[Experimental studies on effect of grafting injury to vein graft]

To study the mechanism of restenosis of the vein graft and the effect of the grafting injury to the vein graft.

One side of the 36 healthy rabbits was randomly chosen as the V-A group, and on the side a 1.5-cm-long femoral vein was obtained, and an 0.5-cm-long segment of the obtained femoral vein was separated as the control group. The remaining 1-cm-long femoral vein was inverted and was autogenously implanted into the femoral artery on the same side of the rabbit. The other side of the rabbits was chosen as the V-V group, and on this side a 1-cm-long femoral vein was obtained ex vivo and then was sutured in situ. The vein grafts on both sides were harvested 4 weeks after operation. The specimens from the harvested vein grafts were stained with HE and the elastic fiber Victoria blue for an observation on the histological changes in the walls of the vein grafts, and the specimens were also stained by the immunohistochemistry of the proliferating cell nuclear antigen (PCNA) for an observation on the wall cell proliferation of the vein grafts. The changes in the ultrastructure of the proliferated wall cells of the vein grafts were observed under electron microscope. The two sides of the rabbits were compared.

The smooth muscle cells of the media developed hyperplasia, but the intima and the media remained unchanged in their thickness (3.50 +/- 0.41 microm, 12.23 +/- 1.59 microm) in the V-V group, with no difference when compared with the control group (3.40 +/- 0.37 microm, 12.14 +/- 1. 62 microm); however, when compared with the V-A group (25.60 micro 3.21 microm, 21.30 +/- 2.47 microm), there was a significant difference in the thickness (P < 0. 01). There were no cells positive for PCNA by the immunohistochemistry examination in the control group. The cells positive for PCNA were found in the intima and the media in both the V-V group and the V-A group; however, the percentage of the cells positive for PCNA in the intima and the media was significantly greater in the V-A group than in the V-V group (16.4% +/- 1.9% and 36.5% +/- 3.7% vs. 5.9% +/- 1.3% and 23.4% +/- 3.4%, P < 0.01). In the V-V group, the endothelial cell could be observed under transmission electron microscope, which was flat and had a process-like villus at its free end, and the endothelial cells were closely arranged and had hyperplasia of the smooth muscle cells in the media. But in the V-A group, the endothelial cells had an obvious hyperplasia with an irregular shape and a widened space between the cells, and in the intima a great amount of the smooth muscle cells could be observed, which had a broken basement membrane. The smooth muscle cells also had an obvious hyperplasia in the media. The shape and alignment of the endothelial cells in the control group were similar to those in the V-V group, but the hyperplasia of the smooth muscle cells was not observed in the media.

The grafting injury can cause hyperplasia of the vascular wall cells, and if the hemodynamics is changed simultaneously, more serious hyperplasia and cell migration can be observed from the media to the intima, resulting in restenosis of the blood vessels. So, if we can reduce the grafting injury and improve the microcirculation of the vein graft. we may find out the methods of preventing restenosis of the vein graft. The animal model of the V-V graft can help to understand the mechanism of restenosis of the vein graft.