INHALED NITRIC-OXIDE IMPROVES LUNG ALLOGRAFT FUNCTION AFTER PROLONGEDSTORAGE

Morbidity caused by early allograft dysfunction, manifested by a progr essive increase in pulmonary vascular resistance and a decrease in oxy genation, remains a serious problem in lung transplantation. Inhalatio n of nitric oxide, an essential homeostatic molecule, has been shown t o have beneficial effects on a variety of acute lung injuries, The pur pose of the present study was to investigate the effect of inhaled nit ric oxide on posttransplant function of canine left lung allografts, F ourteen dogs underwent left lung allotransplantation, Donors received systemic heparin and prostaglandin E(1) followed by pulmonary artery f lush with modified Euro-Collins solution, Donor left lungs were stored for 18 hours at 1 degrees C and subsequently implanted, Immediately a fter reperfusion, the contralateral right main pulmonary artery and br onchus were ligated, The chest was closed and recipients turned to the supine position for the 6-hour assessment period, Hemodynamic and art erial and venous blood gas analyses were made at 15-minute intervals a t an inspired oxygen fraction of 1.0 and 5 cm of water positive end-ex piratory pressure. Animals were killed at the end of the assessment. A llograft myeloperoxidase activity assays and wet/dry weight ratios wer e done, In group I (n = 5), nitric oxide gas was administered continuo usly at concentrations of 60 to 70 ppm before reperfusion and througho ut the 6-hour assessment period. In group II (n = 5), nitric oxide adm inistration was initiated at the same concentration after reperfusion injury had developed, Group HI animals (n = 4) received no nitric oxid e, Significant improvement in gas exchange was apparent in group I, At the end of the 6-hour assessment period, mean arterial oxygen tension was 253.8 +/- 44.7 mm Hg and 114.9 +/- 25.5 mm Hg in groups I and III , respectively (p < 0.05), Group n animals had no improvement in oxyge nation with nitric oxide, Systemic hemodynamics were unaffected by nit ric oxide. However, an immediate decrease in pulmonary vascular resist ance was noted, Group I myeloperoxidase activity was significantly low er than that in control group III (0.24 +/- 0.06 versus 0.36 +/- 0.04 units, respectively; p < 0.05).