INTIMAL HYPERPLASIA OF EXPERIMENTAL AUTOLOGOUS VEIN GRAFT IN HYPERLIPIDEMIC RABBITS WITH POOR DISTAL RUNOFF

Poor distal runoff and hyperlipidemia are factors affecting the fate o f an implanted graft. In the present study, combined effects of poor d istal runoff and hyperlipidemia on intimal hyperplasia (IH) of the vei n graft were examined in a newly developed poor distal runoff model in rabbits. A poor distal runoff model was prepared in the right hindlim b of 30 rabbits. These animals were divided into two groups, depending on the diet provided; normolipidemic diet group (Group NL, n = 14) an d hyperlipidemic 1% cholesterol diet group (Group HL, n = 16). Four we eks after preparing the poor runoff model, the femoral vein was implan ted into the ipsilateral femoral artery. At 2, 4 and 6 weeks, the graf ts were harvested. IH of the graft was measured and macrophages in the IH were examined immunohistochemically. Intimal eel proliferation was also determined by bromodeoxyuridine (BrdU) incorporation. IH of the vein graft was significantly accelerated in cases of poor distal runof f and hyperlipidemia. There were no macrophages in the IH in the NL gr oup, In the HL group, macrophages infiltrated the outer layer of IH, s ometimes just above the internal elastic lamina, and increased with ti me. In the poor distal runoff limbs at 6 weeks, macrophages also appea red in the subendothelial layer but were absent in that layer in the c ontrols. Intimal cell proliferation expressed,as the BrdU labeling ind ex (LI) was maximum at 2 weeks. In the HL group, BrdU LI of IH in the poor distal runoff limb was higher than in the control at 2 and 4 week s. Throughout the experiments, BrdU LIs in the HL group were significa ntly higher than in the NL. Hyperlipidemia accelerates intimal cell pr oliferation to a greater extent, then does IH. In cases of a poor dist al runoff, the enhancement of cell proliferation by hyperlipidemia is augmented. These responses, in the presence of a hyperlipidemia, may b e closely related to the migration of macrophages.