Smoke inhalation with a concurrent systemic stress results in lung alveolar injury.
Smoke inhalation with a concurrent systemic stress results in lung alveolar injury.
复制标题
吸入烟雾并发全身应激会导致肺泡损伤。
DOI：
10.1164/ajrccm.149.1.8111586
复制
发表时间：
1994
影响因子：
24.7
通讯作者：
Fisher,AB
中科院分区：
文献类型：
--
作者：
Thom,SR;Mendiguren,I;VanWinkle,T;Fisher,D;Fisher,AB
烟雾吸入导致肺气道损伤，有时肺泡炎症也会在大约24小时内发生。肺实质损伤的病理生理学尚不清楚，通常是致命的。我们假设远离吸烟相关肺损伤的炎症应激是肺泡损伤发展所必需的。自发呼吸的大鼠仅头部暴露于花旗松木材（DF）、聚氯乙烯（PVC）或DF+PVC组合的无燃烧热解（阴燃）产生的烟雾中。吸入烟雾前4 h腹腔注射无菌牡蛎壳糖原作为额外的炎症刺激。组织学检查显示所有烟雾暴露组均有广泛的气道炎症。单独的糖原腹膜炎不会引起肺损伤，在没有糖原的情况下，吸入烟雾既不会引起肺实质损伤（通过[125I]牛血清白蛋白（BSA）渗漏来评估），也不会引起中性粒细胞浸润（通过髓过氧化物酶（MPO）活性来量化）。然而，在糖原预处理的大鼠中，并在暴露于DF+PVC燃烧产生的烟雾24小时后进行研究，[125I]BSA通透性增加了232 +/- 41% (SE; n = 13)， MPO活性增加了5倍，从2.6 +/- 0.4 （n = 7）增加到13.9 +/- 1.4 (n = 19) A460/min/g肺，组织病理学结果包括广泛的肺部炎症。我们的结论是，当远离肺部的炎症过程存在时，吸入某些类型的烟雾会引发肺损伤。
Smoke inhalation causes injuries to lung airways, and, at times, alveolar inflammation also develops over approximately 24 h. The pathophysiology of parenchymal lung injuries is unknown, and it is often fatal. We hypothesized that an inflammatory stress remote from the smoke-related lung insult was required for development of alveolar injuries. Spontaneously breathing rats were exposed, head only, to smoke generated by nonflaming pyrolysis (smoldering) of Douglas fir wood (DF), polyvinylchloride (PVC), or the combination of DF+PVC. Intraperitoneal injection of sterile oyster shell glycogen 4 h before smoke inhalation was used as an extra inflammatory stimulus. Histologic examinations revealed extensive airway inflammation in all smoke-exposed groups. Glycogen peritonitis alone caused no lung injuries, and in the absence of glycogen, smoke inhalation caused neither parenchymal lung injuries, assessed by [125I]bovine serum albumin (BSA) leakage, nor neutrophil infiltration, quantified by myeloperoxidase (MPO) activity. However, in rats pretreated with glycogen and studied 24 h after exposure to smoke from burning DF+PVC, [125I]BSA permeability was increased by 232 +/- 41% (SE; n = 13), MPO activity was increased 5-fold, from 2.6 +/- 0.4 (n = 7) to 13.9 +/- 1.4 (n = 19) A460/min/g lung, and histopathologic findings included extensive pulmonary inflammation. We conclude that inhalation of certain types of smoke will trigger pulmonary injury when an inflammatory process remote from the lungs is present.