71 Artifacts and histologic pitfalls in the lung Ex vivo smooth muscle contraction The collapse of peripheral lung tissue due to surgical atelectasis has additional morphologic consequences. While the bronchial lumens are essentially unaffected secondary to the presence of cartilaginous rings and plates, bronchiolar luminal patency is greatly affected. In vivo the bronchioles remain under physiologic conditions, expanded by the negative pressure between the parietal and visceral pleura. This ‘‘outward’’ force is transferred by the elastin meshwork between the visceral pleura, alveolar walls, and airways and results in circumferential traction to keep the bronchiolar lumens open. In vivo the actual bronchiolar diameter is a balance between the ‘‘outward’’ tension provided by the elastic fibers and ‘‘inward’’ contraction tension of the smooth muscle cells. At the end of expiration, a slightly lower lumen diameter is noted as compared to the end of inspiration. In the ex vivo situation the outward tension of elastin fibers is abolished, resulting in unopposed smooth muscle forces. Examples of ex vivo smooth muscle contraction are well appreciated in other organs such as uterus (Figure 3, A) and intestinal wall, where the muscle layers of the resected organs contract or shorten as compared to overlying mucosa (not shown). Smooth muscle contraction in the lung leads to a reduction in bronchiolar luminal diameter, with secondary infolding of the mucosa, including the basement membrane and elastin fibers (Figure 3, B and C). The outer diameter of the epithelium, that is, the circumference at the side of the basement membrane, should theoretically be unchanged. It is not clear whether the surface area of underlying connective tissue is unchanged. However, in the presence of a preexisting luminal mucous plug or fibromyxoid connective tissue polyp, the airway lumen is unchanged or only minimally narrowed (Figure 3, D and E). Thus, the bronchiolar epithelium will demonstrate only partial invaginations around the intraluminal material. The smooth muscle contraction was reversible by perfusion fixation (Figure 3, F). The ex vivo bronchiolar smooth muscle contraction causes prominent narrowing of the bronchiolar lumen, which may give a false impression of constrictive bronchiolitis or other small airway diseases, including asthma94–97. This should not be called asthma because of a lack of goblet cell hyperplasia, eosinophilic granulocytes, and thickened basement membrane. In constrictive or obliterative bronchiolitis the airway has luminal narrowing due to subepithelial scarring (ie, between epithelium and smooth muscle cells, which are absent in the ex vivo contraction artifact)97–101. The smooth muscle cells in pulmonary blood vessels will also shrink. However, the architecture in the tunica media is different, as it is able to cope in the pulmonary artery with pressure changes between 4- and 30-mm Hg. Ex vivo during the collapse the pulmonary blood vessels will shrink in the longitudinal direction. In the cross-sectional direction the pulmonary artery will shrink ex vivo owing to the difference in structure, looking more like a rubber band without tension: there will be evidence of a (flexible) remaining lumen. This shrinking may be diminished by intimal fibrosis (Figure 3, G). 5
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