The roles of vascular smooth muscle cells in the aortic wall thinness under prolonged continuous flow left heart bypass.
Aortic wall thinness was one of the most characteristic changes observed in experimental animals under prolonged continuous flow left heart bypass. The goal of this study was to determine the roles of smooth muscle cells in the vascular remodeling process in cases demonstrating aortic wall thinness under prolonged continuous flow left heart bypass. The aortic samples from three goats in which continuous flow left heart bypass was performed were subjected to histological and immunohistochemical analyses. After 4 weeks of observation, the pulse pressure in the goats under the continuous flow left heart bypass was clearly lower than that in the normal healthy goats. The aortic walls of these goats became thinner, an effect caused by the dilation of their internal diameter. These aortic smooth muscle cells maintained contractile formation due to the fact that they contained abundant alpha-smooth muscle actin (SMA) and smooth muscle myosin heavy chain (SMMS). These cells also synthesized redundant matrix metalloproteinase-2 and -9, and the ratio of the SMMS-positive to the SMA-positive area was significantly lower (0.76) than that observed in the control goat (1.00; P < 0.05). The smooth muscle cells demonstrated synthetic-dedifferentiated formation, which is one of the phenotypes of smooth muscle cell function. In conclusion, aortic wall thinness under prolonged continuous flow left heart bypass is caused by over-synthesis of matrix metalloproteinase in smooth muscle cells, and this refers the vascular remodeling process of the extracellular matrix.