胍丁胺对大鼠应激性体温升高的抑制作用

目的：观察胍丁胺（AGM）是否能降低或反转应激性体温过高反应。方法：61只雄性SD大鼠随机分为3部分，每部分再分为对照组和AGM组。在实验过程中，人工气候箱和开放实验箱内的温度均保持在22℃。①用无线遥测技术连续测量大鼠的体温和活动，观察腹腔注射AGM对安静状态下大鼠正常体温和活动的影响（n=8）；②将大鼠放置在开放实验箱中60 min复制应激性体温过高的模型，用无线遥测技术连续测量开放实验箱内大鼠体温和活动的变化（n=7~8）；③用美国哥伦布公司动物代谢分析系统测量AGM对大鼠能量代谢的影响（n=7）。结果：①腹腔注射AGM 80 mg/kg能引起正常大鼠出现明显低温反应（-0.46±0.11）℃，而注射AGM 40 mg/kg则对正常体温无明显影响。②对照组大鼠腹腔注射生理盐水后，置于开放实验箱内体温升高达（0.78±0.16）℃；给大鼠注射AGM 40或80 mg/kg后，置于开放实验箱内60 min时，体温则分别降低（0.34±0.11）℃和（0.81±0.14）℃。③AGM 80 mg/kg能明显降低大鼠的耗氧量和产热量。结论：AGM能引起正常大鼠出现低温反应和明显翻转应激性体温升高反应，其作用可能与AGM能降低能量代谢有关。

Inhibitory effects of agmatine on stress-induced hyperthermia in rats

Objective:To examine whether agmatine (AGM) would alter stress-induces hyperthermic response. Methods:Sixty-one male SD rats were randomly divided into three experiments. Each experiment was divided into control group and AGM group. During the experiments, the animals were maintained in a chamber at 22℃. ①Effects of intraperitoneal injecting 40 or 80 mg/kg AGM on normal core temperature and activity were observed in undisturbed rats using radiotelemetry (n=8). ②Stress-induced hyperthermia model was established by placing rats in an open-field chamber for 60 min. Rats were dosed intraperitoneally with AGM or saline, and placed immediately inside the open-field chamber. Core temperature and motor activity were monitored by radiotelemetry in an open-field chamber (n=7~8). ③Effect of AGM on energy metabolism was measured by Columbus Oxymax Lab Animal Monitoring System (n=7). Results:①Rats administered with 80 mg/kg AMG showed significant hypothermic responses (-0.46±0.11)℃, while 40 mg/kg AMG had no significant effect on the normal core temperature. ②Core temperature of control group increased by (0.78±0.16)℃ during open-field exposure, whereas rats administered 40 and 80 mg/kg AGM underwent a (0.34±0.11)℃ and (0.81±0.14)℃ reductions in core temperature within 60 min, respectively. ③Oxygen consumption and energy metabolism were significantly reduced by AGM (80 mg/kg). Conclusion:The data demonstrated that AGM induced hypothermic responses in rats and reversed stress-induced hyperthermia, and its effect might attribute to the suppression of energy metabolism.