Dipyridamole is a drug that inhibits thrombus formation when given chronically and causes vasodilation when given at high doses over short time. It inhibits the cellular reuptake of adenosine into platelets, red blood cells and endothelial cells leading to increased extracellular concentrations of adenosine. It also inhibits the enzyme adenosine deaminase which normally breaks down adenosine into inosine. This inhibition leads to further increased levels of extracellular adenosine. Dipyridamole also inhibits the enzyme phosphodiesterase- 5 (PDE 5) which normally breaks down cGMP. This results in added benefit when given together with NO or statins. Dipyridamole has shown to lower pulmonary hypertension without significant drop of systemic blood pressure Dipyridamole inhibits formation of pro-inflammatory cytokines (MCP-1, MMP-9) in vitro and results in reduction of hsCRP in patients. Dipyridamole inhibits proliferation of smooth muscle cells in vivo and has shown to prevent AV-shunt failure in dialysis patients. Dipyridamole increases release of t-PA from brain microvascular endothelial cells Dipyridamole treatment in vivo results in increase of 13 - HODE and decrease of 12 - HETE in the subendothelial matrix (SEM) and reduced thrombogenicity of the SEM. Dipyridamole pretreatment reduced reperfusion injury in volunteers. Dipyridamole treatment has shown to increase myocardial perfusion and left ventricular function in patients with ischemic cardiomyopathy. Dipyridamole treatment resulted in reduction of the number of thrombin and PECAM-1 receptors on platelets in stroke patients. Adenosine interacts with the adenosine receptors to cause increased cAMP via adenylate cyclase. cAMP impairs platelet aggregation and also causes arteriolar smooth muscle relaxation. Chronic therapy did not show significant drop of systemic blood pressure.