K. Okabayashi et al., INHALED NITRIC-OXIDE IMPROVES LUNG ALLOGRAFT FUNCTION AFTER PROLONGEDSTORAGE, Journal of thoracic and cardiovascular surgery, 112(2), 1996, pp. 293-299
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).