Platelet Adherence to Thromboemboli in Relation to the Pathogenesis and Treatment of Pulmonary Embolism

THE mechanisms by which pulmonary thromboemboli produce pulmonary hypertension, increased airway resistance, pulmonary edema and even sudden death have not been satisfactorily explained solely by mechanical obstruction of the pulmonary vasculature. The existence of reflex or humoral pathways has been invoked to explain some of these events.1 In a recent study the release of fresh, autologous stasis thrombi to the lungs of dogs was shown to induce rapid development of airway constriction.2 Similar changes were also produced in dogs by platelet microemboli formed by the administration of bacterial endotoxin.3 In both sets of experiments the acute physiologic responses to emboli . . .