ABSTRACT
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.
Subject(s)
Carboxylic Acids/pharmacology , Exploratory Behavior/drug effects , Hypercapnia/drug therapy , Hypnotics and Sedatives/pharmacology , Hypoxia/drug therapy , Neuroprotective Agents/pharmacology , Pyrones/pharmacology , Animals , Anxiety , Drug Evaluation, Preclinical , Hypercapnia/psychology , Hypoxia/psychology , Male , Motor Activity/drug effects , Propofol/pharmacology , Rats, Wistar , Sleep/drug effectsABSTRACT
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.
