Prostaglandin E1 and nitroglycerin reduce pulmonary capillary pressure but worsen ventilation-perfusion distributions in patients with adult respiratory distress syndrome.

Pulmonary artery hypertension associated with adult respiratory distress syndrome (ARDS) may increase microvascular filtration pressure by increasing pulmonary capillary pressure (PCP). To evaluate the potential to reverse this consequence of pulmonary artery hypertension, the effects of short-term vasodilator treatment were compared with prostaglandin E1 (PGE1) or nitroglycerin (NTG) on pulmonary hemodynamics and gas exchange. The two vasodilators were infused in ten patients with mild or moderate ARDS at a dosage rate achieving a 20% reduction of the mean arterial pressure. PCP was estimated by graphic analysis of the pulmonary artery occlusion curve, and continuous ventilation-perfusion (VA/Q) distributions were assessed using the multiple inert gas technique. At the given dosages both drugs induced equivalent reductions of the mean pulmonary artery pressure (PAP) from 28.2 +/- 3.6 to 23.7 +/- 3.2 with PGE1 and to 23.4 +/- 3.2 mmHg with NTG. The right atrial and pulmonary artery wedge pressure (PAWP) were also decreased to the same extent associated with the expected decrease in PCP from 17.4 +/- 2.6 to 15.1 +/- 3.3 with PGE1 and to 15.6 +/- 2.7 mmHg with NTG. The estimated PCP values were closely correlated with the values calculated according to Gaar's equation (r = 0.822. n = 23, P less than 0.001) with a regression close to the identity line. The contribution of pulmonary venous resistances to the resistance of the whole pulmonary vascular bed computed as the ratio (PCP- PAWP)/(PAP-PAWP) was 0.28 and remained unchanged during vasodilator infusion.(ABSTRACT TRUNCATED AT 250 WORDS)