Treatment with the plasminogen activator streptokinase or urokinase has been shown to accelerate lysis of acute pulmonary emboli [23,34,39,45,46] and recent peripheral venous thrombi [5,15,16,25,37]. Although the clinical value of these effects has not been completely defined, it is likely that the rapid lysis of major pulmonary emboli benefits patients by relieving pulmonary artery hypertension in the acute phase of pulmonary embolism, particularly if there is limited cardiopulmonary reserve. Treatment may also reduce the degree of chronic residual pulmonary artery obstruction in patients who have a reduced ability to resolve pulmonary emboli. In addition, early complete lysis of deep leg vein thrombi has been shown to preserve function of venous valves [27,35] and hence may prevent serious late postphlebitic disability. These probable consequences of fibrinolytic therapy have made it an attractive form of treatment in some patients with thromboembolic disease.The presently used dosage schedules for streptokinase and urokinase treatment were derived from the fundamental and applied investigations of Fletcher, Alkjaersig and Sherry [1,9,10] and the work of Verstraete and his associates [2,47]. The use of these regimens has produced encouraging clinical results, but they have some possible disadvantages [24] and are not necessarily the most effective treatment schedules for producing thrombolysis. We have therefore evaluated another approach to achieving thrombolysis, the use of combinations of the anticoagulant drug, heparin, with various dosage schedules of the fibrinolytic agent, streptokinase.