油酸-内毒素序贯致伤引起大鼠急性肺损伤的特点

Characteristics of the acute lung injury induced by oleic acid and lipopolysaccharide in rats

目的 通过复制油酸 内毒素 (OA LPS)介导的大鼠急性肺损伤 (ALI)模型并观察大鼠血浆IL 13含量等变化 ,探讨序贯致伤所引起的急性肺损伤特点。方法 采用OA LPS序贯致伤Wistar大鼠 ,观察伤后大鼠PaO2 、肺含水量、血浆IL 13含量及病理学的变化。结果 OA LPS组大鼠呼吸窘迫 ,PaO2 早期低于 8kPa ,死亡率升高 ,肺含水量显著增加 ,肺水肿、炎细胞浸润等病变严重 ,伴透明膜形成 ,血浆IL 13含量显著升高 ;尤其在间隔 4h两次致伤以后 ,上述各指标变化最大。结论 OA LPS序贯致伤大鼠 ,可以介导严重的ALI/ARDS ,即在第一次致伤后 ,给予第二次低剂量致伤 ,可以引发ARDS ,与机体抗炎细胞因子水平异常升高可能有关 ;并且 ,在两次致伤之间还存在一个“相对敏感期”。

Objective To investigate the characteristics of the acute lung injury induced by oleic acid (OA) and lipopolysaccharide (LPS) in rats. Methods Wistar rats were injured with OA (0.2 mL/kg) and LPS (2 mg/kg) to establish the acute lung injury (ALI) model. The indexes of respiratory rate, PaO 2, wet weight/dry weight (W/D) of lung lobes, plasma IL 13, and pathological changes were observed. Results Acute respiratory distress syndrome (ARDS) was found in rats treated with OA LPS. The level of PaO 2 was lower than 8 kPa at the early stage. Increased death rate, significantly increased water content in the lungs, more serious pulmonary edema and infiltration of inflammatory cells accompanied by formation of hyaline membrane, and significantly increased plasma IL 13 content were also found. There were significant changes of the above indices, especially in OA LPS/4 h group. Conclusion OA LPS might cause serious ALI/ARDS. Injury due to second time low dose OA LPS after the first time injury may induce ARDS, which may be associated with the abnormally increased level of anti inflammatory cytokines. There is a relative sensitivity between the two injuries.