EFFECTS OF NITRIC-OXIDE INHALATION ON PULMONARY SERIAL VASCULAR RESISTANCES IN ARDS

The pulmonary vasculature site of action of nitric oxide (NO) in patie nts with acute respiratory distress syndrome (ARDS) is still unknown. Seven patients were studied during the early stage of ARDS. The bedsid e pulmonary artery single-occlusion technique, which allows estimation of the pulmonary capillary pressure (Pcap) and segmental pulmonary va scular resistance, was used without NO or with increasing inhaled NO c oncentrations (15 and 25 parts per million [ppm]). Systemic circulator y parameters remained unaltered during 15 ppm NO inhalation, whereas 2 5 ppm NO inhalation slightly decreased mean systemic arterial pressure from 76.7 +/- 5.1 (mean +/- SEM) to 69 +/- 5.2 mm Hg (p < 0.01). Mean pulmonary arterial pressure (Ppam) and mean pulmonary capillary press ure (Pcapm) fell during 25 ppm NO inhalation from 27.4 +/- 3.5 to 21 /- 2.2 mm Hg (p < 0.001) and from 14.8 +/- 1.5 to 10.7 +/- 1.4 mm Hg ( p < 0.001) respectively, the total pulmonary resistance decreased by 2 8% (p < 0.01). The resistance of the capillary-venous compartment fell during 25 ppm NO inhalation from 100 +/- 16 to 47 +/- 16 dyn . s . m .(2) . cm(-5) (p < 0.01), whereas the pulmonary arterial resistance wa s unchanged. In these patients NO inhalation during the early stage of ARDS reduces selectively Ppam and Pcapm by decreasing the pulmonary c apillary-venous resistance. This latter effect may reduce the filtrati on through the capillary bed and hence alveolar edema during ARDS.