Pulmonary impairment in the offspring of smoking mothers is well documented by epidemiologic studies. The morphologic bases for the functional impairment are largely unexplored. We studied 17 infant lungs obtained at autopsy, ten from smoking (group 1) and seven from nonsmoking (group 2) mothers, by light (LM), transmission (TEM), and scanning electron microscopy (SEM). By LM, the alveolar mean linear intercept was similar in both groups; the total lung volume and alveolar surface area increased with the increase in gestational age in all lungs studied. By SEM, the sizes of the neuroepithelial bodies (NEB) were larger in group 1 than in group 2. By SEM and TEM, ciliated cells were increased, but the amount of dense core granules was decreased, in the NEB of the smoking group. Maternal smoking during pregnancy appears to alter the size and cellular composition of fetal NEB. The detailed mechanisms of the alteration in NEB and their implications are unclear from this study and needed further clarification.
Interstitial proliferation of striated muscle cells in the lung is rare. A few cases in the literature only document infants with associated lung and other major organ anomalies incompatible with long-term survival. In this report we document a case of diffuse patchy interstitial proliferation of striated muscle cells in the left lung and confirm their nature by immunohistochemistry and electron microscopy. In particular, we show that these skeletal muscle cells express alpha-sarcomeric actin, but not alpha-smooth muscle actin, indicating an antigenetically well-developed striated muscle phenotype despite morphologically embryonal features.
Nicotine, 1 mg/kg body weight/day, was injected subcutaneously in 3 female rabbits during gestational and lactating periods, and the lungs of the offspring were studied by scanning and transmission electron microscopy (SEM and TEM) on days 5, 10, and 25 postpartum. Three other female rabbits served as controls. The size and number of neuroepithelial bodies (NEB) as estimated by SEM were larger in the experimental group than in the control group, especially on days 5 and 25. Moreover, the NEB in the nicotine-exposed groups showed loss of normal boundaries and derangement of cells and granules by TEM. Neural components also became prominent. These findings suggest that chronic maternal exposure to nicotine may directly, or, through the neural route, indirectly induce hyperplasia and dysplasia of the NEB in the offspring of rabbits. Because NEB are suspected to regulate regional bronchial and vascular smooth muscle cells, such alterations may be similar to respiratory functional impairments found in infants of mothers who smoke.
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