Prostaglandin F2 alpha improves oxygen tension and reduces venous admixture during one-lung ventilation in anesthetized paralyzed dogs.

The authors investigated the effect of prostaglandin F2 alpha infused 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, PaO2 was 327 +/- 15 mmHg (mean +/- SD) and venous admixture (Qsp/Qt) was 11 +/- 3%. One-lung atelectasis reduced PaO2 to 91 +/- 12 mmHg and increased Qsp/Qt to 40 +/- 4%. Prostaglandin F2 alpha in doses of 0.4, 0.6, 1.2, and 1.8 micrograms X kg-1 X min-1 was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 micrograms X kg-1 X min-1 there was a dose-dependent reduction in Qsp/Qt to a minimum of 25 +/- 4% and an increase in PaO2 to 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 micrograms X kg-1 X min-1 decreased PaO2 to 156 +/- 32 mmHg and increased Qsp/Qt to 32 +/- 9%. Increased systemic effects of prostaglandin F2 alpha were 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.