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目的研究腹腔注射内毒素(LPS)和(或)静脉注射油酸(OA)的方法致大鼠急性肺损伤(ALI)模型的不同特点及其可能机制。方法将24只雄性Wistar大鼠随机分为4组,每组6只。对照组(C组):腹腔注射生理盐水10ml/kg;内毒素组(LPS组):腹腔注射1%LPS10mg/kg;油酸组(OA组):静脉注射OA0.15ml/kg;内毒素+油酸组(LPS+OA组):腹腔注射1%LPS10mg/kg,30min后静脉注射OA0.15ml/kg。观察120min内各组大鼠平均动脉压和心率变化率的改变。120min后处死动物采集标本。分别检测肺组织核转录因子κB(NF-κB)P65、血清IL-6、肺组织髓过氧化物酶(MPO)含量、动脉血气指标和肺组织湿-干重比(W/D),HE染色观察肺组织病理学改变。结果与C组比较,LPS组肺组织NF-κBp65水平、MPO含量及血清IL-6含量显著增加,肺组织W/D比值及血气分析结果无显著性差异,病理组织学改变轻微;OA组肺组织NF-κBp65水平和MPO含量及血清IL-6含量无显著改变,肺组织W/D比值升高,pH值和PaO2降低,PaCO2升高,肺脏出现严重的肺泡上皮细胞损伤和肺泡结构破坏。LPS+OA组肺组织NF-κBp65水平、MPO含量和W/D比值及血清IL-6含量显著增加,pH值和PaO2降低,PaCO2升高,肺泡破坏严重,大量组织液渗出。结论内毒素复合油酸可以产生协同作用,产生大量致炎细胞因子,并造成大鼠严重的肺脏病理生理改变,临床ALI/ARDS发病过程更为接近,是一种研究ALI发病机制及早期干预的较理想的动物模型。
Objective To investigate the different characteristics of acute lung injury (ALI) induced by intraperitoneal injection of lipopolysaccharide (LPS) and / or oleic acid (OA) and its possible mechanism. Methods Twenty-four male Wistar rats were randomly divided into 4 groups with 6 rats in each group. The rats in the control group (group C) received intraperitoneal injection of normal saline (10ml / kg), LPS group (intraperitoneal injection of 1% LPS 10mg / kg), oleic acid group (OA) Oleic acid group (LPS + OA group): intraperitoneal injection of 1% LPS10mg / kg, 30min after intravenous injection of OA0.15ml / kg. The changes of mean arterial pressure and heart rate in each group were observed within 120 minutes. 120min after the animals were sacrificed to collect specimens. The levels of NF-κB P65, IL-6, MPO, W / D, W / D, Staining to observe the histopathological changes in lung tissue. Results Compared with group C, the levels of NF-κBp65, MPO and the level of serum IL-6 in LPS group were significantly increased. There was no significant difference in W / D ratio and blood gas analysis between the two groups. There was no significant change in NF-κBp65 level, MPO level, serum IL-6 level, W / D ratio in lung tissue, decrease of pH and PaO2, increase of PaCO2, severe pulmonary alveolar epithelial cell injury and alveolar structure destruction. The levels of NF-κBp65, MPO, W / D and serum IL-6 in LPS + OA group were significantly increased, pH and PaO2 were decreased, PaCO2 was increased, and alveolar destruction was serious. Conclusions Endotoxin compound oleic acid can produce a synergistic effect, produce a large number of proinflammatory cytokines and cause severe pulmonary pathophysiological changes in rats, the clinical ALI / ARDS pathogenesis is more similar, is a study of ALI pathogenesis and early intervention The ideal animal model.