Histochemistry of aortic elastin in patients with nonspecific abdominal aortic aneurysmal disease.
Histochemical studies of nine aneurysmal aortas revealed a conspicuous deficiency of iron hematoxylin-reactive elastin in four specimens, in comparison with eight atherosclerotic control specimens. A fibrillar matrix that morphologically resembled elastin was demonstrated in these same specimens under ultraviolet light. The phenomenon of substantial preservation of features of medial architecture suggests that, if the pathogenetic mechanism is enzymatic destruction, the process is highly selective. Comparisons with differences in human fetal vs newborn aortas and in Blotchy mouse vs normal mouse aortas suggest superficial similarities. These latter observations suggest that a hypothesis of maturation arrest might be considered as an alternative to enzymatic destruction. Definitive experiments to test the relative importance of maturation arrest vs enzymatic destruction in the pathogenesis of aneurysmal disease will require further studies.
D000328:Adult; D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism*; D001014:Aortic Aneurysm / Q000378:metabolism*; D004549:Elastin / Q000378:metabolism*; D005260:Female; D005315:Fetal Diseases / Q000378:metabolism; D006416:Hematoxylin; D006651:Histocytochemistry; D006801:Humans; D007231:Infant, Newborn; D007501:Iron; D051379:Mice; D011247:Pregnancy; D013194:Staining and Labeling
D004549:Elastin; D007501:Iron; D006416:Hematoxylin