Background: The pathogenesis of aortic aneurysms remains largely unknown, despite aneurysmal rupture being an increasingly common catastrophe.
Methods: This study was designed to elucidate the mechanism of arterial dilatation histologically and electron microscopically, utilising a new animal model. Elastase, 3.0 mg/ml, was applied to the abdominal aortae of 18 New Zealand white rabbits from the adventitia side for 3 hours. The rabbits were sacrificed at 0, 3, 14, 28, 42 and 90 days after the procedure (n=4, 3, 2, 2, 2, 3).
Results: Two rabbits were found to have developed aortic rupture. On day 0, elastase application induced fusiform aneurysms up to 1.62+/-0.14 times the pre-elastase application aortic diameter. Dilated walls revealed medial elastolysis, degeneration of smooth muscle cells (SMCs) and damaged endothelial cells. By day 3, the smooth muscle cells had changed to the synthetic type. Aneurysms did not progress, and after 42 days, showed gradual shrinkage. By day 90, aortic diameters had nearly normalised.
Conclusions: Aortic walls also returned to the pre-elastase application thickness and some mature medial elastic lamellae showed regeneration. Medial smooth muscle cells reverted to the contractile type. Aortic dilatation induced by peri-aortic application of elastase heals spontaneously, accompanied by regeneration of smooth muscle cells. Irreversible degeneration of medial smooth muscle cells appears to be more critical to aneurysm formation than degeneration of elastic lamellae.