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机构地区:[1]南京市胸科医院麻醉科,210009 [2]东南大学附属中大医院麻醉科
出 处:《中华麻醉学杂志》2009年第11期1040-1043,共4页Chinese Journal of Anesthesiology
摘 要:目的探讨瑞芬太尼对兔内毒素性急性肺损伤(ALI)的影响。方法健康成年雄性新西兰大白兔30只,体重2.5~3.5kg,随机分为5组(n=6):对照组(C组)、ALI组、低剂量瑞芬太尼组(LR组)、中剂量瑞芬太尼组(MR组)和高剂量瑞芬太尼组(HR组)。C组经30Bin静脉输注生理盐水10ml;ALI组经30min静脉输注大肠杆菌内毒素(LPS)0.5mg/kg;LR组、MR组和HR组分别静脉输注瑞芬太尼0.2、0.4和0.8ug·kg^-1·min^-1至处死,输注15min时开始给予LPS,方法同ALI组。于LPS输注前即刻(T0)、输注结束后1、2.5、5.5h时记录平均动脉血压(MAP)、心率(HR)和气道峰压(Ppeak),测定动脉血氧分压(PaO2)和血浆细胞间粘附分子1(ICAM-1)浓度,称量肺组织湿重(W)和干重(D),计算W/D比,并在光镜和电镜下观察肺组织病理学结果。结果与C组比较,ALI组MAP、HR和PaO2降低,W/D比、Ppeak和血浆ICAM-1浓度升高(P〈0.05);与ALI组比较,LR组、MR组和HR组MAP、HR升高,肺组织W/D比降低,Ppeak和血浆ICAM-1浓度降低,PaO2升高(P〈0.05);与LR组比较,MR组和HR组MAP、HR、Ppeak、血浆ICAM-1浓度和肺组织W/D比降低,PaO2升高(P〈0.05);与MR组比较,HR组注肺组织W/D比降低,PaO2升高(P〈0.05)。LR组、MR组和HR组肺组织病理学损伤较ALI组减轻。结论瑞芬太尼可减轻兔内毒素性急性肺损伤,且呈剂量依赖性,其机制可能与抑制ICAM-1的表达有关。Objective To investigate the effects of remifentanil on lipopolysaccharide (LPS)-induced acute lung injury (ALl) in rabbits. Methods Thirty healthy male New Zealand white rabbits weighing 2.5-3.5 kg were randomly divided into 5 groups ( n = 6 each) : group Ⅰ control (group C) ; group Ⅱ ALI; group Ⅲ , Ⅳ, Ⅴ low, median and high dose RF + LPS (group LR, MR, HR). The animals were anesthetized with intravenous 3% pentobarbital sodium 30 mg/kg, tracheostomized and mechanically ventilated. The carotid artery and jugular vein were cannulated for MAP and HR monitoring, blood sampling, and fluid and drug administration. LPS 0.5 mg/kg in 10 ml of normal saline (NS) was infused over 30 rain in group Ⅱ- Ⅴ . Remifentanil 0.2, 0.4 or 0.8 ug·kg^-·min^-1 was infused starting from 15 min before LPS administration until the death of the animals. MAP, HR, peak airway pressure (Ppook), PaO2 and plasma intercellular adhesion molecule 1 (ICAM-1) concentration were measured innnediately before LPS infusion (TO , baseline) and at 1, 2.5 and 5.5 h after the end of LPS infusion. The animals were killed and the lungs were immediately removed for microscopic examination and determination of W/D lung weight ratio. Results MAP, HR and PaO2 were significantly decreased while W/D ratio and Ppeak were significantly increased after iv LPS inlusion as compared with control group. LPS significantly increased plasma iCAM-1 concentration and damaged the structure of lung tissue. Remifentanil infusion significantly attenuated the LPS-induced changes in a dose-dependent manner. Conclusion RF has protective effect against LPS-induced ALI and inhibition of ICAM-1 expression is involved in the mechanism.
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