摘要
在潜艇舱室复杂的气体环境下,有害气体可能刺激气管上皮细胞并损伤肺血管内皮细胞,引起肺组织慢性炎症反应以及氧化与抗氧化功能失衡。肺组织内氧自由基增多与炎症反应相互作用,引起血液和肺组织中超氧化物歧化酶(superoxide dismutase,SOD)、血管内皮素-1(endothelin-1,ET-1)和一氧化氮含量变化,并产生大量炎性细胞以及肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白介素-6(interleukin-6,IL-6)等炎性介质浸润肺组织。这些炎症反应可以导致气管壁的损伤修复过程反复发生,引起气管结构重塑,还可以损伤肺血管,使肺血管平滑肌增生,肺血管阻力增加,形成肺动脉高压,同时,长期炎症反应还可导致肺实质的纤维化,进一步影响肺功能。
Submarine cabin contains very complicated air environment. Harmful gases in this environment may induce chronic inflammatory reaction and oxidant-antioxidant imbalance in the pulmonary tissues by stimulating bronchus epithelial ceils and damaging pulmonary vascular endothelial cells. Increasing oxygen free radicals and inflammatory reactions may lead to changes in the levels of superoxide dismutase, endothelin-1, and nitric oxide in blood and lung tissues, and attract a large number of inflammatory cells and inflammatory mediators such as tumor necrosis factor-or and interleukin-6 which would infiltrate into lung tissues. These inflammatory reactions may lead to airway remodeling, pulmonary vascular smooth muscle proliferation, pulmonary vascular resistance increment, and pulmonary hypertension. At the same time, long-term inflammation can also cause pulmonary fibrosis, deteriorating lung function.
出处
《环境与职业医学》
CAS
北大核心
2013年第11期886-888,共3页
Journal of Environmental and Occupational Medicine
基金
军队中医药科研专项课题(编号:10ZYZ219)
关键词
肺
肿瘤坏死因子
血管内皮素
超氧化物歧化酶
炎症
pulmonary
tumor necrosis factor
endothelin
superoxide dismutase
inflammation