The effect of the beta-agonist, ritodrine HCl, was studied on cardiac output (CO) and pulmonary lymph flow (QL) in sheep. Increased CO is associated with an increase in pulmonary QL in sheep during exercise. Isoproterenol increases CO but has not been shown to increase pulmonary QL. Ritodrine HCl was chosen because of its association with pulmonary edema when used to halt premature labor in pregnant women. Unanesthetized sheep received an intravenous infusion of ritodrine in increasing doses over 4 h up to a maximum of 6.3 micrograms/kg/min. Pulmonary pressure increased 2 mmHg after 1 h and returned to baseline by hours 3 and 4 with no change in left atrial pressure or lymph to plasma protein ratio. Pulmonary QL increased by 61% and CO by 80% at hour 3 of infusion (ritodrine dose 5.4 micrograms/kg/min) and remained at this level. Pulmonary QL and CO (normalized to baseline) correlated, r = 0.72, p less than 0.001, but there was no correlation between pulmonary QL and calculated microvascular pressure. Although an increase in pulmonary microvascular endothelium permeability with concurrent pulmonary vasodilation can not be completely ruled out, it appears from this study that beta-agonist therapy with ritodrine increases pulmonary QL by a CO related recruitment of microvessels.