Platelet rich plasma transforms exogenous prostaglandin endoperoxide H2 into thromboxane A2.
Platelet rich plasma transforms exogenous prostaglandin endoperoxide H2 into thromboxane A2 immediately prior to the initiation of irreversible aggregation. Selective thromboxane synthetase inhibitors block thromboxane A2 formation and aggregation. Thromboxane A2 formation appears to be essential during arachidonate mediated aggregation. The results presented reconcile the previously accepted paradoxical behavior of thromboxane synthetase in platelet rich plasma toward the prostaglandin endoperoxide H2 substrate.
D001095:Arachidonic Acids / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism*; D006801:Humans; D011450:Prostaglandin Endoperoxides, Synthetic / Q000097:blood*; D011462:Prostaglandins G / Q000097:blood; D011463:Prostaglandins H / Q000097:blood; D013928:Thromboxane A2 / Q000096:biosynthesis* / Q000097:blood; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors; D013931:Thromboxanes / Q000096:biosynthesis*
D001095:Arachidonic Acids; D011450:Prostaglandin Endoperoxides, Synthetic; D011462:Prostaglandins G; D011463:Prostaglandins H; D013931:Thromboxanes; D013928:Thromboxane A2; D013930:Thromboxane-A Synthase