Inhaled nitric oxide and vasoconstrictors in acute respiratory distress syndrome

It has been suggested that the increase in Po-2 observed with nitric oxide (NO) should be enhanced by the addition of a vasoconstrictor agent. The vas oconstrictor used in combination with NO should mimic or enhance hypoxic va soconstriction. The aim of this study was to evaluate the respiratory and h emodynamic effects of norepinephrine (a nonspecific vasoconstrictor), almit rine bismesylate (a specific pulmonary vasoconstrictor), and inhaled NO, al one or together. During a 6-mo period, 16 patients presenting with ARDS wer e prospectively investigated. On inclusion, no patient was receiving cardio vasoactive drugs. The protocol consisted of seven consecutive phases: basel ine, norepinephrine (in order to obtain a 3 mm Hg rise in mean pulmonary ar terial pressure [(Ppa) over bar]), almitrine bismesylate (16 mu g/kg/min), inhaled NO (20 ppm delivered during inspiration), norepinephrine + inhaled NO, almitrine bismesylate + inhaled NO, almitrine bismesylate + norepinephr ine + inhaled NO. General factorial analysis of variance showed that inhale d NO and almitrine bismesylate increased oxygenation (p < 0.0001). Norepine phrine had no effect on oxygenation. A synergistic effect between inhaled N O and almitrine bismesylate was found (p < 0.05), whereas norepinephrine di d not affect the response to inhaled NO. Nitric oxide produced a significan t decrease in (Ppa) over bar and pulmonary vascular resistances (PVRI) (p < 0.0001). Both almitrine bismesylate and norepinephrine induced an increase in (Ppa) over bar (p < 0.0001). Norepinephrine increased PVRI (p < 0.002), whereas almitrine bismesylate had no effect on PVRI. The present results s upport the hypothesis that a selective pulmonary vasoconstrictor enhances t he increase in oxygenation induced by inhaled NO, whereas norepinephrine at tenuates this effect.