부산대학교 도서관

olerance to hypoxia can be induced by reducing oxygen consumption. Dexmedetomidine (DEX) decreases locomotor activity and induces bradycardia and hypothermia in mice. The present study examined the hypothesis that DEX improves hypoxia tolerance in mice. Adult mice received an intraperitoneal injection of 1, 5, 10, 20, 40, 80, 160 or 320 μg/kg DEX, 20 mg/kg propranolol or saline. Acute hypoxic conditions were induced by placing the mice in a limited enclosed container with soda lime. Core body temperature (CBT) and heart rate (HR) were measured prior to and 30 min after drug administration. Survival time was monitored in the sealed container. Survival times (mean ± standard deviation) of mice in the saline, 1, 5, 10, 20, 40, 80, 160 and 320 μg/kg DEX, and the 20 mg/kg propranolol groups were 22.4±1.1, 23.4±1.1, 26.0±0.9, 36.9±5.2, 42.4±2.9, 43.2±2.3, 58.2±4.2, 80.5±4.0, 79.2±6.0, and 38.2±2.8 min, respectively. Pretreatment with propranolol and 10, 20, 40, 80, 160 or 320 μg/kg DEX, but not 1 or 5 μg/kg, significantly prolonged survival time compared with saline-injected mice (P<0.05 or P<0.01). CBT and HR decreased in a similar manner. The correlation coefficients between survival time and CBT, and survival time and HR were -0.802 and -0.726, respectively. Thus, DEX dose-dependently enhances hypoxia tolerance in mice. In conclusion, it is suggested that DEX may be used in clinical practice as a novel protective agent for organs and tissues during hypoxic injury. [ABSTRACT FROM AUTHOR]