We investigated the feasibility of developing an in vitro abdominal aortic aneurysm model by mechanically stretching passive porcine aortic tissue after enzymatic degradation of its structural proteins. Individual arterial rings, taken from the thoracic and abdominal porcine aorta were exposed to specific concentrations of collagenase (to degrade collagen) and/or elastase (to degrade elastin). The specimens were then cut into flat strips and subjected to uniaxial incremental creep tests of increasing load amplitude. The plastic strain (strain at zero load) after each creep load cycle was recorded until specimen failure. The maximum plastic strain due to enzymatic degradation and mechanical loading in elastase treated specimens (mean+SD = 45.1±14.7%; p<0.001) was significantly higher than in untreated controls (19.4±7.61%). However, the plastic strain in collagenase treated specimens (18.4±10.3%; p = 0.79) was not significantly different from the controls. Because AAA is associated with a plastic deformation of 200–400%, the results suggest that it is not feasible to develop an in vitro AAA model by enzymatic degradation and biomechanical stretching of passive porcine aorta. Consequently, these findings suggest that aneurysm growth is unlikely to be solely the result of pressure induced passive stretch of a weakened aorta.

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