Prostaglandins in myocardial: with emphasis on myocardial preservation.
Various therapies during early hours of acute myocardial infarction (AMI) have been suggested to protect ischemic myocardium and reduce infarct size. Despite reports that prostaglandins (PGs) are released during myocardial ischemia, and that prostacyclin (PGI2) and thromboxane A2 (TXA2) have opposing effects on vasomotion and platelet aggregation, the physiologic roles of PGs, PGI2 and TXA2 in AMI have not been clearly defined. However, in pharmacologic doses, experimental evidence suggests that vasodilator PGs might be beneficial, and vasoconstrictor PGs might be deleterious, in AMI. Recent recognition that coronary spasm is frequent in AMI has led to the notion that an increased PGI2/TXA2 ratio might be desirable. Thus, exogenous PGE1, exogenous PGI2 or tis more stable analogs, drugs that stimulate PGI2 release, and inhibitors of TXA2 and harmful PGs are potential agents for protective therapy in AMI.
D000527:Alprostadil; D000818:Animals; D004285:Dogs; D011464:Epoprostenol / Q000627:therapeutic use; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000627:therapeutic use; D011465:Prostaglandins, Synthetic / Q000627:therapeutic use*; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000187:drug effects
D011453:Prostaglandins; D011458:Prostaglandins E; D011465:Prostaglandins, Synthetic; D013928:Thromboxane A2; D011464:Epoprostenol; D000527:Alprostadil