Journal of Applied Physiology, Vol 67, Issue 2 528-533, Copyright © 1989 by American Physiological Society
Lack of alveolar O2 during lung reperfusion does not decrease edema formation
P. T. Overand, M. J. Bishop, B. L. Eisenstein, E. Y. Chi, M. Su and F. W. Cheney
Department of Anesthesiology, University of Washington School of Medicine, Seattle 98195.
We previously reported that pulmonary arterial occlusion for 48 h followed
by 4 h of reperfusion in awake dogs results in marked edema and
inflammatory infiltrates in both reperfused and contralateral lungs (Am.
Rev. Respir. Dis. 134: 752-756, 1986; J. Appl. Physiol. 63: 942-950, 1987).
In this experiment we study the effects of alveolar hypoxia on this injury.
Anesthetized dogs underwent thoracotomy and occlusion of the left pulmonary
artery. Twenty-four hours later the dogs were reanesthetized, and a
double-lumen endotracheal tube was placed. The right lung was continuously
ventilated with an inspiratory O2 fraction (FIO2) of 0.35. In seven study
animals the left lung was ventilated with an FIO2 of 0 for 3 h after the
left pulmonary artery occluder was removed. In six control animals the left
lung was ventilated with an FIO2 of 0.35 during the same reperfusion
period. Postmortem bloodless wet-to-dry weight ratios were 5.87 +/- 0.20
for the left lower lobe and 5.32 +/- 0.12 for the right lower lobe in the
dogs with hypoxic ventilation (P less than 0.05 for right vs. left lobes).
These values were not significantly different from the control dog lung
values of 5.94 +/- 0.22 for the left lower lobe and 5.11 +/- 0.07 for the
right lower lobe (P less than 0.05 for right vs. left lobes). All values
were significantly higher than our laboratory normal of 4.71 +/- 0.06. We
conclude that reperfusion injury is unaffected by alveolar hypoxia during
the reperfusion phase.
