Adenosine transport, erythrocyte deformability and microvascular dysfunction: an unrecognized potential role for dipyridamole therapy.
Reperfusion injury and no-reflow phenomenon are known entities that contribute to persistent impairment in myocardial perfusion and regional myocardial dysfunction following restoration of epicardial coronary blood flow after a myocardial infarction. Following prolonged ischemia, oxidative stress and inflammation-mediated alterations in erythrocyte mechanics and microvascular architecture play a major role in ischemia/reperfusion injury and no-reflow phenomenon. An increase in red cell rigidity is an important rheological aspect of RBCs, which facilitates platelet aggregation with the subendothelium. Dipyridamole inhibits the reuptake of adenosine which causes platelet inhibition and vasodilatation. Dipyridamole improves microvascular function by increasing RBC deformability and reducing blood viscosity. In addition, it has anti-oxidant and anti-inflammatory properties that provide protection to the microvasculature. This review discusses the potential role for dipyridamole therapy in the treatment of microvascular dysfunction.
Bhavsar
Jignesh
J
Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, MI, USA.
Rosenson
Robert S
RS
D000241:Adenosine / Q000493:pharmacokinetics* / Q000627:therapeutic use; D001809:Blood Viscosity / Q000187:drug effects; D004176:Dipyridamole / Q000494:pharmacology* / Q000627:therapeutic use; D004907:Erythrocyte Deformability / Q000187:drug effects / Q000502:physiology*; D004912:Erythrocytes / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000188:drug therapy*
D004176:Dipyridamole; D000241:Adenosine