Axial stretch as a means of lengthening arteries: An investigation in organ culture

Arteries remodel in response to mechanical stimuli in vivo. Increased blood pressure causes the arterial wall to thicken while increased flow rate leads to arterial dilation. If axial stretch also leads to remodeling, this may provide a means to engineer new arterial tissue from existing arteries. Such an approach could provide a source of autologous arterial tissue for use in coronary bypass grafting, thereby increasing the supply of native arterial tissue that is suitable for bypass applications. The present study explored the possibility of achieving permanent length increase in arteries by applying axial stretch in organ culture.; Porcine common carotid arteries were cultured in a perfusion system for 7 days under physiologic pressure and flow conditions. A constant axial stress of 250 kPa or an increasing stress of 350 kPa and higher was applied to arteries using closed-loop control of axial force and arterial length. Control arteries were cultured at the physiologic stretch ratio of 1.5.; Permanent arterial length increase was proportional to the maximum axial stretch ratio in culture for stretch ratios above 2.14; otherwise no length increase occurred. The maximum permanent length increase was 23%. Rupture of the structural components of the extracellular matrix appeared to be the main mechanism of length increase, though plastic deformation of matrix fibers may also have played a role. Maximum length increase was limited by arterial rupture, and the average axial stretch ratio at failure for the arteries in these protocols was probably between 2.4 and 2.6.; Medial smooth muscle population increased significantly in stretched arteries when length increase was considered. Necrotic cell death also increased in stretched arteries. However, overall smooth muscle viability remained high in stretched arteries, and the vasomotor function of stretched arteries was comparable to that of control arteries after 7 days. No clear evidence of repair was observed around damaged regions in stretched arteries, indicating a possible limitation of the organ culture model when compared to the in vivo environment.