Background. Nitric oxide (NO) is considered to be one of the endogenou
s inhibitory factors of ischemic reperfusion injury, In this study, th
e NO-producing ability of the preserved lung, flushed at various pulmo
nary artery pressures (flushing pressure), was studied during reperfus
ion using an ex vivo rabbit lung perfusion model. Methods. The lungs w
ere flushed with 200 mi of preservation solution with flushing pressur
es adjusted to 15, 15, 20, and 25 mmHg for groups 1, 2, 3, and 4, resp
ectively (n=5 in each group), In the control group (group 1), the hear
t-lung block was harvested after flushing and the lungs were assessed
without preservation, In the other groups, the harvested blocks were p
reserved at 8 degrees C for 24 hr and reperfused with homologous blood
for pulmonary functional assessment, Pulmonary function was assessed
by measuring mean airway pressure, mean pulmonary arterial pressure, p
artial oxygen tension of pulmonary venous effluent blood, and pulmonar
y wet-dry weight ratio, The sequential changes in the concentration of
NO-related substances (NO-RS) in the serum of reperfused blood were a
lso measured by chemiluminescence. Results. During reperfusion, biphas
ic increases in NO-RS were observed in all groups, In groups 3 and 4,
the increases in NO-RS were significantly lower than those of groups 1
and 2, and pulmonary function deteriorated. Conclusion. These data su
ggest that in order to maintain the endogenous NO-producing ability of
preserved lung, the flushing pressure must be less than 20 mmHg.