Acute thrombogenicity of arterial prostheses exposed to reduced blood flow in dogs: effects of heparin, aspirin, and prostacyclin.

Thrombogenesis is considered the principal cause of early failure of arterial grafts. Although antithrombotic drugs are recommended, their efficiency under low blood flow conditions is still being debated. In this study, we evaluated the ability of three drugs to modify the thrombotic properties of blood and, consequently, to influence platelet and fibrin deposition on the luminal surface of polyester arterial prostheses. In dogs receiving saline (control, n = 10), heparin (100 U/kg, n = 5), aspirin (325 mg, n = 5), or prostacyclin (15 ng/kg/min, n = 5), a 30-cm, woven, loop-shaped, DeBakey arterial prosthesis was implanted as a substitute for the infrarenal aorta and exposed to reduced blood flow (50 ml/min) for 4 h. The parameters of the blood measured included activated clotting time (ACT) and platelet aggregation with collagen, determined before and after each treatment. Blood deposits were quantified using 111In labeled platelets and 125I-labeled fibrinogen. The ACT was significantly prolonged only after heparin treatment, and platelet aggregation, which was decreased by 35% (p < 0.05) after heparin treatment, was almost abolished after aspirin and prostacyclin treatments. As compared with the control group, both platelet and fibrin uptake on the luminal surface of the prostheses were reduced significantly by heparin by 87 and 37%, respectively. Despite their inhibition of platelet aggregation in vitro, aspirin and prostacyclin induced no significant change in platelet and fibrin deposition on the luminal surface of the woven polyester arterial prostheses under low blood flow conditions. Under such conditions, however, thrombin generation with subsequent platelet-fibrin deposition was prevented by use of heparin anticoagulant therapy.