The objective of this work was to assess whether selective proteolysis of elastin and/or collagen in a porcine aorta followed by mechanical creep loading would result in an aneurysm-like permanent tissue stretch. The underlying motivations were to (1) test the feasibility of developing an in vitro abdominal aortic aneurysm (AAA) model, and (2) understand what role, if any, that passive creep-induced stretching plays in aneurysmal dilation. Multiple circumferentially oriented flat specimen strips were cut from the porcine thoracic aorta of ten adult pigs. Specimens were subjected to one of six treatment protocols: Untreated controls (UC;N=23), complete elastin degradation (E;N=10), partial elastin degradation (E(p);N=10), partial collagen degradation (C(p);N=22), and partial degradation of both elastin and collagen (E(p)+C(p);N=3). All specimens were then subjected to cyclic creep (10 min/cycle) with increasing load amplitude until failure. The zero-load strain prior to the creep cycle where failure occurred was defined as load-induced plastic strain. The plastic strain induced by treatment alone, creep loading alone and the total was determined for all specimens. The total plastic strain was significantly greater for E (mean +/- SD = 48.2 +/-17.6,p<0.005), E(p)(41.6+/-11.1,p<0.0005), but not for E(p)+C(p)(48.9+/-21.6,p=0.17) and C(p)(22.2+/-12.8,p=0.14) compared to UC (17.7+/-6.1). Of the total plastic strain, treatment-induced plastic strain was high for those specimens subjected to partial or total elastin degradation (E,E(p),E(p)+C(p)), but not for those where elastin was intact (C(p)). However, load-induced plastic strain in the treated specimens was not different in any of the treated groups compared to controls. Maximum total plastic strain of 78.6% was induced in one porcine aortic tissue from the E group. Even this is far lower than what would be needed for creating a realistic in vitro AAA model. Our findings do not support the feasibility of developing an in vitro AAA by enzymolysis followed by passive stretching of the aorta. The findings also suggest that AAA formation is unlikely to be a passive creep-induced stretching of a proteolytically degraded aortic wall as conventional thinking may suggest, but rather may be predominantly due to growth and remodeling of the aortic wall.