This research project will permit a continuation of studies of the contributions of prostaglandins and other bioactive agents to the cardiopulmonary changes that occur in association with acute pulmonary embolism. During the next year the changes in prostaglandin E2(PGE2) and prostaglandin F2 alpha (PGF2 alpha) will be quantitated and the effects of prostacyclin and thromboxane inhibitors on PGE2 and PGF2 alpha production and on the cardiopulmonary changes will be evaluate. The project will also permit a continuation of the studies of the hazards of autotransfusion. Special emphasis has been placed upon changes in the coagulation and fibrinolytic mechanisms and upon red cell and platelet survival. The effects of tissue blood interfaces upon the autotransfusion process is being studied. Special emphasis during the next year will be directed to the effects of the fibrinolytic activators of mesothelial surfaces upon the coagulation and fibrinolytic parameters of the reinfused blood. Studies will begin to evaluate the role of indium labeled platelets (111 In) in detecting in vivo thromboses and pulmonary emboli in animals. The long-term goals of the research are to find ways to reduce the severity of the cardiopulmonary changes of acute pulmonary embolism and to eliminate some of the hazards of autotransfusions.