In vitro effects of mercury on platelet aggregation, thromboxane and vascular prostacyclin production

Arch Toxicol Suppl. 1983:6:48-51. doi: 10.1007/978-3-642-69083-9_8.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arachidonic Acid
  • Arachidonic Acids / metabolism
  • Blood Vessels / drug effects*
  • Blood Vessels / metabolism
  • Epoprostenol / biosynthesis*
  • In Vitro Techniques
  • Mercuric Chloride
  • Mercury / pharmacology*
  • Platelet Aggregation / drug effects*
  • Rabbits
  • Thromboxanes / blood*

Substances

  • Arachidonic Acids
  • Thromboxanes
  • Arachidonic Acid
  • Mercuric Chloride
  • Epoprostenol
  • Mercury