Schraufnagel D E, Schmid A
Department of Medicine, University of Illinois, Chicago 60680.
Am J Pathol. 1988 Jan;130(1):126-35.
The essential component of pulmonary emphysema is destruction of alveoli. Because capillaries make up much of the alveolar wall, it has been a long-held opinion that capillary loss in this disease parallels the loss of other elements of the alveolar septum. Yet the nature of the damage to capillaries and the occurrence of microvascular remodeling are unknown. Scanning electron microscopy of vascular casts of lungs from rats given intratracheal elastase were studied for identifying capillary changes in this type of experimental emphysema. The pressure-volume curves showed a clear distinction between the elastase and saline control animals, and light microscopy showed alveolar enlargement consistent with mild emphysema. The casts of capillaries in the elastase lungs appeared to have larger alveolar baskets, and capillaries ended abruptly near areas of focally destroyed lung. The elastase animals had more nonconnecting capillary segments on the pleural surface where the emphysema was worse and folds in the capillaries were more pronounced, suggesting weakened alveolar walls. The capillary density was decreased on the pleural surface, although this decrease could have resulted from hyperinflation. No difference in capillary diameters or branching frequency occurred. It appears that in this model of emphysema, decreased elastic recoil occurs before diffuse loss of capillaries.
肺气肿的基本组成部分是肺泡破坏。由于毛细血管构成了大部分肺泡壁，长期以来人们一直认为，这种疾病中毛细血管的丧失与肺泡间隔其他成分的丧失是平行的。然而，毛细血管损伤的本质以及微血管重塑的发生情况尚不清楚。对经气管内注射弹性蛋白酶的大鼠肺血管铸型进行扫描电子显微镜检查，以确定这种实验性肺气肿中的毛细血管变化。压力-容积曲线显示弹性蛋白酶处理组和生理盐水对照组动物之间有明显差异，光学显微镜显示肺泡扩大，符合轻度肺气肿表现。弹性蛋白酶处理组大鼠肺内的毛细血管铸型显示肺泡篮较大，毛细血管在肺局部破坏区域附近突然终止。在肺气肿较严重的胸膜表面，弹性蛋白酶处理组动物有更多不连续的毛细血管段，毛细血管的褶皱更明显，提示肺泡壁薄弱。胸膜表面的毛细血管密度降低，尽管这种降低可能是由于肺过度充气所致。毛细血管直径或分支频率没有差异。在这种肺气肿模型中，似乎弹性回缩力降低发生在毛细血管弥漫性丧失之前。
