Acute asphyxiation of the spinal cord and of other sections of the nervous system

Abstract

Oxygen lack causes an impedance increase of the spinal cord coinciding in time with an asphyxial potential which can be led off from the spinal gray matter against an indifferent electrode. After circulatory arrest the latency of these changes is of the order of 10 sec; after ventilation of the preparation with nitrogen the latency is 20–25 sec. An asphyxial transport of chloride was demonstrated into dendrites of dorsal horn neurons accompanied by a volume increase of these structures. The electrolyte movement can account for the impedance increase by a loss of extracellular ions which are the main carriers of the measuring current. The observed ion movement, taken as an indication of depolarization, suggests that the asphyxial potential is due to dendritic depolarization, the somas (and axons) acting as source. This explanation was supported by the much slower decline of the spinal asphyxial potential as compared with that of a similar potential which can be led off from the cerebral cortex. The difference in the rate of decline reflects the much slower asphyxial depolarization of the somas of spinal neurons as compared with that of cerebral nerve cell bodies which has been observed previously.