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目的：本实验探讨脓毒败血症肺损伤时肺血流动力学和花生四烯酸环氧酶代谢改变．方法：采用盲肠结扎穿孔（ＣＬＰ）模型．结果：小鼠在ＣＬＰ后３０ｈ累积死亡率为５５％；而家兔ＣＬＰ后Ｐａｏ２，Ｐａｃｏ２，ｐＨ都呈下降趋势；在ＣＬＰ后８～１１ｈ肺动脉压升高，肺血流量下降，肺血管阻力增加；在ＣＬＰ后１２ｈＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α均有显著升高，但３０ｈ后以６－ｋｅｔｏ－ＰＧＦ１α增高为主．ＣＬＰ后支气管肺泡灌洗液中白蛋白含量显著升高，提示肺通透性增加．结论：ＴＸＡ２和ＰＧＩ２的变化可能是引起其它改变的原因之一．
Objective: This study was to investigate the changes of pulmonary hemodynamics and arachidonic acid cyclooxygenase metabolism in the septic septic lung injury. Methods: Cecal ligation and puncture (CLP) model was used. Results: The cumulative mortality rate of mice after CLP was 55% at 30h after CLP. The Pao2, Paco2 and pH of rabbits decreased after CLP. Pulmonary arterial pressure increased, pulmonary blood flow decreased and pulmonary vascular resistance increased at 8 ~ 11h after CLP ; After 12h CLP, the levels of TXB2 and 6-keto-PGF1α were significantly increased, but the increase of 6-keto-PGF1α was the main one after 30h. After CLP, albumin in bronchoalveolar lavage fluid was significantly increased, suggesting increased pulmonary permeability. Conclusion: Changes in TXA2 and PGI2 may be responsible for other changes.