VASCULAR-PERMEABILITY AND EPITHELIAL TRANSPORT EFFECTS ON LUNG EDEMA FORMATION IN ISCHEMIA AND REPERFUSION

To determine the role of various Na+ transport systems in the edema fl uid accumulation after ischemia and reperfusion in the lung, we evalua ted the effect of amiloride (a Na+ channel blocker), ouabain (a Na+-K-adenosinetriphosphatase blocker), and phloridzin (a Na+-glucose cotra nsport blocker) in isolated rat lungs. Ischemia and reperfusion (I/R) significantly increased the edema accumulation, with the wet-to-dry we ight ratios increasing to 10.14 +/- 0.58 from 6.03 +/- 0.05 in control lungs (P < 0.04). Amiloride significantly augmented the amount of ede ma 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 endothel ial 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 ac tive Na+ absorption transport system, are very important in opposing e dema fluid accumulation in rat lungs subjected to I/R injury and opera te as an edema safety factor. However, if the endothelial damage assoc iated with I/R is allowed to persist, then the transport processes, ev en if operative, are insufficient to prevent continuous edema accumula tion.