Roles of serotonin in glass-bead pulmonary microemboli

Abstract

We investigated the role of serotonin release from aggregating platelets in glass-bead microemboli on isolated perfused rabbit lungs. The perfusion was performed at 70 ml/min with a roller pump. The temperature of the perfusion circuit was maintained at 37 +/- 1 degrees C by means of a heat exchanger. 100 microns-diameter glass beads (1 g) were infused via the main pulmonary artery. We examined the concentration of serotonin and the number of platelets in the perfusate and the mean pulmonary arterial pressure before and after glass bead embolization. Administration of PRP (platelet-rich plasma) to the perfusate caused the concentration of serotonin to significantly increase after microembolization. Specific serotonin S2 receptor antagonist (DV-7028) inhibited the increase of serotonin concentration in the perfusate, platelet aggregation, and vasoconstriction. We concluded that in the glass-bead embolization model, serotonin was released from aggregating platelets surrounding the glass beads, and constricted pulmonary microvessels via serotonin S2 receptors on the vascular smooth muscles cells.