Ultrastructure of the afferent arteries of experimental femoral arteriovenous fistulae in rabbits
- 1 January 1995
- Vol. 27 (4) , 333-338
- https://doi.org/10.1080/00313029500169253
Abstract
Summary Using transmission electron microscopy, the aorta and iliofemoral arteries of 12 normocholesterolemic rabbits with femoral arteriovenous fistulae were investigated (49 to 895 days postoperatively) to determine whether the fibrofatty lesions in arteries proximal to chronic fistulae were ultrastructurally consistent with human atherosclerosis. The contralateral ilio-femoral arteries from the same animals and the vessels of 4 additional rabbits (2 with femoral arteriotomies) served as control material for comparison. There were microfractures adjacent to complete tears of the internal elastic lamina which had abrupt margins. These tears were observed mostly in the ilio-femoral arteries proximal to the fistula. They were most numerous, extensive and associated with considerable intimal proliferation near the fistula. Further proximally the tears were associated with progression to severe atrophy of the wall, the media in places being reduced in width to no more than 2 or 3 smooth muscle cells without any evidence of cellular degeneration. Intimal proliferation near the fistula and the naturally occurring intimal thickenings at branching sites proximal to the fistula, not only extended peripherally and progressed with time post-operatively, but exhibited ultra-structural changes consistent with atherosclerosis. These changes comprised dystrophic basement membrane, granulovesicular degeneration (matrix vesicles) and necrosis of smooth muscle cells, disruption of the elastic laminae, the appearance of extracellular and to a lesser extent intracellular lipid, adherence of monocytes, accumulation of foam cells, intimal fibrin deposition and sub-endothelial hemorrhage. Such results indicate that augmented hemodynamic stresses associated with femoral arteriovenous fistulae are consistent with those of human atherosclerotic lesions.Keywords
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