The protection against the cerebral and pulmonary effects of hyperbaric oxygen by pharmacological agents and lithium salts in mice

The effect of three phenothiazines, a barbiturate, a ureide, two oxazolidine diones, γ-aminobutyrate, γ-hydroxybutyrate and n-dipropylacetate, in diminishing the incidence of convulsions and pulmonary oedema induced by hyperbaric oxygen at pressures up to 6 bars was studied in mice. The order of effectiveness in protection was chlorpromazine (6 mg/kg) > LiCl (600 mg/kg) > γ-hydroxybutyrate (200 mg/kg) > prochlorpemazine (5 mg/kg) > phenobarbitone (5 mg/kg). If a drug protected the mouse against convulsions, the pulmonary hydration did not increase. The findings generally supported the hypothesis that the protection from hyperbaric oxygen was due to these drugs preventing the fall of γ-aminobutyrate in the brain caused by hyperbaric oxygen.     

Effect of aligeron and cinnarizine in models of general and local depression of the cortical bioelectrical activity in cats

The effect of aligeron (5 mg/kg i.v.) and cinnarizine (10 mg/kg i.v.) on general and local depression of cortical bioelectrical activity was studied in acute experiments on cats. Asphyxic anoxia and hypoventilation hypoxia were used as models of general depression. Local depressions were caused by topical application of potassium chloride (KCl) and adenosine-5'-monophosphate (AMP) on the cortex. In hypoventilation hypoxia aligeron and cinnarizine increased cortical resistance to hypoxia and accelerated the recovery of cortical bioelectrical activity. In KCl- and AMP-induced depressions the drugs showed a protective effect manifested in a decrease of the degree and duration of the depression. In asphyxic anoxia their effect was insignificant.