RECOVERY FROM INCREASED PRESSURE OR INCREASED LEAKINESS EDEMA IN PERFUSED SHEEP LUNGS

Two routes by which interstitial pulmonary edema liquid may leave the lung during recovery are reabsorption into the pulmonary circulation a nd clearance by lung lymphatics. We hypothesized that reabsorption of edema liquid of low protein concentration into the pulmonary circulati on would be greater than reabsorption of edema liquid of high protein concentration because of the greater protein osmotic gradient in the f ormer. On the basis of previous studies, lymph flow should contribute minimally to the recovery. In 22 in situ perfused sheep lungs with lym ph fistulas, we produced similar to 100 g of osmotic or hydrostatic ed ema (low protein) or increased leakiness edema by calcium depletion (h igh protein). To induce reabsorption, we changed the perfusate from lo w- (1% albumin, osmotic pressure = 4 cmH(2)O) to high-protein (7% albu min, osmotic pressure = 22 cmH(2)O) solution in the osmotic group, dec reased capillary pressure from 29 +/- 9 to 11 +/- 6 cmH(2)O in the hyd rostatic group, or reversed leakiness by adding CaCl2 to the perfusate in the increased leakiness group. Reabsorption occurred only during r ecovery from osmotic (40 +/- 22% of filtered liquid) and hydrostatic ( 15 +/- 11%) edema. Total lung lymph flow during recovery from osmotic, hydrostatic, or increased leakiness edema was 4.9 +/- 3.4, 4.3 +/- 3. 4, or 3.5 +/- 1.9 g, respectively. We conclude that during recovery fr om pulmonary edema interstitial liquid is reabsorbed into the circulat ion in inverse proportion to its protein concentration. We confirm tha t only a small fraction of the interstitial edema liquid is cleared by the lymphatics during recovery from any type of edema.