高温复合脂多糖应激大鼠血清尿素和肌酐的变化特点

Changes of serum urea and creatinine concentrations in rats with lipopolysaccharide and heat co-exposure

目的探讨高温与脂多糖(LPS)复合应激大鼠血清尿素、肌酐含量等指标的动态变化特点。方法雄性SPF级Wistar大鼠随机分为常温+生理盐水组(C组)、高温+生理盐水组(H组)、常温+LPS组(L组)、高温+LPS组(HL组)。置动物于模拟气候舱,HL组、H组暴露环境干球温度为(35.0±0.5)℃,L组、C组Tdb为(26±0.5)℃;HL组、L组动物经尾静脉注射LPS8mg/kg,H组、C组动物经尾静脉注射0.9%NaCl8ml/kg。检测动物应激0、40、80、120min时血清尿素、肌酐等物质含量的变化。结果肌酐在不同温度、时间、药物水平间不存在显著性差异(P>0.05);不同温度、时间、药物水平间动物血清尿素存在显著性差异(P<0.01),时间与药物、温度与药物、时间与温度交互效应显著(P<0.01)。应激40min起各组间尿素差异显著,HL组尿素显著高于其余3组(P<0.01)。尿素水平与TNF-α含量存在正相关关系(r=0.730,P=0.000)。结论高温与LPS复合应激可促发、扩大全身炎症反应综合征,造成肾损伤。

Objective To investigate the effects of lipopolysaccharide （LPS） and heat co-exposure on serum urea and creatinine （Cr） concentrations in rats. Methods Male Wistar rats were randomized into normothermic saline injection control group （group C）, heat exposure saline injection group （group H）, normothermic LPS injection group （group L）, and heat exposure LPS injection group （group HL）. The rats in groups H and HL were exposed to heat in a chamber at an dry bulb temperature （Tdb） of 35.0±0.5 %, and those in groups C and L were kept in a chamber at Tdh of 26±0.5 %. LPS （8 mg/kg） was injected via the tail vein in the rats in groups L and HL to induce endotoxemia, while those in groups C and H were given normal saline injection （8 ml/kg） via the tail vein. The serum levels of urea and Cr were determined at the time points of 0, 40, 80, and 120 min after the injections. Results No significant difference was found in serum Cr level at any level of the main effects of time, drug, or Tdb （P〉0.05）, but serum urea level varied significantly between the different time points, different levels of Tdb, and the drug injections （P〈0.01）. Significant interactions were identified between the time after injection, injected agents, and Tdb （P〈0.01）. Except for those in the group C, all rats showed elevated serum urea levels 40 min after the injection, particularly those in group HL. The serum urea levels were positively correlated to the level of tumor necrosis factor-α （P〈0.01）. Conclusion Co-exposure to LPS and heat in rats may elicit and worsen systemic inflammatory response syndrome and kidney injury.