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 a rterial grafts. Although antithrombotic drugs are recommended, their e fficiency under low blood flow conditions is still being debated. In t his study, we evaluated the ability of three drugs to modify the throm botic properties of brood and, consequently, to influence platelet and fibrin deposition on the luminal surface of polyester arterial prosth eses. 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 implante d as a substitute for the infrarenal aorta and exposed to reduced bloo d flow. (50 ml/min) for 4 h. The parameters of the blood measured incl uded activated clotting time (ACT) and platelet aggregation with colla gen, determined before and after each treatment. Blood deposits were q uantified using In-111 labeled platelets and I-125-labeled fibrinogen. The ACT was significantly prolonged only after heparin treatment, and platelet aggregation, which was decreased by 35% (p < 0.05) after hep arin treatment, was almost abolished after aspirin and prostacyclin tr eatments. As compared with the control group, both platelet and fibrin uptake on the luminal surface of the prostheses were reduced signific antly 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 s urface 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.