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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。
In a complex gaseous environment in a submarine compartment, the noxious gases may stimulate the tracheal epithelial cells and damage the pulmonary vascular endothelial cells, causing chronic inflammation of the lung tissue and an imbalance of oxidation and anti-oxidant functions. The increase of oxygen free radicals in the lung tissue interacted with the inflammatory response, causing the changes of superoxide dismutase (SOD), endothelin-1 (ET-1) and nitric oxide in blood and lung tissue , And produced a large number of inflammatory cells and tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and other inflammatory mediators infiltrated lung tissue. These inflammatory reactions can lead to repeated tracheal wall injury repair process, causing tracheal remodeling, but also can damage the pulmonary blood vessels, pulmonary vascular smooth muscle hyperplasia, increased pulmonary vascular resistance, the formation of pulmonary hypertension, while chronic inflammation can also lead to lung Substantial fibrosis further affects lung function.