Ultrastructural evidence of the effects of shear stress variation on intimal thickening in dogs with arterially transplanted autologous vein grafts. Based on our findings that changes in wall shear stress, not the rate of blood flow, were the main hemodynamic factor related to intimal hyperplasia of autologous vein grafts, we further investigated the effect of wall shear stress variation on sequential ultrastructural changes in the intimal hyperplasia of arterially transplanted autovein grafts, using canine models. As noted, wall shear stress variation (tau-variation) could be defined by the variation in wall shear stress within a cardiac cycle, using a desktop flow waveform analyzer. In Group I, which had a high flow rate of 78.4 +/- 4.6 ml/min and low tau-variation of 36.1 +/- 2.2 dynes/cm2, intimal hyperplasia was significant. Ultrastructurally, there was a marked transformation of intimal smooth muscle cells to secretory cells 2 to 4 weeks after implantation. The surface of the intima was lined with modified smooth muscle cells at 2 weeks after implantation. In Group II, which had a low flow rate of 5.6 +/- 2.2 ml/min and normal tau-variation value (174.6 +/- 13.0 dynes/cm2), intimal hyperplasia was minimal, and there were several layers of contractile type smooth muscle cells, with characteristic myofibrillae. The surface of the intima was lined with endothelial cells at 2 weeks after implantation. These findings suggest that, in regions of low wall shear stress variation, intimal smooth muscle cells of autovein grafts may well become secretory cells, and enhanced platelet adherence could occur during early intimal repair, causing intimal hyperplasia to develop. 