Ultrastructural studies of vascular lesions in experimental amyloidosis of mice.
Definite lesions of arteriolar capillaries have been demonstrated in early amyloid lesions of mice. Pathologic changes include multiple endothelial gaps, the loss of an identifiable basal lamina, variable degrees of endothelial alteration, and the presence of the developing amyloid lesions surrounding the affected vessels. Despite these changes, the vessels remain functional part of the local microcirculation as demonstrated by intravascular injection of electron dense markers. These structural changes of arteriolar capillaries explain the presence of circulating plasma as a constant and major component of the early amyloid lesions in these animals and on this basis may determine the time of onset and site of formation of the lesions. The vascular injury appears to be caused by immunologic reactions to injected foreign antigens which gain a close relation to the structures of these vessels.
D000682:Amyloid / Q000378:metabolism; D000686:Amyloidosis / Q000473:pathology*; D000818:Animals; D001808:Blood Vessels / Q000473:pathology / Q000648:ultrastructure*; D002196:Capillaries / Q000473:pathology / Q000648:ultrastructure; D005293:Ferritins / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D008854:Microscopy, Electron; D013154:Spleen / Q000098:blood supply / Q000473:pathology / Q000648:ultrastructure
D000682:Amyloid; D005293:Ferritins