To determine the role of various Na+ transport systems in the
edema fluid accumulation after
ischemia and reperfusion in the lung, we evaluated the effect of
amiloride (a Na+ channel blocker),
ouabain (a Na(+)-K(+)-
adenosinetriphosphatase blocker), and
phloridzin (a Na(+)-
glucose cotransport blocker) in isolated rat lungs.
Ischemia and reperfusion (I/R) significantly increased the
edema accumulation, with the wet-to-dry weight ratios increasing to 10.14 +/- 0.58 from 6.03 +/- 0.05 in control lungs (P < 0.04).
Amiloride significantly augmented the amount of
edema fluid (wet-to-dry weight ratio 12.26 +/- 0.77), and
ouabain further increased the amount of
edema (wet-to-dry weight ratio 18.58 +/- 1.00).
Phloridzin did not significantly affect
edema formation associated with I/R.
Isoproterenol decreased the amount of
edema formation in the presence and absence of
amiloride. This occurred because the endothelial permeability as assessed by filtration coefficient was restored to normal values and less
edema formed. The present study indicates that Na+ channels and Na(+)-K(+)-
adenosinetriphosphatase, components of the active Na+ absorption transport system, are very important in opposing
edema fluid accumulation in rat lungs subjected to I/R injury and operate as an
edema safety factor. However, if the endothelial damage associated with I/R is allowed to persist, then the transport processes, even if operative, are insufficient to prevent continuous
edema accumulation.