Electroencephalographic protective action of pyridoxylate during acute hypoxia and subsequent recovery in the rat.

Pyridoxylase at a concentration of 0.6 mmol/kg body weight injected intraperitoneally in rats, increased the resistance of animals to severe hypoxia (O2:3.2%; N2; 96.,%). The electrocorticogram (ECoG) was used to indicate the effectiveness of the drug in lowering the delay of electrographic silence, in 19 control rats and 12 pretreated rats. The ECoG was also recorded period under pure oxygen. In pretreated rats, the ECoG records became flat in a mean time of 551 s, compared with 269 s in the control group. The latent periods of successive steps during cerebral anoxia were significantly delayed in pyridoxylate-pretreated rats subjected to hypoxia. During the recovery period, pyridoxylate improved the recovery of the normal ECoG, particularly when values were expressed as a function of the duration of the hypoxic period. These findings are in good agreement with the significant protection afforded by pyridoxylate on the cerebral rate of energy-rich phosphate bond utilization during hypoxia studied in a separate work.

[Evaluation by electrocorticogram of the protective action of piridoxilate against cerebral hypoxia in rats]. / Evaluation sur l'électrocorticogramme du rat de l'action protectrice du piridoxilate contre l'hypoxie cérébrale.

Piridoxilate, at the concentration of 120 mg/kg i.p. in rats, enhanced resistance of these animals to hypoxia (N2 : O2 3,2 %). The electrocorticogram (ECOG) is used to indicate the effectiveness of the drug in lowering the time of electrographic silence, on control (n=19) and pretreated rats (n=12). The ECOG was recorded also during the recovery period under pure oxygen. In pretreated rats, the ECOG records became flat in approximately 551 sec (versus 269 sec on the control group). The latent period of successive steps of cerebral anoxia were delayed in pretreated rats exposed to hypoxia. During the recovery period, piridoxilate seems to enhance the restoration of normal ECOG, as a function of the duration of hypoxia.

[Experimental study of neural and neuro-muscular conduction during simulated diving in dogs and rabbits: anatomo-pathologic correlations]. / Etude expérimentale de la conduction nerveuse et neuro-musculaire au cours de la plongée fictive chez le chien et le lapin: corrélations anatomo-pathologíques.

Five dogs and twelve rabbits were submitted to simulated diving at 6 ATA (compressed air) and 13-15 ATA (normoxic oxygen + nitrogen). Progressive decompressions were carried on for the first, rapid for the lasts. Motor nerve conduction velocity and nerve-muscle delays were measured. No variations could be observed neither for nerve conduction velocity nor for muscular and nerve action potentials. Nevertheless optic and electronic microscopy observations shew some nerve, neuronal and a few muscular alterations occuring during rapid decompression.

What EEG criteria for diving fitness?

The authors have tried to consider EEG criteria applicable to fitness for diving. In a study of 90 professional divers, 37 (41%) displayed patterns susceptible of being interpreted as falling outside of strict normalcy. These patterns have sometimes been considered incompatible with diving, or even pathological by some authors. Considering the fact that these subjects were in good health, the value of these EEG signs is discussed in comparison with the literature. A general guideline is proposed placing subjects in three groups: fit, unfit, and questionable. In the last case, a final decision is taken in each individual case in agreement with the other medical examinations and based on the type of diving considered. Some explicit EEG criteria of definitive or temporary fitness and unfitness are proposed.

[Hyperbaric oxygen: effect of sodium dipropylacetate and dipropylacetamine on convulsion seizures and pulmonary lesions in the mouse]. / Oxygène hyperbare: effets du dipropylacétate de Na et du dipropylacétamide sur les crises convulsives et les lésions pulmonaires chez la souris

It was shown that oxygen at high pressure (OHP) induced epileptic seizures and pulmonary damages on mice. Dipropylacetate protected mice against nervous syndrome better than did dipropylacetamide. No significant pulmonary protection was observed with both drugs.

The uptake and efflux of L-phenylalanine and L-tyrosine from rat brain cerebral cortex slices.

The uptake of radioactive l-phenylalanine and l-tyrosine into the tissue water of rat brain cerebral cortex slices was shown to have saturation kinetics. The apparent K(m) for the uptake of l-phenylalanine was 0.86mm and for l-tyrosine was 1.64mm; for phenylalanine the apparent V(max.) value was 0.64mumol/min per ml of tissue water, and for l-tyrosine it was 0.98mumol/min per ml of tissue water. The accumulation of the two amino acids by the tissue was depressed in the absence of O(2), at 0 degrees C, or in the presence of metabolic inhibitors. The influxes and effluxes of both l-isomers were more rapid than those of the d-isomers. Competition between these two amino acids and each with l-tryptophan in respect of uptake into tissue water was shown. Their rates of influx were faster, and rates of efflux were slower, in the presence than in the absence of Na(+). It was concluded that these amino acids were taken up by active transport via a carrier mechanism.

The uptake and efflux of glycine from rat cerebral-cortex slices.

The kinetics of the influx and efflux of radioactive l-glycine was studied in slices of rat cerebral cortex. The influx showed saturation kinetics and was inhibited by l-alanine. Influx was dependent on the presence of Na(+) ions and a metabolizable substrate. The efflux of glycine was accelerated by alanine. It was concluded that carrier-mediated facilitated diffusion was the mechanism of glycine uptake by, and efflux from, cerebral slices.

Hyperbaric oxygen: effects on metabolism and ionic movement in cerebral cortex slices.

The incubation of slices of cerebral cortex under hyperbaric oxygen pressures from 1 to 10 atmospheres in the presence of radioactive glucose, pyruvate, succinate, fumarate, L-glutamate, and gamma-aminobutyric acid causes a marked diminution of tissue oxidative reactions. There is a simultaneous decrease in phosphocreatine and adenosine triphosphate, and a reduction of the apparent intracellular ionic gradients. The increase of lipid peroxides, measured directly, is attributed to the toxic effects of hyperbaric oxygen.