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Clinically available alternatives of vascular access for long-term haemodialysis—currently limited to native arteriovenous fistulae and synthetic grafts—suffer from several drawbacks and are associated to high failure rates. Bioprosthetic grafts and tissue-engineered blood vessels are costly alternatives without clearly demonstrated increased performance. In situ tissue engineering could be the ideal approach to provide a vascular access that profits from the advantages of vascular grafts in the short-term (e.g. early cannulation) and of fistulae in the long-term (e.g. high success rates driven by biointegration). Hence, in this study a three-layered silk fibroin/polyurethane vascular graft was developed by electrospinning to be applied as long-term haemodialysis vascular access pursuing a ‘hybrid’ in situ engineering approach (i.e. based on a semi-degradable scaffold). This Silkothane® graft was characterized concerning morphology, mechanics, physical properties, blood contact and vascular cell adhesion/viability. The full three-layered graft structure, influenced by the polyurethane presence, ensured mechanical properties that are a determinant factor for the success of a vascular access (e.g. vein-graft compliance matching). The Silkothane® graft demonstrated early cannulation potential in line with self-sealing commercial synthetic arteriovenous grafts, and a degradability driven by enzymatic activity. Moreover, the fibroin-only layers and extracellular matrix-like morphology, presented by the graft, revealed to be crucial in providing a non-haemolytic character, long clotting time, and favourable adhesion of human umbilical vein endothelial cells with increasing viability after 3 and 7 d. Accordingly, the proposed approach may represent a step forward towards an in situ engineered hybrid vascular access with potentialities for vein-graft anastomosis stability, early cannulation, and biointegration.
Ex vivo systems represent important models to study vascular biology and to test medical devices, combining the advantages of in vitro and in vivo models such as controllability of parameters and the presence of biological response, respectively. The aim of this study was to develop a comprehensive ex vivo vascular bioreactor to long-term culture and study the behavior of native blood vessels under physiologically relevant conditions. The system was designed to allow for physiological mechanical loading in terms of pulsatile hemodynamics, shear stress, and longitudinal prestretch and ultrasound imaging for vessel diameter and morphology evaluation. In this first experience, porcine carotid arteries (n = 4) from slaughterhouse animals were cultured in the platform for 10 days at physiological temperature, CO2 and humidity using medium with blood-mimicking viscosity, components, and stability of composition. As expected, a significant increase in vessel diameter was observed during culture. Flow rate was adjusted according to diameter values to reproduce and maintain physiological shear stress, while pressure was kept physiological. Ultrasound imaging showed that the morphology and structure of cultured arteries were comparable to in vivo. Histological analyses showed preserved endothelium and extracellular matrix and neointimal tissue growth over 10 days of culture. In conclusion, we have developed a comprehensive pulsatile system in which a native blood vessel can be cultured under physiological conditions. The present model represents a significant step toward ex vivo testing of vascular therapies, devices, drug interaction, and as basis for further model developments.
and therefore loss of elastin is believed to be the main characteristic of aneurysms.In the last years, aneurysm development has been increasingly linked to impaired collagen homeostasis (Lindeman et al., 2010). However, studies based on the analysis of collagen content in AAA tissue showed discordant results, observing a decrease (McGee et al., 1991), an increase (He and Roach, 1994;Rizzo et al., 1989) or no changes (Gandhi et al., 1994) in collagen content. Collagen crosslinking has been shown to be increased in AAA (Carmo et al., 2002;Lindeman et al., 2010;Wågsäter et al., 2013), and alterations in collagen microarchitecture in AAA and Marfan's syndrome tissue resulted in tissue mechanical failure (Lindeman et al., 2010). However, the exact role of collagen in aneurysm pathophysiology and whether the loss of elastin function or collagen crosslinking or their combination triggers the pathology is still unknown.To optimize treatment and better understand aneurysm pathophysiology, several in vivo animal models have been developed IntroductionAbdominal aortic aneurysm (AAA) is a life-threatening and often asymptomatic cardiovascular disease consisting of an abnormal dilation of the aorta owing to vessel wall weakening, which develops until rupture. The prevalence of AAA is ≈ 5% in men and ≈ 1% in women older than 60 years (Golledge and Norman, 2011); rupture carries a 90% overall mortality (Giugliano et al., 2018;Upchurch and Criado, 2009). The etiology and pathogenesis of aneurysms are poorly understood. It seems that aneurysm formation is associated with a significant increase in stiffness of the arterial wall compared to healthy
and therefore loss of elastin is believed to be the main characteristic of aneurysms.In the last years, aneurysm development has been increasingly linked to impaired collagen homeostasis (Lindeman et al., 2010). However, studies based on the analysis of collagen content in AAA tissue showed discordant results, observing a decrease (McGee et al., 1991), an increase (He and Roach, 1994;Rizzo et al., 1989) or no changes (Gandhi et al., 1994) in collagen content. Collagen crosslinking has been shown to be increased in AAA (Carmo et al., 2002;Lindeman et al., 2010;Wågsäter et al., 2013), and alterations in collagen microarchitecture in AAA and Marfan's syndrome tissue resulted in tissue mechanical failure (Lindeman et al., 2010). However, the exact role of collagen in aneurysm pathophysiology and whether the loss of elastin function or collagen crosslinking or their combination triggers the pathology is still unknown.To optimize treatment and better understand aneurysm pathophysiology, several in vivo animal models have been developed IntroductionAbdominal aortic aneurysm (AAA) is a life-threatening and often asymptomatic cardiovascular disease consisting of an abnormal dilation of the aorta owing to vessel wall weakening, which develops until rupture. The prevalence of AAA is ≈ 5% in men and ≈ 1% in women older than 60 years (Golledge and Norman, 2011); rupture carries a 90% overall mortality (Giugliano et al., 2018;Upchurch and Criado, 2009). The etiology and pathogenesis of aneurysms are poorly understood. It seems that aneurysm formation is associated with a significant increase in stiffness of the arterial wall compared to healthy
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