• L Miskolczi, L R Guterman, J D Flaherty, I Szikora, and L N Hopkins.
• Toshiba Stroke Research Center, Department of Neurosurgery, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, USA.
• Neurosurgery. 1997 Jul 1; 41 (1): 220-8; discussion 228-9.

ObjectiveTo develop a new saccular aneurysm model in vitro using elastase to study aneurysm initiation, growth, and rupture and to create a new in vivo aneurysm model to test endovascular therapies.MethodsSeventeen common carotid arteries excised from freshly killed pigs and sheep were treated with seven different methods of elastase delivery. The arteries were mounted in a saline-filled flow chamber. They received pulsatile flow for 48 hours, or until the resulting aneurysms ruptured. Changes were continuously monitored with video camera recordings and validated with histological sections.ResultsAll eight arteries treated topically, either on the intimal or on the adventitial surface, with elastase concentrations greater than 1 U/mm2, developed saccular aneurysms; five of them ruptured within 48 hours. All four arteries treated with surface concentrations of 0.1 U/mm2 via microcatheter infusion into the lumen developed fusiform aneurysms. None of the arteries that received surface concentrations less than 0.1 U/mm2 developed aneurysms. Histological sections revealed a reduced number of cellular element in a stretched collagen matrix at the dome of the saccular aneurysms.ConclusionAfter empirically testing several methods of elastase delivery, we were able to induce saccular, bifurcation-type aneurysms in animal arterial specimens. These aneurysms are histologically similar and more authentic than surgical models. The procedure is easy and reproducible. Our results suggest a possible enzymatic role in aneurysm formation and highlight the dramatic effects of selective arterial elastic damage. Also, the rapid growth of our experimental aneurysms may reflect the speed of the natural process.

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