NITRIC-OXIDE POTENTIATES ACUTE LUNG INJURY IN AN ISOLATED RABBIT LUNGMODEL

Background. The effect of inhaled nitric oxide (NO) treatment on pulmo nary function in the setting of adult respiratory distress syndrome is controversial. We examined the effect of inhaled NO on pulmonary func tion in an isolated rabbit lung model of oleic acid (OA)-induced acute lung injury. We hypothesized that NO would decrease pulmonary artery pressure and improve oxygenation. Methods. Rabbit heart-lung blocks we re isolated, flushed in vivo, harvested, and immediately perfused with whole blood and ventilated with 50% oxygen (O-2). Pulmonary artery pr essure was determined every 15 seconds for 60 minutes of perfusion. Ox ygenation was determined by blood gas analysis of pulmonary venous eff luent at 0, 20, 40, and 60 minutes after initiation of OA infusion. Ra bbits were randomized into four study groups: saline control; OA contr ol, which received a 20-minute infusion of 50% OA/ethanol solution; NO treatment (20 ppm NO inhaled before OA infusion); and NO control, whi ch underwent NO (20 ppm) pretreatment, followed by saline infusion. Pu lmonary artery pressure, oxygenation (arteriovenous O-2 difference), c ompliance, and wet/dry lung weight were determined. Results. Pretreatm ent with NO caused significant increases in pulmonary artery pressure (NO treatment versus NO control and saline control; no significant dif ference between NO treatment group and OA control group), and did not improve oxygenation in our model. Conclusions. Contrary to our hypothe sis, pretreatment with NO potentiates acute lung injury in our isolate d lung model. There was significant exacerbation of pulmonary hyperten sion and no improvement in oxygenation. Further investigation of the p ossible deleterious effects of NO in acute lung injury are needed, esp ecially in the early acute phases of this process. (C) 1998 by The Soc iety of Thoracic Surgeons.