Intimal hyperplasia: the permeation of serum-derived substance into the arterial autovein graft under abnormal blood flow.

The etiology of intimal hyperplasia in autogenous vein grafts used for arterial replacement was experimentally studied in dogs. We previously developed an experimental model, which mimicked a human extremity with poor run-off of peripheral arteries. This model characterized the abnormal flow by a weak fluctuation of wall shear stress at the site adjacent to the vessel wall. In this model we found that an autogenous vein implanted into the femoral artery under such abnormal flow conditions exhibited remarkable intimal thickening; 200-400 micron at 1 month and 300-500 micron at 6 months. A fluorescence microscopic study revealed that Evans blue-albumin complex entered the inner wall of vein grafts transplanted in abnormal flow conditions until about 2 weeks after implantation, after which further permeation was no longer observed. A similar observation was made in the fibrinogen distribution of subendothelial tissue. These results showed that abnormal flow conditions enhance the permeation of certain substances into immaturely repaired intimal tissues of autovein grafts. This phenomenon is thought to be responsible for the proliferation of smooth muscle cells, leading to hyperplasia of autovein grafts.