摘要
目的：进一步探索肺氧中毒的机理。方法：在大鼠常压高浓度氧（97％±2％）暴露的早期，观察肺血管紧张素转化酶（ACE）活性、脂质过氧化物（LPO）水平及肺泡毛细血管超微结构的变化。结果：随着肺ACE活性的下降和LPO水平的升高，部分肺泡内皮细胞（EC）出现胞浆水肿，同时肺泡毛细血管内白细胞、血小板明显增多。结论：肺泡EC胞膜功能的受损，尤其是胞膜结合的ACE活性下降所致对炎性介质清除的减少，可能起动了以肺泡EC胞膜通透性增高和炎细胞粘附为特征的早期肺氧中毒。
Aim: To further investigate the mechanism of pulmonary oxygen toxicity. Methods:The changes of pulmonary a ngiotensin- converting enzyme (ACE ) activity, lipid peroxide (LPO ) level and ultrastructure of alveolar capillary were observed in the early stage of normobaric hyper-oxygen (97%±2% ) exposure in rats. Results: Cytoplasm edema occurred in a part of endothelial cells (EC) with a decrease of ACE activity(P<0. 05) and an elevation of LPO level (P<0. 01 ). Meanwhile, the platelets and leukocytes increased greatly in the alveolar capillary lumen. Conclusion: The impairment of alveolar EC membrane function, especially the reduced elimination of inflammatory mediator due to the decreased membrane joined ACE activity, may have initiated the early pulmonary oxygen toxicity characterized by an increase in EC membrane permeability together with the adherence of platelets and leukocytes to the EC.
关键词
氧中毒
肺
内皮细胞
结构
功能
Lung Poisoning, oxygen Endothelial cell Angiotensin-converting enzyme
