Platelets and arachidonic acid derivatives in myocardial ischemia in animal models.
The accumulated evidence indicates that myocardial ischemia is a complex process involving dysfunction of various cellular elements as well as coronary narrowing. A homeostatic imbalance of endogenously produced vasoactive compounds, released locally as a result of intricate platelet, neutrophil, and endothelial cell-cell interactions, participates in the eventual outcome of tissue ischemia. This imbalance is frequently caused by the formation of an intracoronary platelet thrombus. Therapeutic strategy aimed to modulate intrinsic eicosanoid biosynthesis and neutrophil platelet function may reduce ischemia and benefit patients with ischemic heart disease.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D001792:Blood Platelets / Q000502:physiology*; D002319:Cardiovascular System / Q000187:drug effects; D003324:Coronary Artery Disease / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000187:drug effects; D007962:Leukocytes / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D011453:Prostaglandins / Q000378:metabolism / Q000494:pharmacology; D013189:SRS-A / Q000494:pharmacology / Q000502:physiology
D001095:Arachidonic Acids; D011453:Prostaglandins; D013189:SRS-A; D016718:Arachidonic Acid