The role of serotonin in thrombogenesis.

摘要: Serotonin, a weak activator on its own, elicits strong platelet reactions (aggregation, arachidonate metabolization, release reaction) through amplification. Such amplification operates via 5-HT2-serotonergic receptors which are linked to the turnover of polyphosphoinositides and increases intracellular [Ca2+]i concentrations as signal transducing systems. In experimental animals, selective blockade eliminates arterial thrombus formation over sites endothelial injury in stenosed canine coronaries; combination with manipulation TXA2, it prevents coronary thrombotic reocclusion after fibrinolysis rt-PA, inhibits drastic activation, elicited by injections collagen vivo. These observations suggest that serotonergic substantially contributes aggregation platelets damaged vessels offers perspectives for an improved antithrombotic approach.