Venous thrombosis (VT) and its sequelae, pulmonary embolism (PE) are significant national healthcare concerns. Thrombus and vessel wall damage promotes the up-regulation of adhesion molecules, tissue factor (TF), and inflammatory mediators in vivo. Utilizing animal models, my laboratory and others have defined the contribution that adhesion molecules, TF, and cytokines play during thrombosis. Recent research suggests that hypoxic and chemical injury to vascular endothelium contributes to the pathogenesis of several cardiovascular diseases. My research evaluates the effects venous endothelium dysfunction post oxidative injury. Our goal is to define the role of oxidative injury in the pathogenesis of venous thrombosis.