Cox Robert A, Burke Ann S, Soejima Kazutaka, Murakami Kazunori, Katahira Jiro, Traber Lillian D, Herndon David N, Schmalstieg Frank C, Traber Daniel L, Hawkins Hal K
Shriners Hospital for Children, Department of Anesthesiology, University of Texas Medical Branch, Galveston, TX 77550, USA.
Am J Respir Cell Mol Biol. 2003 Sep;29(3 Pt 1):295-302. doi: 10.1165/rcmb.4860.
The goals of this study were (i) to compare the degree and (ii) temporal changes in airway obstruction in sheep with pulmonary injury induced by smoke inhalation and/or burn; (iii) to qualitatively assess the cellular and mucous content of obstructive material; and (iv) to statistically assess a possible relationship between the degree of airway obstruction and pulmonary dysfunction. Using masked histologic slides, we estimated the degree of luminal obstruction in all cross-sectioned airways. The mean degree of bronchial, bronchiolar, and terminal bronchiolar obstruction was significantly greater in animals with smoke injury alone or combined smoke inhalation and burn (S+B) injury, compared with animals with burn injury alone or uninjured animals (P < 0.05). In S+B animals, the degree of bronchial obstruction was maximal at 24 h, with a progressive decrease over 72 h. In contrast, the degree of bronchiolar obstruction increased over time. Qualitatively, bronchial casts were largely composed of mucus at early times after injury, whereas neutrophils were the principal component of bronchiolar obstructive material. Localization of specific mucin subtypes in S+B tissues suggests that increasing bronchiolar obstruction is derived, in part, from upper airway material. Multiple linear regression analysis of airway obstruction scores compared with PaO2/FIO2 values showed a correlation coefficient of r = 0.76, with bronchial and bronchiolar scores predictive of PaO2/FIO2, (P < 0.05). These results suggest that strategies to remove or decrease formation of upper airway obstructive material may reduce its deposition into small airways and parenchyma and may improve respiratory function in victims of smoke inhalation injury.
（i）比较烟雾吸入和/或烧伤诱导的肺损伤绵羊气道阻塞的程度；（ii）比较其随时间的变化；（iii）定性评估阻塞性物质的细胞和黏液成分；（iv）统计评估气道阻塞程度与肺功能障碍之间的可能关系。我们使用盲法组织学切片，估计所有横切气道的管腔阻塞程度。与单纯烧伤动物或未受伤动物相比，单纯烟雾损伤或合并烟雾吸入和烧伤（S+B）损伤的动物，支气管、细支气管和终末细支气管阻塞的平均程度显著更高（P<0.05）。在S+B组动物中，支气管阻塞程度在24小时时最大，在72小时内逐渐降低。相比之下，细支气管阻塞程度随时间增加。定性分析显示，损伤后早期支气管铸型主要由黏液组成，而中性粒细胞是细支气管阻塞性物质的主要成分。S+B组织中特定黏蛋白亚型的定位表明，细支气管阻塞的加重部分源于上呼吸道物质。气道阻塞评分与PaO2/FIO2值的多元线性回归分析显示，相关系数r = 0.76，支气管和细支气管评分可预测PaO2/FIO2（P<0.05）。这些结果表明，清除或减少上呼吸道阻塞性物质形成的策略可能会减少其在小气道和实质中的沉积，并可能改善烟雾吸入性损伤患者的呼吸功能。
