Uncontrolled deposition of platelets on thrombogenic surfaces may lead to the occlusion of vessels, a condition associated with numerous pathophysiological changes, such as acute myocardial infarction and unstable angina, or the ischemic complications of coronary intervention and stroke. Studies show that antiplatelet agents can prevent development of thrombotic disorders, such as myocardial infarction and peripheral vascular diseases. In vitro screening methods are described. Selection of volunteer blood donors and preparation of platelets and platelet aggregation assays are discussed. Washed platelets are prepared by the method of Rho et al and platelet aggregation is determined by a standard turbidometric method using an aggregometer. In vitro platelet aggregation is measured with a whole blood electrical impedance aggregometer. Preparation of gel-filtered platelets, preparation of fixed platelets, and platelet adhesion are described. Acid soluble collagen is injected into the aortic arch of rabbits via the carotid artery and serial platelet counts performed on blood withdrawn subsequent to collagen administration. In vivo screening methods are discussed. A model of electrolytic injury-induced carotid artery occlusive thrombus formation is used. The experimental procedure results in the formation of platelet-rich intravascular thrombus along with a few erythrocytes and a rough fibrous coating at the site of an endothelial lesion induced by electrolytic injury in proximity to distal arterial stenosis. Arterial thrombosis and thrombotic occlusion occurs in response to intimal damage, after which the vessel segment is ligated, both proximal and distal to the point of injury, and removed without disturbing the intravascular thrombus. Photochemically induced thrombosis model in rats are discussed. The right jugular vein and artery are cannulated for the injection of dye and the monitoring of arterial blood pressure and heart rate, respectively. Studies of antiplatelet efficacy in rheusus monkeys are discussed.