Thromboxane, prostacyclin, and leukotrienes in cerebral ischemia.
Our understanding of the biochemistry and biologic actions of AA metabolites has been greatly expanded in recent years. The discoveries of TXA2, PGI2, and LTs have fostered new concepts of the pathophysiology of cerebral ischemia. New approaches to treatment of ischemia include seeking an optimal dose of aspirin, developing drugs that selectively inhibit or antagonize TXA2 or LTs, and administering PGI2 or its analogues. Altering the dietary content of essential fatty acids for prophylaxis is also being studied. Though the results of this thrust are still preliminary, the exploration of these therapeutic strategies in cerebrovascular disorders based on further understanding of the pathophysiologic roles of TXA2, PGI2, LTs and probably other AA metabolites is anticipated with some optimism.
D001792:Blood Platelets / Q000378:metabolism; D004032:Diet; D011464:Epoprostenol / Q000378:metabolism* / Q000627:therapeutic use; D007213:Indomethacin / Q000627:therapeutic use; D002546:Ischemic Attack, Transient / Q000188:drug therapy / Q000378:metabolism*; D007975:Leukotriene B4 / Q000378:metabolism*; D013189:SRS-A / Q000378:metabolism; D013928:Thromboxane A2 / Q000096:biosynthesis / Q000378:metabolism*; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism
D013189:SRS-A; D007975:Leukotriene B4; D013928:Thromboxane A2; D011464:Epoprostenol; D013930:Thromboxane-A Synthase; D007213:Indomethacin