In vitro effects of mercury on platelet aggregation, thromboxane and vascular prostacyclin production.
Mercuric chloride [25-50 micrograms/ml platelet-rich plasma (PRP)] lowers the threshold concentration of arachidonic acid (AA) required for triggering rabbit platelet aggregation and causes a marked increase of thromboxane production. The metal, added as HgCl2, does not modify (50 micrograms/ml PRP) or block (100 micrograms/ml PRP) the platelet aggregation wave induced by a normal aggregating dose of AA. Whether or not AA-induced platelet aggregation takes place, a large increase in thromboxane production is observed. Methyl mercury, assayed as reference drug, induces platelet aggregation and a significant increase of thromboxane levels. Finally, HgCl2 and methyl mercury, in a concentration range of 0.125-0.5 micrograms/microliters in the incubation liquid, induce an increased prostacyclin release from rat aortic tissue.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001808:Blood Vessels / Q000187:drug effects* / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis*; D066298:In Vitro Techniques; D008627:Mercuric Chloride; D008628:Mercury / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects*; D011817:Rabbits; D013931:Thromboxanes / Q000097:blood*
D001095:Arachidonic Acids; D013931:Thromboxanes; D016718:Arachidonic Acid; D008627:Mercuric Chloride; D011464:Epoprostenol; D008628:Mercury