瑞芬太尼对脓毒症大鼠能量代谢影响的实验研究

Experimental Study of Remifentanil on Energy Metabolism in Sepsis Induced Rats

目的观察瑞芬太尼对脓毒症大鼠能量代谢指标乳酸、丙酮酸、肾上腺素表达的影响,为瑞芬太尼治疗脂多糖(LPS)诱导的脓毒症提供理论依据。方法采用雄性清洁级Wistar大鼠54只,随机分为3组,即对照组21只、LPS组18只,瑞芬太尼处理组15只。LPS组于20 min内尾静脉注射LPS 15 mg/kg制作脓毒症模型,对照组应用相同量的生理盐水代替;瑞芬太尼处理组,先注射等量LPS后再给予瑞芬太尼(0.04 mg/kg)尾静脉泵入40 min。测定各组大鼠造模后6 h的心、肾组织能量代谢指标表达情况,采用生化法检测乳酸、丙酮酸水平,ELISA检测肾上腺素水平。结果与对照组比较,LPS组大鼠心、肾组织的乳酸、丙酮酸、肾上腺素水平明显增加(P<0.05),而瑞芬太尼显著改善上述指标的变化。LPS组大鼠心、肾组织的乳酸、丙酮酸水平与肾上腺素水平呈正相关(P<0.05)。结论瑞芬太尼可通过调节机体能量代谢,减轻能量代谢紊乱所致的组织缺氧,保护LPS所致的脓毒症组织损伤。

Objective To observe the effects of remifentanil on the expression of lactic acid,pyruvate and adrenaline in energy metabolism indexes in sepsis rats,and to provide a theoretical basis for remifentanil in the treatment of lipopolysaccharide(LPS)-induced sepsis.Methods Fifty-four male clean Wistar rats weighing 270-320 g were randomly divided into three groups:21 in the control group,18 in the LPS group,and 15 in the remifentanil treatment group.In the LPS group,15 mg/kg LPS was injected into the tail vein in 20 mins to make a sepsis model.The control group was replaced with the same amount of normal saline.In the remifentanil treatment group,an equal amount of LPS was injected first,and then the remifentanil(0.04 mg/kg)was administered to the tail vein for 40 mins.After 6 hours,the expression of energy and metabolic indexes in the heart and kidney tissues of rats in each group was determined.Biochemical method was used to detect the levels of lactic acid and pyruvate,and ELISA was used to detect the level of adrenaline.Results Compared with the control group,the levels of lactic acid,pyruvate,and adrenaline in the heart and kidney tissues of rats in the LPS group increased(P<0.05),while remifentanil significantly improved the changes of the above indicators.The levels of lactic acid and pyruvate in the heart and kidney tissues of rats in LPS group were positively correlated with the levels of adrenaline(P<0.05).Conclusion Remifentanil can reduce tissue hypoxia caused by disturbance of energy metabolism and protect sepsis tissue damage caused by LPS by regulating energy metabolism.