Lung resection mag be complicated by postpneumonectomy pulmonary oedema. Ox
idant generation following surgery-induced ischaemia-reperfusion may be res
ponsible.
This hypothesis was tested utilizing isolated, in situ, blood perfused rode
nt lungs subjected to continuous perfusion (control subjects); one lung ven
tilation followed by pneumonectomy (group 1); or one lung ventilation follo
wed by reinflation of the collapsed lung (group 2).
In control subjects, no significant changes in markers of oxidant damage, o
xygenation, pulmonary artery pressure or extravascular albumin extravasatio
n were detected. In group 1 lungs, hydroxyl radical-like damage was detecte
d in association with impaired oxygenation (p<0.05), and increased pulmonar
y artery pressure and extravascular albumin accumulation in both lungs. In
group 2, there,vas evidence of hydroxyl radical-like damage, and a fall in
oxygenation (p<0.05) occurred during one lung ventilation. There was a tran
sient rise in pulmonary artery pressure following lung reinflation and extr
a vascular albumin accumulation was significantly increased in both lungs (
right>left, p<0.05). Both changes were attenuated (p<0.05) following treatm
ent with the reactive oxygen species (ROS) scavenger superoxide dismutase (
group 2a) and the nitric oxide synthase inhibitor N-G-nitro-L-arginine meth
yl ester (group 2b). Hydroxyl radical-like damage was undetectable followin
g nitric oxide synthase inhibition.
Oxidant stress may contribute to the pathologies seen in this model of lung
injury.