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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 copy the model of acute lung injury (ALI) in aged rats and lay the foundation for further exploring its pathogenesis. Methods Two hundred and twenty-two Wistar rats, 24 months old, were randomly divided into three groups: oleic acid + lipopolysaccharide group (O + L PS group), oleic acid group (O group) and lipopolysaccharide group (L PS group). O + L PS group was injected with oleic acid 0.75 ml / kg, and then injected with lipopolysaccharide 2.5 mg / kg 8 hours later. O and L PS groups were injected with oleic acid 0.751g / kg and lipopolysaccharide 2.5mg / kg respectively. 1.5 L / min after injection of oxygen for 4 h (except after injury lh group). Arterial blood gas changes were observed before and after injury at 1, 6, 12, 24, 72, 120 h after injury. Pathological changes of lung tissue, incidence of systemic inflammatory response, AL I incidence and mortality were observed. Results The Pa O2 in O + L PS group was lower than that in O group and L PS group (P <0.01), and the lung histopathological score in O + L PS group was higher than that of O group and L PS group (P <0.01) ). The incidence of SIRS, ALI and mortality in O + L PS group were 64.9%, 54.4% and 38.3%, respectively, which were higher than those in O group and LPS group (P <0.01). Conclusion This model better simulates the progression from secondary infection to ALI after lung injury and is a good animal model for studying the pathogenesis of senile ALI.