Activation of thrombotic processes contributes to microvascular dysfunction in a variety of disease states such as sepsis and ischemia-reperfusion. Statins inhibit platelet activity by several mechanisms, including increased endothelial NO and adenosine release and decreased platelet thromboxane production and cholesterol content. Tissue factor expression and activity in response to thrombin is reduced in EC by simvastatin at concentrations as low as 100 nM. The fibrinolytic system may also be favorably affected by statins. An increase in tissue plasminogen activator and a decrease in plasminogen activator inhibitor type I in EC in response to statins have been demonstrated, but these effects require fairly high concentrations and human studies have been inconsistent.
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