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七氟醚对脂多糖诱导的大鼠急性肺损伤的保护效应 被引量:8

Effects of sevoflurane postconditioning on lungs of rats with lipopolysaccharide-induced acute lung injury
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摘要 目的:评估七氟醚后处理对脂多糖(LPS)致急性肺损伤(ALI)大鼠肺的影响。方法:随机将30只大鼠分为5组(n=6):生理盐水组、脂多糖组:气管内滴注生理盐水1 ml/kg或脂多糖5 mg/kg;七氟醚30 min组、七氟醚1 h组、七氟醚2 h组:气管内滴注脂多糖后4 h,分别吸入2.4%七氟醚0.5,1,2 h。各组于滴注生理盐水或脂多糖后6 h放血处死。检测各组肺组织病理切片和肺泡灌洗液(BALF)中TNF-α,IL-1β和IL-10的浓度。结果:与生理盐水组比较,脂多糖组病理切片示肺泡正常结构破坏严重,灌洗液中TNF-α,IL-1β和IL-10浓度显著升高(P<0.01)。与脂多糖组比较,七氟醚组病理切片示肺泡结构破坏较轻,灌洗液中TNF-α,IL-1β和IL-10浓度降低(P<0.05);且1,2 h组七氟醚改善病理形态和抑制TNF-α,IL-1β的效果更佳。结论:七氟醚后处理能减轻脂多糖致急性肺损伤大鼠肺部炎症反应,且吸入时间长有更佳的效果。 Objective: To investigate the effect of sevoflurane postconditioning on lungs of rats with LPS-induced acute lung injury.Methods: Thirty rats were randomly divided into 5 groups(n=6): NS group,LPS group,NS(1 ml/kg) or LPS(5 mg/kg) was instilled in rats′ airway.Sevoflurane groups(S 0.5 h group,S 1 h group,S 2 h group): Four hours after LPS instillation,rats received sevoflurane inhalation(2.4%) respectively for thirty minutes,one hour or two hours.Six hours after NS or LPS instillation,all groups were exsanguinated.Histopathological examinations were performed for the lung specimens and concentration of TNF-α,IL-1β and IL-10 in BALF were measured.Results: Compared with the NS group,after LPS instillation,the alveolar structure was severely altered.Concentration of TNF-α,IL-1β and IL-10 in BALF were significantly increased(P0.01).Compared with the LPS group,in sevoflurane groups,the alveolar structure was improved.Concentration of TNF-α,IL-1β and IL-10 were reduced(P0.05).It was more effective to improve pathohistology and reduce TNF-α,IL-1β levels in S 1 h group and S 2 h group than S30min group.Conclusion: Sevoflurane postconditioning could attenuate lung inflammation in rats with lipopolysaccharide induced acute lung injury,it was more effective during longer inhalation time.
作者 杨芬 方志源
出处 《江苏大学学报(医学版)》 CAS 2010年第3期223-225,I0002,共4页 Journal of Jiangsu University:Medicine Edition
关键词 七氟醚 脂多糖 急性肺损伤 炎症反应 sevoflurane lipopolysaccharide acute lung injury lung inflammation
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参考文献8

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