Effect of Potassium Comenate on CNS Functional Status in Rodents Exposed to Combined Hypoxia and Hypercapnia in Comparison with Normally Ventilated Animals.

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.

Neuroprotective effect of potassium comenate against glutamate toxicity on the model of cultured rat cerebellar neurons.

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.