心源性肺水肿发病机制的研究进展  

Advance in pathogenesis of cardiogenic pulmonary edema

作　　者：欧典强(综述) 邓华钊(审校) OU Dian-qiang;DENG Hua-zhao(Guangdong Medical University,Zhanjiang 524000,Guangdong,CHINA)

机构地区：[1]广东医科大学,广东湛江524000

出　　处：《海南医学》2021年第5期647-650,共4页Hainan Medical Journal

摘　　要：过去,人们使用Starling方程进行解释心源性肺水肿形成,但这种传统机制现已受到越来越多研究的挑战。心源性肺水肿的始动因素是静水压的升高,但后续发展过程中还有血气屏障的受损、表面活性物质功能障碍、一氧化氮的增加以及炎症反应等事件的参与。这些事件可能会导致肺通透性的改变,肺泡表面张力的增加,从而导致心源性肺水肿的形成。升高的静水压也会抑制钠水转运系统以减少肺泡液的清除,同时促使肺泡液从吸收相向分泌相的转化。因此,对心源性肺水肿的治疗不应只局限于静水压管控,更应从发病机制入手考虑更多相关的事件。此综述将对这些事件展开讨论,以期为心源性肺水肿的治疗提供新的思路。In the past,the Starling equation is used to explain the formation of cardiogenic pulmonary edema,which has been challenged by increasing research.Cardiogenic pulmonary edema is initiated by increased hydrostatic pressure,but is followed by impaired blood gas barrier,dysfunction of surfactant,increased nitric oxide,and inflammatory reactions.These events may result in changes in lung permeability and increased alveolar surface tension,leading to the formation of cardiogenic pulmonary edema.The increased hydrostatic pressure also inhibits the sodium water transport system to reduce the clearance of alveolar fluid,and promotes the conversion of alveolar fluid from the absorption phase to the secretion phase.Therefore,the treatment of cardiogenic pulmonary edema should not only be limited to hydrostatic control,but also should consider more related events in terms of the pathogenesis.These events will be discussed in this review with a view to providing new ideas for the treatment of cardiogenic pulmonary edema.

关 键 词：心源性肺水肿 血气屏障损伤 一氧化氮 肺表面活性物质 肺水清除功能 

分 类 号：R563[医药卫生—呼吸系统]