RESUMO
OBJECTIVE: The aim: To study the antihypoxic activity of 2,6-dimethylpyridine-N-oxide in mice using the various experimental models of acute hypoxia under orally or intraperitoneally administration. PATIENTS AND METHODS: Materials and methods: The studies were performed on male CD-1 (SPF) mice. The antihypoxic activity of 2,6-dimethylpyridine-N-oxide was studied in three experimental models of acute hypoxia - hypercapnic hypoxia or hypoxia in a closed space, hemic hypoxia and histotoxic hypoxia at orally administration at doses 0.07; 7.1 and 71 mg/kg (respectively 1/20000, 1/200 and 1/20 of LD50) and at intraperitoneally administration at doses 7.1 and 71 mg/kg in comparison with reference drug Armadin. RESULTS: Results: It is established, that 2,6-dimethylpyridine-N-oxide shows a antihypoxic activity in the all experimental models of acute hypoxia (hypoxia in a closed space, hemic hypoxia and histotoxic hypoxia). Its antihypoxic activity in acute hemic hypoxia and in acute hypoxia in a closed space was significantly higher than of reference drug Armadin, but during acute histotoxic hypoxia did not differ from Armadin. Also at intraperitoneal administration of 2,6-dimethylpyridine-N-oxide demonstrates less pronounced antihypoxic activity than at oral administration in all experimental models of acute hypoxia, but the coefficient efficiency is higher than in the reference drug Armadin. CONCLUSION: Conclusions: 2,6-dimethylpyridine-N-oxide may be recommended for further detailed experimental studies as a perspective antihypoxant.
