Differential response of arteries and vein grafts to blood flow reduction

Abstract

In this model, arteries and VG responded to flow reduction by wall thickening, but the mechanism differed. Arteries underwent medial remodeling, lumen caliber reduction, and shear stress normalization, whereas VG responded by an upward modulation of the proliferative response that follows graft placement. These data support a primary role for tangential stress and a secondary role for shear stress in determination of VG dimensions.

Comparison of the Effects of Mechanical Stimulation on Venous and Arterial Smooth Muscle Cells in vitro

“…The causes of intimai hyperplasia are complex and poorly understood. A variety of factors that may serve as stimuli for SMC proliferation have been suggested, and these include injury to the saphenous vein during surgical har vesting [16][17][18], elevated wall tension with subsequent mechanical wall deformation [10,11], and alterations in blood flow velocity and shear stress [19][20][21][22], In this study we have focused upon a possible role for mechanical forces in vascular remodeling by comparing the effects of pulsatile stretch on the proliferation of vascular ECs and SMCs in vitro.…”

“…However, the success of saphenous vein grafts depends upon long-term patency, and the patency rate for these grafts varies from 50 to 70% 10 years after surgery [1,2], Anastomotic neointimal hyperplasia caused by the proliferation of smooth muscle cells (SMCs) with superimposed atheroma is the major cause of late graft occlusion [3,4], The cellular events which may con tribute to neointimal hyperplasia following bypass graft ing are described in studies using pathological specimens [5,6] as well as in detailed time course experiments using a number of animal models suggest that wall tension and inereased transmural pressure produced by these changes in pressure and flow serve as stimuli for SMC prolifera tion [10,11].…”

Long-Term Behavior of an Arterial Autograft: A New Role for Intimal Hyperplasia?

“…The long-term myointimal development of the arterial graft segment may be explained as a compensatory phe nomenon to restore shear stress and tensile stress in accor dance with the work by Galt et al [25]. The participation of this myointimal layer in adaptive modifications has been shown in other models [26][27][28], Factors other than shear and tense stress that may cause or contribute to intimal hyperplasia in this model include traumatic injury, denervation [29], ischemic damage [30], and inflammation in the adventitia due to nonsterile conditions [30].…”

Computational Simulation of the Adaptive Capacity of Vein Grafts in Response to Increased Pressure

“…Vein graft failure results primarily from thrombosis during the acute period (<1 month), wall thickening during the intermediate period (1-12 months), and atherosclerosis in the long-term (3-5 yr) [5]. There is substantial evidence relating hemodynamic loads to vein graft remodeling [8][9][10][11]. Understanding the kinetics of these (mal)adaptative processes could be facilitated by a computational model that relates macroscopic hemodynamic quantities and structural adaptations to underlying cellular mechanisms, thus providing a mechanobiological understanding of vein adaptation versus maladaptation or failure.…”

“…This approach is motivated by prior studies that show medial thickening to associate best with increased intramural circumferential stress or strain [16]. There is also evidence that circumferential stress plays a primary role and wall shear stress plays a secondary role in determining overall vein graft dimensions [10], though shear stress likely controls neointimal formation [17]. Toward this end, we first identify constitutive parameters for a normal mouse vena cava based on published experimental data from pressure-diameter and axial force-length tests [18].…”