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肺脂质与疾病

Lung lipids and disease.

作者信息

Higenbottam T

机构信息

Department of Respiratory Physiology, Papworth Hospital, UK.

出版信息

Respiration. 1989;55 Suppl 1:14-27. doi: 10.1159/000195747.

Abstract

Pulmonary surfactant is a complex mixture of proteins and phospholipids which possesses unique physical properties. It is no longer viewed just as a system for lowering surface tension but may play a protective role particularly with reference to inhalation of noxious substances. Derangement of the surfactant system may proceed to the development of disease by opening the way to toxic injury of the delicate epithelial lining of the lungs. Currently, it is believed that surfactant, which is synthetised, stored and secreted by type II alveolar pneumocytes, spreads rapidly on release to form a monomolecular layer covering the squamous surface lining of the alveoli. Furthermore, physiological and histological studies show that this monolayer extends into the bronchioli and possibly bronchi also. Effectively, the inspired air encounters an extensive and continuous 'oily' surface. It has been known for some time that cigarette smokers appear to sequester pulmonary surfactant into alveolar macrophages, leaving less free surfactant on the alveolar and bronchiolar surfaces. This process may be initiated by physical inactivation of surfactant by tobacco smoke. The tar of tobacco smoke alters the surface properties of surfactant as well as the compliance of the lung in vitro. This process may not only lead to the associated increase in the number of alveolar macrophages found in smokers, but could, by lessening the effective protective role of surfactant, lead to direct toxic injury of the lung and the development of chronic obstructive lung disease.

摘要

肺表面活性物质是蛋白质和磷脂的复杂混合物,具有独特的物理特性。它不再仅仅被视为降低表面张力的系统,而是可能发挥保护作用,特别是在吸入有害物质方面。表面活性物质系统的紊乱可能通过为肺的脆弱上皮内衬的毒性损伤开辟道路而导致疾病的发展。目前,人们认为由II型肺泡上皮细胞合成、储存和分泌的表面活性物质在释放后迅速扩散,形成覆盖肺泡鳞状表面内衬的单分子层。此外,生理学和组织学研究表明,这个单分子层还延伸到细支气管,甚至可能延伸到支气管。实际上,吸入的空气会遇到一个广泛而连续的“油性”表面。一段时间以来,人们已经知道吸烟者似乎会将肺表面活性物质隔离到肺泡巨噬细胞中,从而使肺泡和细支气管表面的游离表面活性物质减少。这个过程可能是由烟草烟雾对表面活性物质的物理失活引发的。烟草烟雾中的焦油在体外会改变表面活性物质的表面特性以及肺的顺应性。这个过程不仅可能导致吸烟者肺泡巨噬细胞数量的相应增加,而且可能通过削弱表面活性物质的有效保护作用,导致肺的直接毒性损伤和慢性阻塞性肺疾病的发展。

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