Adrenalectomized rats exposed to high pressure oxygen (OHP) until convulsion convulse much later than sham-operated or normal rats. No significant changes in the concentration of noradrenaline (NA) and total catecholamines (TC) in the brain were noted in sham-operated or adrenalectomized rats resulting from sham or real surgery and no change occurred in these variables in normal sham-operated or adrenalectomized animals after OHP leading to convulsion. Brain adrenaline (A) concentration, however, decreased significantly in all three groups following OHP-induced convulsions. Activity of catecholamine O-methyltransferase (COMT) decreased significantly only in adrenalectomized rats. Brain γ-aminobutyric acid (GABA), glutamate, and other amino acid level remained unchanged after adrenalectomy whereas the concentration of ammonia decreased significantly when normal rats were adrenalectomized. After OHP-induced convulsions, the concentrations of brain GABA and glutamate decreased and ammonia and glutamine plus asparagine increased significantly in normal, sham-operated, and adrenalectomized rats. In the blood no significant difference was noted in the concentration of the catecholamines, ammonia, and amino acids either in normal or sham-operated rats. In adrenalectomized rats, the blood A and NA concentrations decreased significantly and tyrosine increased significantly. The concentration of NA, ammonia, and glutamine plus asparagine in rats from all three groups increased after OHP-induced convulsions, whereas the concentration of glutamate decreased significantly. Since the concentration of A increased significantly after convulsions in normal and sham-operated rats but did not change in adrenalectomized rats, it might be proposed that adrenalectomy protects against OHP-induced convulsions by reducing the circulating concentration of A and ammonia.However, these are not the only factors involved in the protection since the sham-operated rats also convulsed much later than normal rats but had similar ammonia and A concentrations to normal animals.
High-pressure oxygen rewires glucose metabolism of patient-derived glioblastoma cells and fuels inflammasome response
