Research Article

Comparison of Pulmonary and Systemic NO- and PGI2-Dependent Endothelial Function in Diabetic Mice

Figure 1

Histology of the lungs and ultrastructure of pulmonary endothelial cells from the control (a, c, e, g) and diabetic (b, d, f, h) lungs (db/db mice). (a) Histological structure of the control lungs. (b) Inflammation in the lung tissue: increased amount of cells (including granulocytes and macrophages) and (d) collagen in parenchyma of the diabetic lung tissue as compared to control; visible decreased aerial space in diabetic lungs as compared to the control (c). (e) Microphotographs of ultrastructure of the control lungs—blood-air barrier (alveolar–capillary barrier) with normal endothelial layer. (f, g, h) Microphotographs of ultrastructure of the lungs from the db/db mice. (f) Capillary endothelial cells (arrows) with numerous plasmalemmal vesicles (caveolae) on thickened blood-air barrier (bab). In the center: collapsed pulmonary alveoulus, on the right: blood platelet (plt) inside the vessel. (g) A presence of convoluted apical region in endothelial cells with cytoplasmic extensions on hyperplastic basal laminae enriched with elastine (el); on the bottom: red blood cell (rbc). (h) Endothelial cells of various heights (arrows) separated by thickened blood-air barrier (bab) from pulmonary alveolus; neighbouring red blood cell (rbc). Representative images of at least 3 independent experiments.
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