果糖二磷酸钠镁对失血性休克大鼠肾脏的保护作用

Protective effects of sodium magnesium fructose diphosphate on the kidney in hemorrhagic shock rats

目的探讨果糖二磷酸钠镁(FDPM)对失血性休克大鼠肾脏的保护作用及其机制。方法按照Wiggers改良法建立失血性休克模型,模型成功后分别自股静脉注射FDPM(90.0、45.0、22.5mg.kg-1),1.6-二磷酸果糖(37.5mg.kg-1),硫酸镁(3.4mg.kg-1)及等容量生理盐水,于休克前、休克末、给药后10、、30、60min及回输血后0、30、60min检测平均动脉压的变化,并测定血清中的尿素氮(BUN)、肌酐(Cr)含量和肾脏组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)、Na+-K+-ATPase、Mg2+-ATPase、Ca2+-ATPase活性的变化。结果FDPM能够升高失血性休克大鼠的平均动脉压(MAP),减少血清中的BUN和Cr含量,同时降低肾脏组织MDA含量和提高SOD、Na+,K+-ATPase、Mg2+-ATPase、Ca2+-ATPase活性。结论FDPM能够有效的减轻失血性休克大鼠肾脏组织缺血缺氧性损伤,改善能量代谢,增加ATP酶活性,减轻自由基损伤,从而起到保护肾脏的作用。

Aim To study the protective effects of sodium magnesium fructose diphosphate （FDPM） on the kidney in hemorrhagic shock rats. Methods The study utilized Wiggers hemorrhagic shock model. Sixty Wistar rats were divided into six groups randomly： normal saline control group, three doses of FDPM group （90.0, 45.0, 22.5 mg·kg^-1）, 1,6-fructose diphosphate group （37.5 mg·kg^-1） and magnesium sulfate group （3.4 mg·kg^-1）. Mean arterial pressure was monitored before shock, 10, 30 and 60 minuts after drug administration and 0, 30 and 60 minuts after shed blood reinfusion Blood urea nitrogen and creatinine, the content of malondiadehyde, and the activity of Na^＋-K^＋-ATPase, Ca^2＋-ATPase, Mg^2＋-ATPase, and superoxide dismutase in kidney were also measured. Results FDPM significantly improved mean arterial blood pressure of hemorrhagic shock rats, reduced blood urea nitrogen and creatinine, decreased the content of malondiadehyde and increased the activity of Na^＋, K^＋-ATPase, Ca^2＋-ATPase, Mg^2＋-ATPase and superoxide dismutase in kidney. Conclusion FDPM had protective effects on the ischemia-hypoxia injury of kidney by improving energy metabolism and attenuating tissue injury caused by free radicals in hemorrhagic shock.