Experimental Arterial Thromboembolism in Baboons: Mechanism, Quantitation and Pharmacologic Prevention

A quantitative primate model of arterial thromboembolism has been developed that involves the kinetic measurements of ⁵¹Cr-platelets and ¹²⁵I-fibrinogen by femoral arteriovenous cannulae in chaired baboons. Cannula platelet consumption (CPC) correlated directly with exposed cannular area for irradiated Silastic (IS) end polyurethane (correlation coefficients of 0.940 and 0.901 respectively; p < 0.001) and remained steady state for months. Fibrinogen was not measurably destroyed. CPC was independent of cannula flow rate, platelet count, heparin anticoagulation and ancrod defibrinogenation

In-platelet imaging of IS eannulae demonstrated luminal accumulation and subsequent embolization of irregular platelet masses that progressively occluded glomerular vessels with non-fibrin containing platelet thromboemboli.

Oral administration of dipyridamole and sulfinpyrazone decreased cannula platelet consomption in a dose dependent manner with complete interruption at 20 and 250 u mol/kg body wt/day (in three divided doses) respectively, whereas oral acetylsalicylic acid (10-330 umol/kg/day) had no measurable effect on cannula platelet consumption. We conclude that this primate model simulates arterial thrombotic processes in man and that this model is suitable for the in vivo evaluation of biomaterials and of drugs that modify platelet behavior.