Fm. Wagner et al., In-vivo measurement of free radicals - A new technique for direct analysisof reperfusion mechanism after lung ischemia, LANG ARCH S, 1999, pp. 691-696
Introduction: Increased oxygen free radical (OFR) production with disruptio
n of vascular and parenchymal homeostasis is assumed to cause reperfusion i
njury after lung transplantation. Up to now direct measurement of this reac
tion in an in vivo model has not been introduced. In an in vivo pig model o
f warm pulmonary ischemia followed by reperfusion levels of OFR, NO and per
oxidation of serum lipids were determined by chemiluminescent measurements
(CM).
Methods: After anesthesia ventilated animals underwent left lateral thoraco
tomy and dissection of the left pulmonary hilum. Two groups were studied: i
n Group I (n = 6) left lung warm ischemia was maintained for 90 min after c
lamping of the hilum and flushing of the PA with ringers lactate followed b
y a 4 hour reperfusion period. In Group II (control; n = 6) animals underwe
nt surgery without clamping. Hemodynamics and gas exchange were assessed du
ring the whole study period. CM measurements were performed in whole blood
samples taken hourly from the pulmonary artery and left atrium.
Results: All animals in group I showed a statistically significant decrease
in Pa O-2 and developed a variant degree of pulmonary edema during reperfu
sion. In this group two peaks of OFR production were observed: one at 2 hou
rs after hilum dissection, followed by second peak that occurred 120 to 180
min after initiation of reperfusion. 30 to 60 min after these time points
an increase of lipid peroxidation of HDL/LDL as well as of NO production wa
s measured. In the control group no changes of lipid peroxidation and NO le
vels occurred, however, one similar first peak of OFR was observed.
Conclusion: We conclude that reliable detection of OFR activity, subsequent
lipid peroxidation and NO production as a result of pulmonary reperfusion
injury in an in vivo model is feasible and should allow further analysis of
the pathophysiology of reperfusion injury after lung transplantation. Alth
ough surgery alone seems to induce production of OFR.