RESUMO
The effects of potassium comenate on functional state of CNS in mice and rats were studied in the open-field and hole-board tests under control conditions and after acute exposure to hypoxia-hypercapnia. The effects of potassium comenate on CNS were also studied in rodents subjected to propofol-induced sleep. Preliminary administration of 4 mg/kg potassium comenate for 3 days attenuated the posthypoxic changes in behavioral reactions (emotional anxiety/reactivity). The pronounced stress-protective effect of potassium comenate was observed both on days 1 and 14 after exposure to hypoxia-hypercapnia. Under normal conditions, potassium comenate moderated behavioral reactions and augmented somniferous effect of propofol. We hypothesized that the antihypoxic effect of potassium comenate is determined by its stress-protective and sedative potencies.
Assuntos
Ácidos Carboxílicos/farmacologia , Comportamento Exploratório/efeitos dos fármacos , Hipercapnia/tratamento farmacológico , Hipnóticos e Sedativos/farmacologia , Hipóxia/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Pironas/farmacologia , Animais , Ansiedade , Avaliação Pré-Clínica de Medicamentos , Hipercapnia/psicologia , Hipóxia/psicologia , Masculino , Atividade Motora/efeitos dos fármacos , Propofol/farmacologia , Ratos Wistar , Sono/efeitos dos fármacosRESUMO
The study demonstrated neuroprotective action of novel chemical agent, potassium salt of comenic acid, against the glutamate-induced cytotoxicity on the model of cultured cerebral neurons. Potassium comenate (0.001-1.0 mM) significantly decreased the rate of glutamateinduced neuronal death. The highest viability of the cultured neurons during postglutamate time was observed when potassium comenate was applied in a concentration of 0.1 mM.