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Pulmonary surfactant is essential for maintaining lung function. In the present study we attempted to gain insight into the mechanisms underlying changes in surfactant in old age. We examined the ultrastructure of surfactant-producing lamellar bodies of the alveolar epithelial cells and of extracellular tubular myelin unfolding from the lamellar bodies in the lungs of two contrasting age-groups of rats: young, 2-3 months old and senescent, 26 months old. The study also focused on the plausible role of surfactant protein insufficiency in the process of surfactant aging. To this end, puromycin, a protein synthesis inhibitor, was used in vivo in young rats (12 mg/100 g body weight, i.p.) and its effects on surfactant ultrastructure were compared with the surfactant status in senescent rats. Lungs were rapidly dissected after being perfused with a mixture of aldehyde fixative and the tissue was subjected to the routine transmission electron microscopic procedures. Electronograms of the senescent lungs show that the alveolar epithelial lining layer and the lamellar bodies of type II cells, producing surfactant, displayed profound degenerative alterations. No regularly shaped myelin-tubular mesh, so characteristic of young lungs, could be recognized in the old ones. The aqueous, protein-containing hypophase of the alveolar epithelial lining, consisting of myelin tubules, no longer formed a solid layer integrated with the plasma membrane of type II cells. The effects of puromycin-induced inhibition of protein synthesis on the alveolar lining layers in the young lungs were reminiscent of the picture seen in the untreated aged lungs. The similarity of surfactant changes after puromycin to those present in senescent lungs is suggestive of the possible role of decaying surfactant proteins in the natural process of surfactant aging. We conclude that protein deficiency possibly developing in old age may underlie surfactant degradation which may impact lung function in old age.

Surgical brain injury causes neovascularization in the disrupted brain parenchyma, which occurs with the participation of endothelial-like cells. Differentiation of angioblasts from embryonic mesothelial cells has been proposed on the ground of biochemical and antigenic similarities between mesothelial and endothelial cells. Therefore, a transient localization of cytokeratin, the main mesothelial intermediate filament protein, to some embryonic vessels and endothelial progenitors, prompted us to use it to identify the source of cells participating in vessel formation after surgical brain injury. To determine the immunophenotypes of immature endothelial cells involved in new vessel formation following surgical rat brain injury, we used immunohistochemical and electron microscopic immunocytochemical techniques. Subcellular localization of protein markers: Flk-1, cytokeratin, and vimentin was examined in the cells investigated. Our results confirmed the existence of a diversity of immunophenotypes of immature endothelial cells in case of surgical-related brain injury.