We have previously shown that the pulmonary venoconstriction produced by a stable thromboxane A 2 analogue (STAJ is attenuated by prostacyclin (PGIi), but PGI, increases the STA 2 -induced edema. The present study was designed to determine the effects of STA 2 and PGI 2 on the fluid balance in isolated blood-perfused newborn lamb lungs. Vascular permeability was evaluated by use of the fluid filtration coefficient (Kf) and the osmotic reflection coefficient for total proteins (cr,

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... tein double indicator technique), and pulmonary capillary pressure (Pc) was estimated by the double occlusion technique. All lungs had a period of hydrostatic stress induced by elevation of the left atriai pressure from 5 to 20 mm Hg to promote fluid filtration, and the rate of lung weight gain (AW/AT) during this period was determined. Studies were made in four groups; before the hydrostatic stress, lungs were given 1) STA 2 (50 /*g, n=6), 2) PGI 2 (0.4 /ig/kg/min, n = 6), 3) both PGI 2 and STA 2 (n=6), or 4) vehicles (control, n=5). Measurements of Kf were made at the baseline period and after the hydrostatic stress. Kf was significantly increased by 76% with STA 2 , by 121% with PGI 2 , and by 157% with both PGI 2 and STAj, but remained constant in controls. In comparison with control lungs, a similar AW/AT was observed with less of an increase in Pc during the hydrostatic stress in the STA 2 group, and greater values of AW/AT were obtained with smaller elevations in Pc in the groups receiving PGI 2 or both PGI 2 and STA 2 . The <r of 0.66 ±0.07 in the control group was the highest in these experiments. Treatments with STA 2 and/or PGIj significantly decreased <T. These results suggest that both STA 2 and PGI 2 may increase pulmonary microvascular permeability to protein. Furthermore, PGI 2 may increase fluid filtration by increasing vascular surface area.