Inhaled prostacyclin reduces cardiopulmonary bypass–induced pulmonary endothelial dysfunction via increased cyclic adenosine monophosphate levels

Cardiopulmonary bypass triggers a systemic inflammatory response that alters pulmonary endothelial function, which can contribute to pulmonary hypertension. This study was designed to demonstrate that inhaled prostacyclin, a selective pulmonary vasodilator prostaglandin, prevents pulmonary arterial endothelial dysfunction induced by cardiopulmonary bypass.