The concentrations and application methods of elastase in the rabbit aneurysm model were optimized to control the initiation of aneurysms and to cause rupture in a stepwise, controlled fashion. The common carotid artery of male Japanese albino rabbits was exposed. No aneurysm was generated if the adventitia was not dissected. After gentle removal of the adventitia, a two-fold dilution series of elastase was applied to the lesion and observed over a period of 2 hours. Various stages of aneurysmal lesions, from spindle-shaped enlargement to rupture, were produced in proportion to the elastase concentration. Application of elastase stock solution (5 U/mg of type I porcine pancreatic elastase) resulted in rupture within 30 minutes in all six animals. Elastase 1:2 solutions caused oozing in all animals, but subsequent rupture in only three of six animals. Histological examination found serious destruction of the internal elastic lamina and media, with expansion of the very thin wall. Elastase 1:4 to 1:16 solutions caused spindle-like distention of the entire artery and the development of tortuosity at the lesion. Elastase 1:32 or weaker solutions caused only localized dilatations. Overall, the destruction of the tunica media became less severe with decreased elastase concentration. Furthermore, the bursting pressure of the aneurysms decreased with increasing elastase concentrations. In particular, aneurysms produced by the elastase 1:2 solution ruptured at less than 150 mmHg, whereas aneurysms induced by the elastase 1:4 or weaker solutions did not rupture within the physiological range of blood pressure. The present aneurysm model requires shorter preparation time and enables accurate control of aneurysm development and rupture.