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目的 :探讨过氧亚硝基阴离子 (ONOO-)对肺微血管内皮屏障功能的影响和在急性肺损伤发生中的意义。方法 :向SD大鼠气管内推注不同浓度的ONOO-、分解ONOO-或溶剂 2h后 ,检测肺微血管壁通透性变化和肺组织病理学变化 ,并检测ONOO-引起正常肺匀浆MDA含量变化。结果 :ONOO-推入气管后 ,肺系数、肺湿干重比以及肺含水量和伊文思兰含量明显增高呈现剂量效应关系 ;并可导致肺泡明显萎陷、肺泡壁毛细血管明显扩张充血及局灶性出血 ,内皮细胞肿胀、核深染及脱落。ONOO-造成正常肺匀浆MDA含量增加。结论 :外源性ONOO-气管推注后可导致明显的肺微血管内皮屏障功能障碍 ,提示肺内源性ONOO-生成增多时可能参与介导急性肺损伤的发生。
Objective: To investigate the effect of peroxynitrite (ONOO-) on the function of pulmonary microvascular endothelial barrier and its significance in the pathogenesis of acute lung injury. Methods: After the ONOO- was injected intratracheally into the trachea of SD rats, ONOO- or solvent was decomposed for 2h, the permeability of pulmonary microvascular wall and pathological changes of lung were detected, and the ONOO- Variety. RESULTS: After ONOO-T pushed into the trachea, the pulmonary coefficient, the wet-to-dry weight ratio of lung and the lung water content and the Evans blue content increased obviously. It could cause the obvious alveolar collapse, the obvious expansion and congestion of the alveolar wall capillaries Focal hemorrhage, endothelial cell swelling, nuclear stained and shedding. ONOO- caused normal lung homogenate MDA content increased. Conclusions: Exogenous ONOO-tracheal bolus can lead to significant dysfunction of pulmonary microvascular endothelial barrier, suggesting that the increase of endogenous ONOO- may be involved in the mediation of acute lung injury.