An Imbalance between the Excretion of Thromboxane and Prostacyclin Metabolites in Pulmonary Hypertension

THE pathogenesis of pulmonary hypertension is incompletely understood. The histologic features of the small pulmonary arteries of patients with this disease suggest that the coagulation system on the endothelial surface may be activated as either a primary or a secondary process. 1 2 3 4 5 6 Vasoconstriction is a variable feature of pulmonary hypertension; some patients, but not all, respond to vasodilator drugs with a substantial reduction in pulmonary vascular resistance and pressure. 7 8 9 10 Thromboxane A 2 is both a potent pulmonary vasoconstrictor and a procoagulant, whereas prostacyclin has opposing effects, and an imbalance between the release of these two mediators could be involved in the . . .