Serotonin can induce pulmonary hypertension, hypoxia and bronchoconstriction, and ketanserin has been shown to reverse these effects on various experimental models of acute respiratory failure. In the present study, the hemodynamic and gasometric effects of ketanserin were studied during acute respiratory failure induced by an air infusion at a rate of 10 ml/min in dogs. During a 60-min air infusion, 10 dogs received 4 mg of ketanserin i.v. and 10 dogs served as control. Ketanserin-treated dogs had similar pulmonary hypertension even though more significant decreases in arterial pressure and systemic vascular resistance characterized the systemic effects of ketanserin. Similarly, a marked increase in hematocrit observed in control dogs (from 36.9 to 43.8%, p < 0.01) was totally prevented by ketanserin (from 40.3 to 40.4%, NS). Hypoxia was similar, although the increase in pulmonary shunt was attenuated (259 instead of 468%). Therefore, the influence of serotonin is very limited in acute respiratory failure secondary to air embolization. Serotonin might have a more important influence on the systemic than on the pulmonary vasculature in these conditions.