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In platelets, arachidonic acid is converted by cyclo-oxygenases in prostaglandins G2 and H2 - PG2 and PGH2. Thromboxane synthetase converts these into thromboxane A2 - TXA2. TXA2 is a potent aggregator and vasoconstrictor.
However, in endothelial cells, PGH2 is instead converted to prostacyclin I2 - PGI2. PGI2 has exactly the opposite effects to TXA2.
The production of PGI2 may be one means of temporally and spatially limiting the extent of the thrombus. The balance between PGI2 and TXA2 may be involved in atherosclerosis and is the modulated by aspirin.
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