NITRIC-OXIDE AND PROSTACYCLIN AS TEST AGENTS OF VASOREACTIVITY IN SEVERE PRECAPILLARY PULMONARY-HYPERTENSION - PREDICTIVE ABILITY AND CONSEQUENCES ON HEMODYNAMICS AND GAS-EXCHANGE

Background - In patients with primary pulmonary hypertension who respo nd to vasodilators acutely, survival can be improved by the long term use of calcium blockers. However, testing for response with calcium ch annel blockers or prostacyclin (PGI(2)) may cause hypotension and adve rsely affect gas exchange. Nitric oxide (NO), which does not have thes e effects, could be a better test agent.Methods - NO (10, 20, and 40 p pm for 15 minutes), PGI(2) (1- > 10 ng/kg/min), and oral nifedipine (1 0 mg, then 20 mg/h) were administered sequentially to 10 patients afte r determination of the 24 hour spontaneous variability of their pulmon ary and systemic mean arterial pressures. Patients were considered res ponders if the mean pulmonary artery pressure or pulmonary vascular re sistance decreased by 20% or more. Results - Six patients (60%) respon ded to all three agents, and three to none of the agents. One patient responded to PGI(2) only. In those who responded to vasodilators, NO h ad no major effect on gas exchange or systemic haemodynamics, while PG I(2) and nifedipine both induced systemic hypotension (mean (SD) syste mic arterial pressure 72 (14) versus 89 (19) mm Hg with PGI(2) and 72 (15) versus 86 (17) mm Hg with nifedipine, p < 0.05) and hypoxaemia (P aO2 8.7 (1.4) versus 10.8 (1.0) kPa with PGI(2) and 8.6 (1.4) versus 1 0.2 (1.5) kPa with nifedipine, p < 0.05) and increased venous admixtur e (28 (9) versus 14 (4)% with PGI(2) and 22 (9) versus 13 (5)% with ni fedipine, p < 0.05). Conclusions - NO inhalation can accurately predic t a vasodilator response to nifedipine in patients with severe pulmona ry hypertension without adverse effects on systemic haemodynamics and gas exchange. This absence of side effects may make it a more appropri ate agent for testing the vasodilator response.