Abstract

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.

Highlights

  • Arterial dissection refers to separation of the inner layers of the arterial wall

  • Depending on the direction of blood flow, the circulatory pressure will either press the tissue flap to the wall or act to propagate the dissection. The former often results in the dissection remaining benign, whereas the latter can eventually progress to create a large tissue flap that blocks downstream blood flow in the true lumen and encourages flow into the newly formed false lumen between the flap and remaining artery wall

  • The effects of collagenase, elastase and glutaraldehyde treatments on the uniaxial elastic and failure behaviour of arterial tissues were investigated. We expand on those results by investigating the effects of these treatments on dissection resistance

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Summary

Introduction

Arterial dissection refers to separation of the inner layers of the arterial wall. This is almost always initiated by trauma, either directly to the vessel wall, e.g. a catheter piercing or tearing the intimal layer of the vessel during an endovascular procedure [20], or indirectly via external trauma, for instance from motor vehicle crashes [31]. Depending on the direction of blood flow, the circulatory pressure will either press the tissue flap to the wall or act to propagate the dissection (figure 1) The former often results in the dissection remaining benign, whereas the latter can eventually progress to create a large tissue flap that blocks downstream blood flow in the true lumen and encourages flow into the newly formed false lumen between the flap and remaining artery wall. The increasing use of endovascular treatment methods renders desirable the development of new medical devices such as endovascular catheters Research in this area requires access to large supplies of arterial tissue - preferably diseased, to reflect the state of real patient tissues - for physical testing of designs. The cheapness and ready availability of porcine arterial tissue (often considered a waste product in meat preparation), and avoidance of aforementioned ethical issues, suggests tissue models produced in this way can ameliorate the cost and complexity of medical device design

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