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作 者:吴周晏 吉杰梅[1] 谷万杰[1] 刘文志[1] 刘敬臣[1]
机构地区:[1]广西医科大学第一附属医院麻醉科,南宁530021
出 处:《国际麻醉学与复苏杂志》2014年第6期502-505,共4页International Journal of Anesthesiology and Resuscitation
摘 要:目的 探讨右美托咪定(dexmedetomidine,Dex)预先给药对脂多糖(lipopolysaccharide,LPS)诱导大鼠急性肺损伤(acute lung injury,ALI)的保护作用. 方法 气管滴注LPS 5 mg/kg,建立大鼠ALI模型.30只雄性SD大鼠,采用随机数字表法分为3组,每组10只:空白对照组(C组,输注生理盐水)、LPS对照组(L组,腹腔注射生理盐水30 min后气管滴注LPS)、Dex预先给药组(D组,腹腔注射Dex 50 μg/kg 30 min后气管滴注LPS).注射LPS后6h处死动物,行动脉血气分析、检测肺组织髓过氧化物酶(myeloperoxidase,MPO)活性、肺组织湿/干重比(wet/dry ratio,W/D)、肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)和白介素-6(interleukin-6,IL-6),观察肺组织病理学的改变. 结果 D组与L组比较,MPO活性水平分别为(0.70±0.06)和(1.01 ±0.05)(P<0.01)、肺组织W/D值分别为(4.44±0.08)和(4.76±0.10)(P<0.01)、动脉血氧分压(oxygen partialpressure of the artery,Pa02)值分别为(94.0±2.6) mmHg(1 mmHg=0.133 kPa)和(78.0±4.7) mmHg(P<0.05)、血清TNF-α值分别为(39±9) ng/L和(92±14) ng/L(P<0.05)、IL-6值分别为(72±16) ng/L和(95±16)ng/L(P<0.05),且D组肺损伤的病理的严重程度比L组轻. 结论 Dex预先给药对LPS诱导大鼠AH有一定的保护作用,与抑制中性粒细胞在肺内聚集、激活和TNF-α、IL-6等炎性因子的释放有关.Objective To investigate the protective effect of dexmedetomidine(Dex) pretreatment on acute lung injury(ALI) induced by lipopolysaccharide (LPS) in rats.Methods A total of 30 male Sprague-Dawley rats were randomly divided into three groups(n=10):control gronp (group C),the LPS group (group L) and the Dex pretreatment group (group D).The rats in the LPS group were intratracheally administered with LPS (5 mg/kg) to duplicate an acute lung injury model.In the group D,the rats were given 50 μg/kg of Dex intraperitoneally 30 min before LPS application.Six hours after LPS administration,arterial blood was drawn for interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) measurement,and the pulmonary tissues were harvested for pathological evaluation,wet/dry (W/D) ratio measurement,biochemical analysis of myeloperoxidase (MPO).Results The Dex pretreatment group compared with LPS group,the levels of wet/dry weight ratio were (4.44±0.08) and (4.76±0.10) respectively (P〈0.O1),the levels of MPO activities were (0.70±0.06) and (1.01±0.05) respectively (P〈0.01).The value of the oxygen partial pressure in the arteries were (94.0±2.6) mmHg (1 mmHg=0.133 kPa) and (78.0±4.7) mmHg respectively (P〈0.05).The levels of TNF-α were (39±9) ng/L and (92±14) ng/L respectively(P〈0.05).The levels of IL-6 were (72±16) ng/L and (95±16) ng/L respectively(P〈0.05).The pulmonary tissue damage in histopathology in LPS group was more severe than in Dex pretreatment group.Conclusions Dex pretreatment can protect acute lung injury induced by LPS through inhibition of activation of neutrophil in lung tissue and expression of TNF-α and IL-6.
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