PREVENTION OF ISCHEMIA-REPERFUSION LUNG INJURY BY INHALED NITRIC-OXIDE IN NEONATAL PIGLETS

Lung ischemia-reperfusion results in a decrease in the release of nitr ic oxide (NO) by the pulmonary endothelium. NO may have lung-protectiv e effects by decreasing neutrophil accumulation in the lung. We tested whether NO inhalation would attenuate reperfusion-induced endothelial dysfunction and increases in microvascular permeability and total pul monary vascular resistance (RT) by preventing neutrophil lung accumula tion. After baseline determinations of RT, coefficient of filtration ( K-fc), and circulating neutrophil counts, isolated neonatal piglet lun gs were subjected to a l-h period of ischemia followed by a l-h period of blood reperfusion and reventilation with or without additon of NO (10 ppm). NO prevented reperfusion-induced increases in RT and K-fc, a s well as the decrease in circulating neutrophils. After reperfusion, increases in K-fc were correlated with decreases in circulating neutro phils. NO prevented reperfusion-induced decrease in endothelium-depend ent relaxation in precontracted pulmonary arterial rings. This demonst rates that inhaled NO prevents microvascular injury, endothelial dysfu nction, and pulmonary neutrophil accumulation in a neonatal piglet mod el of lung ischemia-reperfusion.