ABSTRACT
Initially described by Moncada and Vane in 1976, prostacyclin (epoprostenol, PGI2) is a member of the prostacylin family produced by the vascular endothelial cells (1,2). PGI2 is a major metabolite of arachidonic acid formed via the cyclooxygenase pathway, and is a potent vasodilator of both the pulmonary and systemic vascular beds, as well as an inhibitor of platelet aggregation (1,2). Chronically, PGI2 has antiproliferative effects and has been shown in vitro to inhibit smooth muscle cell growth (3). PGI2 may also have positive inotropic effects, although this is controversial. Interest in the use of PGI2 as a treatment for pulmonary arterial hypertension (PAH) commenced in the early 1980s, even before the recognition of the relative imbalance between vasodilating and vasoconstricting prostacyclin metabolites in this population (4,5). Several smaller observations during the 1980s paved the way for the landmark trials that established the role of prostanoids for PAH.
