烟雾吸入性急性肺损伤／急性呼吸窘迫综合征与细胞应激

Acute lung injury/acute respiratory distress syndrome after smoke inhalation and cell stress

烟雾吸入性急性肺损伤／急性呼吸窘迫综合征是火灾后患者的最主要死亡原因，其发病机制仍未完全清楚，近年来的研究发现其同细胞应激反应关系密切。其中热应激最早发生，产生各种热休克蛋白；氧化应激可诱导各种酶类及氧自由基的产生及释放；缺氧性应激可产生缺氧诱导因子。这些应激蛋白的产生可以提高细胞抗应激能力，维持细胞的稳态以利细胞在应激条件下生存，但若应激过强过久则诱导损伤细胞的凋亡来保护机体。本文就近年来烟雾吸入性急性肺损伤／急性呼吸窘迫综合征的研究与细胞应激的相关联系作一阐述。

Acute lung injury/acute respiratory distress syndrome after smoke inhalation is the major cause of death in the fire victims. The mechanisms are still not so clear. Recent studies show that this severe lung injury syndrome is related to cell stress. When smoke is inhaled, stresses such as heat shock begin earlier and make different kinds of heat shock proteins, oxidative stress induces the expression of various enzymes and reactive oxygen species, while hypoxia stress induces hypoxiinducible factors. The biological significance of such stress proteins is the increased resistance against further perturbations of cell homeostasis, and thus, enhanced survival. However, when stress is persistent or cellular functions are severely impaired, apoptotic pathways are activated to protect the organism by eliminating the damaged cells.