目的 观察并评估内毒素性急性肺损伤大鼠吸入一氧化氮后外周血中内皮祖细胞和炎症介质的变化情况。方法 90只SPF级健康大鼠分为3组,A组为正常对照组(n=30),B组为急性肺损伤组(ALI)(n=30), C组为一氧化氮(NO)组(n=30)。分别计算各组外周血内皮祖细胞(Endothelial progenitor cells,EPCs) 数量,同时监测肺组织中白细胞介素-10(Interleukin-10,IL-10)水平和髓过氧化物酶(Myeloperoxidase,MPO)活性。结果 我们成功建立了大鼠的ALI肺损伤模型, C组EPCs数量、MPO活性上升幅度均小于B组、而IL-10上升水平均高于B组,差异有统计学意义(P<0.05)。结论 大鼠吸入一氧化氮可减轻内毒素所致急性肺损伤程度,其机制可能与外周血中内皮祖细胞数量及MPO水平下降和IL-10水平上升有关。

Objective To investigate the effect of nitric oxide(NO) inhalation in endotoxin-induced acute lung injury mice. Methods Ninety SPF mice were randomly assigned to the normal group(group A), ALI group(group B)and ALI+NO group(group C). The number of endothelial progenitor cells was counted and the level of Interleukin-10(IL-10) and myeloperoxidase (MPO) were measured. Results Endotoxin administration resulted in pulmonary edema. The pulmonedema was lightened and the level of MPO were decreased by the inhalation of nitric oxide while the level of IL-10 increased. Conclusion NO inhalation can mitigate acute lung injure. The decline of EPCs and MPO and the increase of IL-10 may be one of the mechanism.