nervous centers recovered before higher. In general, recovery of reflexes proceeded from the head caudad. If animals had been promptly resuscitated, vision and the hopping and placing reactions returned within 10 min. In the following hr. residual ataxia disappeared and normal activity returned in 2 hrs. Permanent central nervous damage occurred in 5 animals after from 12-21 daily hypoxia trials at 3.5% O2. These cats showed lasting impairment characterized by blindness, deafness, anorexia, loss of hopping and placing reactions and general depression of activity. In these animals and others in which artificial respiration was purposely withheld for from 30-145 sec., cardiac recovery was slow following the last exposure. Two were maintained for several mos. and recovered from the major disabilities but developed permanent hyperactivity and a stereotyped cage-scratching behavior. Brain sections of these animals showed scattered cell damage from cerebral cortex to medulla, including marked chromatolysis in all neocortical layers, particularly in the outer pyramids and most marked in the primary visual cortex. Damage was also marked in lateral geniculate and moderate in superior and inferior colliculi, thalamic midline nuclei, medullary reticular formation, and nucleus gracilis. Electrocorticograms of the impaired animals showed continuous 3 C.P.S. dysrhythmia compared with 6 to 10 C.P.S. in normal cats. Under the test conditions used, the margin of safety between the time of appearance of central nervous damage and irreversible circulatory failure is apparently very narrow.

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