主动脉夹层(AD)体外循环(CPB)术后低氧血症(PHO)是临床重要并发症，死亡率高且尚未得到有效解决，症结在于现有措施不能既增加机体氧供、又促进肺损伤修复。臭氧因有效改善氧合而应用于缺血性疾病的治疗，但机制不清；CPB围术期应用臭氧防治PHO更未见报道。前期，我们证实臭氧通过抑制NLRP3、增强Nrf2抗氧化，减轻鼠肺缺血-再灌注损伤；体外实验证实了Ozone人体应用的安全性和有效性；预实验观察到AD患者实施CPB后血清HIF-2α、Nrf2减少且臭氧上调其表达。鉴此，我们推测臭氧除增加氧供外，还可激活Nrf2/HO-1/HIF-2α信号通路维护肺泡-毛细血管上皮屏障而减轻肺损伤。为证实该假说，本研究将通过细胞-动物-人体三维度，应用分子生物学、电镜等技术和干预手段，阐明臭氧改善CPB术后肺损伤的分子机制，为PHO临床防治提供新思路和新方法。

Aortic dissection (AD) related postoperative hypoxemia (PHO) is an important complication after cardiopulmonary bypass (CPB), with high mortality and the problem hasn’t been resolved yet due to lack of effective measures which neither increase the oxygen supply nor promote the repair of lung injury. Ozone (O3) has been used in the treatment of some ischemic diseases because it can provide improve oxygenation. However, the mechanisms are seldom discussed. There are no reports on the application of Ozone to prevent PHO during the perioperative period of CPB. Previously, we confirmed that Ozone was proved to reduce lung ischemia-reperfusion injury in rats by inhibiting NLRP3 and enhancing the antioxidant capacity of Nrf2. In vitro experiments confirmed the safety and effectiveness of Ozone in human application. In the preliminary experiment, it was also found that HIF-2α and Nrf2 decreased after CPB operation and Ozone could up-regulate their expression. Therefore, it is speculated that Ozone, in addition to increasing oxygen supply, can also activate Nrf2/HO-1/HIF-2αsignaling pathway to maintain alveolar-capillary epithelial barrier and reduce lung injury. This study will verify or falsify this hypothesis by applying molecular biology, electron microscopy and other techniques and various interventions in three dimensions of cells-animal-human body, so as to clarify the molecular mechanism of Ozone to improve lung injury from a new perspective and provide new ideas and methods for clinical treatment of PHO.