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- W2004755168 abstract "Abstract Ultrastructural aortic endothelial cell changes were examined in 14- and 25-week spontaneously hypertensive (SHR) and normotensive (WKY) rats. Scanning and transmission electron microscopy revealed the presence of blister-like protrusions and cavity-like defects along intercellular junctional areas, resulting from dilatation of the intercellular space, subsequent elevation of the overlying marginal fold, and cellular breakage of this attenuated cellular extension. Junctional complexes, despite the presence of dilatated intercellular spaces, appeared intact. This form of endothelial damage, therefore, does not appear to result in abnormal, indiscriminate vascular permeability, at least to large macromolecules. This was confirmed by examination of representative segments of various SHR and WKY vessels after intravenous injection of colloidal carbon tracers. Only SHR mesenteric postcapillary venules (diameter 9–32 μm) showed permeability alterations, mediated through the formation of interendothelial gaps. In addition, these vessels were extensively fibrinized and occasionally showed evidence of hyalinization. The absence of permeability to colloidal carbon in arteries and arterioles in SHR may reflect the protective function of adaptive wall changes found in chronically hypertensive animals. In addition to changes in the media, these adaptive wall changes may also include endothelial cell alterations such as elongation of marginal folds, an increase in cellular overlap, and an increase in the complexity of intercellular connections, as observed in this study." @default.
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- W2004755168 date "1980-04-01" @default.
- W2004755168 modified "2023-09-27" @default.
- W2004755168 title "Endothelial alterations and colloidal carbon permeability in the peripheral vasculature of the spontaneously hypertensive rat" @default.
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- W2004755168 doi "https://doi.org/10.1016/0014-4800(80)90055-6" @default.
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