| The blood vessel cells in vivo are subjected in complicated circumferential stress, flow shear stress and pressure, etc., and those stresses are changing with the pulstile flow of blood. Abnormal changes in stretch usually instigate adaptive vascular remodeling, including abnormal growth and proliferation of vascular smooth muscle cells as well as extracellular matrix. High blood pressure (hypertension) is implicated to be a crucial reason for the blood vessel remodeling and thus is the main cause of atherosclerosis.Lesions of atherosclerosis are always observed at certain parts of the arterial system, such as curves or bifurcations, where the blood flow is disturbed, causing much lower or higher wall shear stress. That will affect the function of blood vessel cells and the deposition of blood plasma lipoproteins as well. It has been proved that blood plasma lipoproteins, especially the low density lipoprotein (LDL), play an important role in the development and progress of atherosclerosis, and LDL uptake by cells is mostly depended on the concentration of the deposited LDL particles on the vessel wall.In the first part, we used bovine aortic endothelial cells (EC) and smooth muscle cells (SMC) co-cultured ePTFE vascular grafts with different original cell seeding densities subjected to 0 (as a control), 80, 100 and 120mmHg hydrostatic pressure for 7 days, and the increase of cell layer thickness under high pressure was observed. It was concluded that moderately high pressure resulted in cell proliferation and increase of collagen type IV synthesis of the cells on ePTFE vascular grafts. When the original cell seeding density doubled, the thickness of cell layer increased dramatically after 19 days culture (ever since SMC seeding) under the pressure of both 0 and 100mmHg.In the second part, we examined different flow conditions on the cell growth of EC-SMC co-cultured ePTFE vascular graft by using expended and non-expended circular tube flow apparatus. After 7 days flow, we found that the cells exposed to... |
