Prostaglandins and prostaglandin inhibitors in ischemic heart disease.
The evidence for a role of the prostaglandin system in myocardial ischemia and its consequences is still fragmentary. We review the factors that alter the relation between thromboxane A2 and prostacyclin production such that vasoconstriction, platelet aggregation, and the tendency toward thrombus formation are increased. Strategies to prevent platelet aggregation by interfering with the production of thromboxane A2 or by stimulation or administration of prostacyclin are currently under investigation in a number of centers. The ubiquity of the prostaglandin system and our incomplete understanding make careful long-term clinical trials and observations essential if we are to be sure that the net effect of these attempts is beneficial.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects; D001808:Blood Vessels / Q000187:drug effects; D003327:Coronary Disease / Q000178:diet therapy / Q000188:drug therapy* / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors; D011464:Epoprostenol / Q000502:physiology; D006801:Humans; D010741:Phospholipases A / Q000037:antagonists & inhibitors; D011448:Prostaglandin Antagonists / Q000627:therapeutic use*; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology; D013928:Thromboxane A2 / Q000502:physiology; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors
D016861:Cyclooxygenase Inhibitors; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011458:Prostaglandins E; D013928:Thromboxane A2; D011464:Epoprostenol; D010741:Phospholipases A; D013930:Thromboxane-A Synthase