The authors investigated the effect of prostaglandin F2αinfused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, Pao2was 327±15 mmHg (mean±SD) and venous admixture (Q±sp/Q1) was 11±3%. One-lung atelectasis reduced Pao2to 91±12 mmHg and increased Q±sp/Qtto 40±4%. Prostaglandin F2αin doses of 0.4, 0.6, 1.2, and 1.8 μg ± kg−1· min−1was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 μg · kg−1· min−1there was a dose-dependent reduction in Q·sp/Qtto a minimum of 25±4% and an increase in Pao2to 168±25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 μg · kg−1· min−1decreased Pao2to 156±32 mmHg and increased Q±sp/Qtto 32±9%. Increased systemic effects of prostaglandin F2αwere observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.