While both acute and chronic hypoxia increase the expression of COX-2 in the lung [42], insights regarding the role of COX-2 activity in pulmonary hypertension and pulmonary hypertensive vascular remodeling can now be gained by comparing the reported eicosanoid metabolic profiles and hemodynamic data of monocrotaline and chronic hypoxia-induced PH in COX-2 KO mice [25,26] with the data obtained in the present study in the SuHx model of severe PAH and COX-2 inhibitor treated SuHx rats. This evidence concerns the gene PTGS2 and pulmonary hypertension.