prostaglandin-h2 and methylmercuric-chloride

(1) When platelets form TXA2 from endogeneous AA, PGH2 reaches concentrations very similar to those of TXA2 and high enough to produce strong platelet activation. Therefore, platelet activation by TXA2 appears to go along with an activation by PGH2. (2) PGH2 is a more potent stimulus of platelet shape change and aggregation than U 46619. (3) The agonism of PGH2 is limited by the formation of inhibitory prostaglandins, especially PGD2 at higher concentrations. That is why thromboxane synthase inhibitors in PRP and at a physiological HSA concentration do not augment platelet activation. (4) HSA promotes the formation of inhibitory PGD2 at the expense of agonistic PGH2.

Topics: Blood Platelets; Humans; Imidazoles; In Vitro Techniques; Methylmercury Compounds; Platelet Aggregation; Prostaglandin Endoperoxides; Prostaglandin Endoperoxides, Synthetic; Prostaglandin H2; Prostaglandins H; Thrombin; Thromboxane A2; Thromboxane B2; Thromboxane-A Synthase