The impact of deletion of the prostacyclin receptor on the thrombotic (left panel) and proliferative (right panel) response to catheter-induced carotid vascular injury in mice. The endothelium of the common carotid artery was denuded in this model using a fine wire. This activates platelets, as reflected by an enhanced biosynthesis of thromboxane (Tx) A₂ (left panel), and causes neointimal formation, which can be quantified on histological crossections two weeks after the procedure (right panel). The procedure-related platelet activation and thromboxane biosynthesis, as reflected by urinary excretion of its metabolite 2,3 dinor TxB₂, was augmented in mice deficient for the prostacyclin receptor (IP). Deletion of the thromboxane receptor (TP) reduced the procedure-related increment in thromboxane biosynthesis. Simultaneous deletion of both receptors (IPTP) compensated for the effects of the individual receptors.

Redrawn with permission from Cheng Y, Austin SC, Rocca B, et al. Role of prostacyclin in the cardiovascular response to thromboxane A₂.