摘要
目的评价联合2%氢气吸入的液体复苏方案对脂多糖(LPS)诱导的脓毒性休克大鼠心肌的保护。方法60只Wistar大鼠随机分成4组(每组15只):正常对照组(C),脓毒性休克对照组(S),脓毒性休克+液体复苏组(R),脓毒性休克+2%氢气吸入联合液体复苏组(R+H。)。大鼠麻醉后予呼吸机辅助通气,R+H2组给予2%氢空混合气,其余3组给予单纯空气吸入。LPS10mg/kg静脉注射,建立脓毒性休克模型,c组给予等量生理盐水静脉注射。R组和R+H组给予相同液体复苏方案,维持平均动脉压(MAP)于正常水平。4h后,大鼠经腹主动脉放血处死,留取血液及心脏标本。结果联合2%氢气吸入的液体复苏方案与单纯液体复苏比较,明显降低血清cTnI水平、氧化应激损伤及心肌TNF-α、IL-6表达水平。结论联合2%氢气吸入的液体复苏方案对脓毒症所致心肌损伤具有更好的保护作用。
Objective To investigate the therapeutic effects of a novel fluid resuscitation protocol (early fluid resuscitation plus 2% hydrogen inhalation) on heart injury during septic shock induced by lipopolysaccharide (LPS) in rats. Methods Male Wistar rats (n =60) were randomly divided into 4 groups (n =15 per group) : control group (C), septic shock group (S), septic shock with early fluid resuscitation group (R) , and septic shock with early fluid resuscitation plus 2% hydrogen inhalation group (R + H2 ). The rats were ventilated, and a 2% hydrogen mixture was used in group R +H2. LPS (10 mg/kg) was administered to establish the septic shock model in rats and fluid resuscitation was performed in group R and group R +H2. Results Fluid resuscitation with 2% hydrogen inhalation decreased serum cTnI levels. It also reduced oxidative stress injury and decreased heart tumor necrosis factor-α and interleukin-6 levels compared with fluid resuscitation alone. Conclusions Early fluid resuscitation plus 2% hydrogen inhalation provided more protection against heart injury during septic shock.
基金
国家自然科学基金资助项目(No.81571882)
关键词
脓毒性休克
心肌损伤
液体复苏
氢气
septic shock
heart injury
fluid resuscitation
hydrogen