DIFFERENTIAL ACTION OF ANOXIA, ASPHYXIA AND CARBON DIOXIDE ON NORMAL AND CONVULSIVE POTENTIALS

Abstract

The effect of anoxia, asphyxia and inhalation of 10% CO2 on normal and convulsive potentials was studied in anesthetized cats with the following results: Anoxia induced by inhalation of 4% O2 or of N2 abolishes convulsive potentials at a time when normal potentials are practically unchanged. On readmission of air, normal potentials appear in the previously convulsive areas before the convulsive spikes reappear. There is no indication of an excitatory phase in anoxia. Asphyxia induced by cessation of artificial respiration likewise abolishes spikes before normal potentials and leads to an earlier reappearance of the latter on readmission of air. In addition, asphyxia causes a temporary excitation characterized by an increased frequency of spikes and, in the normal cortex, by an increase in background potentials and a decrease in "dial" potentials. When anoxia or asphyxia is carried out until convulsive and normal grouped (dial) potentials are abolished, their restitution on re-oxygenation is preceded by continuous small potentials which are considered to be the equivalent of the increased post-anoxic excitability. Convulsive potentials may be replaced in the course of anoxia or asphyxia by dial potentials which are absent in the same cortical area as long as convulsive activity persists. Moreover, under favorable conditions, progressive anoxia and asphyxia is accompanied by a decreasing spike amplitude, re-oxygenation is followed by an increase. These data seem to indicate that anoxia and asphyxia induce a progressive decruitment of cortical cells and re-oxygenation a recruitment. The limiting factor which determines the number of discharging neurons and the degree of their activity (convulsive vs. non-convulsive) seems to be the supply of oxygen. The restitution of normal oxygenation of the blood after anoxia and asphyxia is often accompanied by a rebound which is shown in the normal cortex in the form of more frequently appearing groups of dial potentials and in the convulsive cortex as increase in frequency of spikes. During this rebound, convulsive potentials may appear which were absent under control conditions due to the application of subthreshold concns. of the convulsant drug. Hypercapnia induced by inhalation of 10.6% CO2 causes excitation of normal and particularly of convulsive potentials (increase in frequency).