Thorning D R, Howard M L, Hudson L D, Schumacher R L
Hum Pathol. 1982 Apr;13(4):355-64. doi: 10.1016/s0046-8177(82)80225-6.
Inhalation of smoke can adversely affect pulmonary function; however, the lack of detailed knowledge of exposure conditions and the overall complexity of ensuing clinical problems generally preclude an understanding of the specific role played by smoke in human victims. Using controlled exposures of rabbits to white pine wood smoke, an animal model of smoke inhalation has been created. Light and electron microscopic examinations of injured respiratory tissues from these animals have revealed a reproducible, necrotizing tracheobronchial epithelial cell injury. By six hours after injury, the epithelium remains largely intact but is infiltrated by inflammatory cells; by 24 hours its ciliated and secretory lining cells are largely destroyed, the inflammatory reaction is maximal, but basal epithelial cells retain their normal structural appearances; by 72 hours, its surfaces are largely covered by a nonciliated, stratified reparative epithelium, apparently derived from proliferating and migrating basal cells. The acute injury and early reactions to injury resemble lesions observed in the lungs of human smoke-injured victims, and suggest several physiologic consequences that would provide likely explanations for some of the disabilities observed in these victims.
吸入烟雾会对肺功能产生不利影响;然而,由于缺乏对暴露条件的详细了解以及后续临床问题的总体复杂性,通常难以理解烟雾在人类受害者中所起的具体作用。通过对兔子进行白松木烟雾的控制性暴露,建立了烟雾吸入动物模型。对这些动物受损呼吸组织的光镜和电镜检查显示,气管支气管上皮细胞出现了可重复性的坏死性损伤。损伤后6小时,上皮大体保持完整,但有炎症细胞浸润;24小时时,其纤毛和分泌性衬里细胞大部分被破坏,炎症反应达到高峰,但基底上皮细胞保持正常结构外观;72小时时,其表面大部分被非纤毛的复层修复上皮覆盖,显然源自增殖和迁移的基底细胞。急性损伤和对损伤的早期反应类似于在人类烟雾损伤受害者肺部观察到的病变,并提示了几种生理后果,这可能为在这些受害者中观察到的一些残疾提供解释。