Arterial Venous Grafts

Effect of Saratin on Venous Anastomotic Intimal Hyperplasia in a Canine Dialysis Access Model

In this model of human dialysis access graft stenosis, PTFE grafts were placed using end-to-side anastomoses between the femoral artery and the femoral vein. The venous anastomosis was exposed to saratin (0.6mL, 1mg/mL) or placebo for 5 minutes prior to closure.  Four weeks after surgery the animals were sacrificed and the degree of intimal hyperplasia at the venous anastomosis – the usual site of graft failure in human dialysis patients – was assessed histologically using computer-assisted morphometry.

In control animals marked intimal hyperplasia occurred, occluding nearly half of the lumen. Saratin almost completely abolished this effect and markedly reduced the ratio of intima to wall thickness in the region of the anastomosis. Saratin had no effect on platelet count or bleeding time.


Placement of the AV graft in the canine model. 

The letter designations depict the position of the section with respect to the AV graft placement. 

Representative elastin-stained histomicrographs of blocks at the venous anastomosis comparing the control group with the saratin group. 

The PTFE material, vein wall, luminal stenosis, and intimal hyperplasia response are labeled.  Sections of through blocks C and D incorporated the PTFE graft and vein wall as well as the vascular anastomosis.  Blocks A through E are labeled with the calculated percent luminal stenosis due to the intimal hyperplasia response.

Intimal hyperplasia (IH) thickness as a ratio of vein wall thickness for blocks C and D in both control and saratin-treated groups.

Mean ± SEM for the ratio of IH versus wall thickness for blocks C and D in both control and saratin-treated groups at 4 weeks after graft placement. 




Smith, TP, Alshafie, TA, Cruz, CP, Fan, CY, Brown, AT, Wang, Y, Eidt, JF andMoursi, MM.  Saratin, an Inhibitor of collagen-Platelet Interaction, Decreases Venous Anastomotic Intimal Hyperplasia in a canine Dialysis Access Model.  Vasc. Endovasc. Surg. 2003;37:259-269.


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