摘要
急性肺损伤(ALI)和急性呼吸窘迫综合症(ARDS)是机体受到感染、误吸、创伤和脓毒症等打击以后肺组织产生的广泛而过度的炎症反应,病理学特点是肺组织出现大量的炎性细胞浸润和肺血管通透性增加。其发病机制复杂,病死率高,是近年来研究的热点。虽然新的保护性通气策略和新的药物的应用对ALI/ARDS的生存率有所改善,但还要继续努力用多种方法(生物、基因和基因组学等)阐释ALI/ARDS的发生机制。这一章我们从ALI/ARDS分子机制、基因组学易感性、动物模型和机械通气相关性肺炎的发生机制等方面的进展作一总结。
Acute lung injury(ALI) and acute respiratory distress syndrome(ARDS) are inflammatory disorders of the lung that are caused by pneumonia,aspiration,trauma and sepsis.Both ALI and ARDS result from widespread lung inflammation and increased pulmonary vascular permeability.Their pathogenesis is complicated and the mortality is high.With the implementation of new protective ventilatory strategies and drug therapies in recent years,some investigators have reported an improvement in survival rates.Even with these recent successes,there is still a tremendous need for continued research efforts utilizing multiple(biological,genomic and genetic) approaches to provide clarity to the underlying pathophysiological mechanisms of ALI/ARDS.In this manuscript,we provide a brief overview of the molecule mechanisms,genetic mechanisms of susceptibility,animal model and ventilation associated pneumonia that are all involved in the development of ALI.
出处
《中国继续医学教育》
2011年第10期63-77,157,共15页
China Continuing Medical Education
关键词
急性肺损伤
急性呼吸窘迫综合症
机制研究
Acute lung injury
acute respiration distress syndrome
mechanism research