Circulation, Vol 82, 973-981, Copyright © 1990 by American Heart Association
S Anidjar, JL Salzmann, D Gentric, P Lagneau, JP Camilleri and JB Michel
An experimental in vivo model of aortic aneurysm was established by
perfusing an isolated segment of rat abdominal aorta with pancreatic
elastase. Ten rats were used in each protocol. Saline-perfused aortas
developed no aneurysmal dilations. Elastase-perfused aortas contained
aneurysms in the perfused area and a total loss of elastic tissue. Control
aortas contained no elastic tissue lesions. There was a quantitative
relation between the amount of elastase perfused and aneurysm formation:
1-2 units induced neither macroscopic nor microscopic lesions; 3-6 units
induced microscopic elastic tissue damage without macroscopic aneurysm; and
more than 6 units produced aneurysmal dilation in all cases. In situ
elastase secretion by macrophages was induced by perfusing rat aortas with
thioglycollate- activated macrophages or with thioglycollate alone. There
was aortitis without true aneurysm and a total loss of elastic tissue in
the vicinity of activated macrophages within the aortic media. Perfusion of
infra-aneurysmal amount of elastase (1 or 2 units) or thioglycollate plus
plasmin (2 units) always induced a large aneurysm, whereas plasmin alone
induced neither macroscopic nor microscopic lesions. These morphological
results were supported by the significantly elevated elastolytic activity
within the aortic wall of animals perfused with thioglycollate plus plasmin
9 days, after perfusion (207.6 +/- 54.8 micrograms elastin-rhodamine
lysed/18 hr; control rats, 25.43 +/- 11.13). The results suggest that the
presence of elastase within the aortic media leads to aneurysm formation.
Activated macrophages within the aortic media may be responsible for
elastase secretion and elastic tissue destruction. Plasmin may enhance
elastase activity and aggravate the aneurysmal lesion.
ARTICLES
Elastase-induced experimental aneurysms in rats
INSERM U36-17, Paris, France.
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