Improved oxygenation with prostaglandin F_2α with and without inhaled nitric oxide in dogs

Dogs of mixed breed ( n = 7) were anesthetized, right lung atelectasis was established, and the cyclooxygenase pathway was blocked with ibuprofen. Measurements of pulmonary gas exchange were performed (fractional concentration of inspired O2 = 0.95) after infusions of prostaglandin F2α(PGF2α; 2 μg ⋅ kg−1 ⋅ min−1), ventilation with nitric oxide (NO; 40 ppm), or both (PGF2α + NO) in random order. The arterial [Formula: see text]([Formula: see text]) under control conditions was 117 ± 16 Torr (shunt = 33 ± 2.5%), was unchanged with NO alone ([Formula: see text] = 114 ± 17 Torr; shunt = 35.7 ± 3.1%), but was significantly improved with PGF2α alone ([Formula: see text] = 180 ± 28 Torr; shunt = 23.2 ± 2.8%) and with the combination of PGF2α + NO ([Formula: see text]= 202 ± 30 Torr; shunt = 20.9 ± 2.5%). The addition of NO did not significantly enhance the effectiveness of the PGF2α on[Formula: see text]. Simulation of these data in a computer model, combining pulmonary gas exchange and pulmonary blood flow, reproduced the results on the basis that vasoconstriction with PGF2αwas maximal under hypoxia in the atelectatic lung and reduced by hyperoxia in the ventilated lung, consistent with the hypothesis of O2 dependence of PGF2α vasoconstriction.