Thrombosis is the end result of two closely interrelated processes: the coagulation cascade and the platelet aggregation process. To determine their relative contribution, we used pharmacologic agents that selectively block each process. The specific effect of each pharmacologic agent on either fibrin deposition or platelet activity was confirmed morphologically by scanning electron microscopy and was substantiated with ADP-induced platelet aggregation and blood clotting time determinations. Forty-two rats had both femoral arteries subjected to a standardized crush-avulsion injury. A total of 84 femoral microvascular anastomoses were subsequently performed. None of the 24 control anastomoses treated with saline remained patent, whereas 6 of 24 of the anastomoses treated with dazmagrel (a selective thromboxane synthetase and platelet aggregation inhibitor), 2.5 mg/ kg IV, remained patent and 18 of 24 of those treated with a single dose of heparin, 200 U/kg IV, remained patent. All 12 anastomoses treated with both drugs remained patent but developed a 33 percent hematoma rate. We conclude that in this microvascular model, fibrin mesh deposition is a more significant factor than platelet aggregation in the pathogenesis of occlusional thrombosis within traumatized arteries. Its temporary inhibition with a single dose of heparin yielded a 75 percent improvement in patency rate. © 1990 American Society of Plastic Surgeons.
