Increased force generation and smooth muscle remodeling follow the implantation of saphenous vein as an arterial bypass graft. Previously, we characterized and mapped 129 proteins in human saphenous vein medial smooth muscle using two-dimensional (2-D) PAGE and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Here, we focus on actin filament remodeling in response to simulated arterial flow. Human saphenous vein was exposed to simulated venous or arterial flow for 90 min in vitro, and the contractile medial smooth muscle was dissected out and subjected to 2-D gel electrophoresis using a non-linear immobilized pH 3-10 gradient in the first dimension. Proteins were analyzed quantitatively using PDQuest 2-D software.
Human saphenous vein (HSV)1 remains a common conduit of choice for bypass grafting in humans because HSV is readily accessed, relatively plentiful, easily harvested (1), and provides adequate flow to the recipient artery. In the arterial bypass situation, the vessel experiences an abrupt change from the low-pressure, minimally pulsatile venous circulation to the high-pressure, pulsatile arterial circulation. The adaptation of HSV to the altered hemodynamic environment is a crucial process in graft maturation and patency.In the artery wall, smooth muscle cells are organized circumferentially and spirally, allowing efficient conduction of the arterial pulse. In contrast, the smooth muscle cells of saphenous vein are orientated both longitudinally and circumferentially. Re-orientation of the medial smooth muscle cells of saphenous vein into co-ordinated circumferential and spiral units is a crucial adaptive response observed in vein grafts. The thin-walled vein dilates in response to arterial pressure. Restoration of a smaller graft lumen with increase in wall thickness, to reduce wall tension, is achieved by migration of smooth muscle cells into the intima, with alteration to a synthetic, proliferative phenotype. This healing response of intimal hyperplasia can be locally excessive, particularly at the anastomoses, and is an important underlying cause of vein graft failure (2, 3). There are very early changes in the contractile properties of HSV following exposure to arterial heFrom the ‡Department