Jackson R M
Division of Pulmonary and Critical Care Medicine, University of Alabama, Birmingham.
Clin Chest Med. 1990 Mar;11(1):73-86.
The pathogenesis of O2 toxicity involves intracellular production of partially reduced O2 metabolites, which increases with O2 partial pressure. Cytotoxic O2 metabolites impair enzyme function and inhibit DNA, protein, and surfactant lipid biosynthesis. Compounds used clinically that increase O2 metabolism or that are metabolized through free radical intermediates may increase pulmonary O2 toxicity. Recent development of liposome-encapsulated and polyethylene glycol-conjugated antioxidant enzyme preparations may provide a clinically useful means of minimizing O2 toxicity and other oxidant injuries. Human pulmonary O2 toxicity is characterized initially by acute edematous lung injury followed by fibrosis and pulmonary hypertension. Functional changes due to O2 toxicity include diffusion impairment, worsening of ventilation/perfusion relationships, decreased lung compliance, and small airways dysfunction. It is likely that new data derived from molecular and cellular studies of O2 toxicity will continue to enrich the clinical atmosphere and allow more directed approaches to therapy of acute lung injuries, including ARDS.
氧中毒的发病机制涉及细胞内产生部分还原的氧代谢产物，其会随着氧分压的升高而增加。具有细胞毒性的氧代谢产物会损害酶的功能，并抑制DNA、蛋白质和表面活性物质脂质的生物合成。临床上使用的可增加氧代谢或通过自由基中间体代谢的化合物可能会增加肺部氧中毒。脂质体包裹和聚乙二醇结合的抗氧化酶制剂的最新进展可能会提供一种临床上有用的方法，以尽量减少氧中毒和其他氧化损伤。人类肺部氧中毒最初的特征是急性肺水肿性肺损伤，随后出现纤维化和肺动脉高压。氧中毒引起的功能变化包括弥散障碍、通气/灌注关系恶化、肺顺应性降低和小气道功能障碍。很可能来自氧中毒分子和细胞研究的新数据将继续丰富临床知识，并为包括急性呼吸窘迫综合征（ARDS）在内的急性肺损伤的治疗提供更具针对性的方法。
