Abstract
Prostacyclins in PAH - Pathobiological Rationale Endothelial dysfunction is the cornerstone event in the pathobiology of pulmonary arterial hypertension (PAH), a rapidly evolving clinical syndrome of dyspnoea and fatigue eventually leading to right ventricular failure and death.1 In the pulmonary vascular bed, endothelial cells are the major source of mediators modulating pulmonary vascular tone, platelet aggregation and muscular cell growth. These mediators include endothelin-1 (ET-1), nitric oxide (NO) and prostacyclin (PGI2).
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