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New Developments in the Pathogenesis of Smoke Inhalation-Induced Pulmonary Edema

机译:烟雾吸入引起的肺水肿发病机制的新进展

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摘要

Smoke inhalation causes most of the deaths in fire-related injuries, with pulmonary edema as a major determinant in the outcome of smoke-inhalation injury. The pathophysiology of pulmonary edema is thought to be related to the products of incomplete combustion. Damage to the integrity of the alveolar epithelium is one of the determinants of the development of smoke-induced pulmonary edema. In recent studies using lung clearance of aerosolized pentetic acid (DTPA [diethylenetriaminepentaacetic acid]) labeled with technetium Tc 99m to assess the permeability of the alveolar epithelium, several factors were identified that may increase a person's susceptibility to smoke-induced acute lung injury. These are increased initial alveolar permeability and alterations in the number and activity of alveolar macrophages. Clinical measurement of 99mTcDTPA clearance may provide a sensitive and convenient method for the early detection and serial assessment of smoke-induced alveolar epithelial permeability changes.
机译:烟雾吸入导致火灾相关伤害的大部分死亡,肺水肿是烟雾吸入伤害后果的主要决定因素。肺水肿的病理生理学被认为与不完全燃烧的产物有关。肺泡上皮完整性的损害是烟雾诱发的肺水肿发展的决定因素之一。在最近的研究中,使用标记为Tc 99m的气雾化戊酸(DTPA [二亚乙基三胺五乙酸])的肺清除率来评估肺泡上皮的通透性,发现了一些因素,这些因素可能会增加人们对烟雾诱发的急性肺损伤的敏感性。这些是增加的初始肺泡通透性以及肺泡巨噬细胞数量和活性的改变。 99m TcDTPA清除率的临床测量可能为烟雾诱导的肺泡上皮通透性变化的早期检测和系列评估提供一种灵敏而方便的方法。

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