Controlled peel testing of a model tissue for diseased aorta.

In this study, we examine the effect of collagenase, elastase and glutaraldehyde treatments on the response of porcine aorta to controlled peel testing. Specifically, the effects on the tissue׳s resistance to dissection, as quantified by critical energy release rate, are investigated. We further explore the utility of these treatments in creating model tissues whose properties emulate those of certain diseased tissues. Such model tissues would find application in, for example, development and physical testing of new endovascular devices. Controlled peel testing of fresh and treated aortic specimens was performed with a tensile testing apparatus. The resulting reaction force profiles and critical energy release rates were compared across sample classes. It was found that collagenase digestion significantly decreases resistance to peeling, elastase digestion has almost no effect, and glutaraldehyde significantly increases resistance. The implications of these findings for understanding mechanisms of disease-associated biomechanical changes, and for the creation of model tissues that emulate these changes are explored.

Creating a model of diseased artery damage and failure from healthy porcine aorta.

Large quantities of diseased tissue are required in the research and development of new generations of medical devices, for example for use in physical testing. However, these are difficult to obtain. In contrast, porcine arteries are readily available as they are regarded as waste. Therefore, reliable means of creating from porcine tissue physical models of diseased human tissue that emulate well the associated mechanical changes would be valuable. To this end, we studied the effect on mechanical response of treating porcine thoracic aorta with collagenase, elastase and glutaraldehyde. The alterations in mechanical and failure properties were assessed via uniaxial tension testing. A constitutive model composed of the Gasser-Ogden-Holzapfel model, for elastic response, and a continuum damage model, for the failure, was also employed to provide a further basis for comparison (Calvo and Peña, 2006; Gasser et al., 2006). For the concentrations used here it was found that: collagenase treated samples showed decreased fracture stress in the axial direction only; elastase treated samples showed increased fracture stress in the circumferential direction only; and glutaraldehyde samples showed no change in either direction. With respect to the proposed constitutive model, both collagenase and elastase had a strong effect on the fibre-related terms. The model more closely captured the tissue response in the circumferential direction, due to the smoother and sharper transition from damage initiation to complete failure in this direction. Finally, comparison of the results with those of tensile tests on diseased tissues suggests that these treatments indeed provide a basis for creation of physical models of diseased arteries.