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作 者:吴国明[1] 徐智[1] 钱桂生[1] 王兴胜[1] 陈维中[1] 李淑平[1] 薛桥[2] 王士雯[2]
机构地区:[1]第三军医大学新桥医院全军呼吸内科研究所,重庆400037 [2]中国人民解放军301医院老年心血管病研究所,100853
出 处:《西部医学》2004年第3期193-196,共4页Medical Journal of West China
基 金:国家重点基础研究发展规划资助项目 ("973"项目 ;No:G2 0 0 0 0 570 0 4 )
摘 要:目的 复制老年鼠急性肺损伤 (AL I)模型 ,为进一步探讨其发病机制奠定基础。 方法 将 2 10只 2 4月龄Wistar大鼠随机分为油酸 +脂多糖组 (O+L PS组 )、油酸组 (O组 )、脂多糖组 (L PS组 )。 O+L PS组注射油酸 0 .175 ml/kg,8h后再注射脂多糖 2 .5 mg/ kg。 O组和 L PS组分别注射油酸 0 .175 ml/ kg和脂多糖 2 .5 mg/ kg。注射后持续 1.5 L /min给氧 4 h(伤后 lh组除外 )。观测伤前及伤后 1、6、12、2 4、72、12 0 h的动脉血气变化、肺组织病理改变、全身炎症反应发生率、AL I发生率及死亡率。结果 O+L PS组 Pa O2 低于 O组和 L PS组 (P<0 .0 1) ,O+L PS组肺组织病理学评分高于O组和 L PS组 (P<0 .0 1)。 O+L PS组的 SIRS发生率、AL I发生率、死亡率分别为 6 4 .9%、5 9.4 %、38.3% ,均高于 O组和 L PS组 (P<0 .0 1)。结论 本模型较好地模拟了肺脏损伤后继发感染发展为 AL I的过程 ,是用于老年 AL I发病机制研究较好的动物模型。Objective To establish a model of acute lung injury (ALI) in aged rats for studying the pathogenesis of ALI in the elderly.Methods Two hundred and ten 24 month old rats were randomly divided into three groups( n=70) :oleic acid+lipopolysaccharide group (O+LPS group), oleic acid group (O group), lipopolysaccharide group (LPS group).O+LPS group received intravenous injection of 0.175 ml/kg oleic acid at first and intravenous injection of 2.5 mg/kg lipopolysaccharide eight hours later. O group and LPS group received intravenous injection of oleic acid or lipopolysaccharide respectively. After injection, all rats received 1.5 L/min oxygen therapy for four hours except the 1 h post injection group. At the time before intravenous injection and then at 1,6,12,24,72,120 h after injection, the PaO 2 was measured and pathological change of lung was examined. In addition, the incidence of systemic inflammatory response syndrom (SIRS) and ALI, mortality of each group were observed.Results The PaO 2 of O+LPS group was less than that of O group and LPS group ( P<0.01) . The pathologic score of lung, incidence of SIRS and MODS, mortality of O+LPS group were higher than those of O group and LPS group( P<0.01) .Conclusion It is successful to imitate the development of ALI after lung injury and secondary infection by injection of oleic acid and lipopolysaccharide subsequently. This is a suitable model for studying the pathogenesis of ALI in the elderly.
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