Permeability edema in dog lung depleted of blood components.

We perfused the isolated dog lung lobe with a 6% dextran (mol wt 60,000-90,000) balanced salt solution to determine the importance of blood components in lung fluid balance following injury with oleic acid (OA). The ventilated lower left lobe (LLL) was perfused at constant vascular pressure and weighed continuously as an index of transvascular fluid exchange. Each LLL was washed out with at least 600 ml of perfusate before recirculation started. All LLLs perfused with 6% dextran ion solution (group I) rapidly developed a permeability edema. The addition of 10% serum (vol/vol) from the lobe donor to the 6% dextran ion solution greatly improved LLL stability. One group of dextran-serum perfused LLLs (group II, n = 6, control) was infused with 2.0 ml normal saline; a second group (group III; n = 5) was given 45 microliters/kg body wt OA. Group II showed a linear rate of weight gain that averaged 7.9 g X h-1 X 100 g-1 over 3 h compared with an average rate of 249 g X h-1 X 100 g-1 in group III. In contrast to no change in group II, group III exhibited a decline in PO2 (P less than 0.05), and lobar compliance (P less than 0.05) and airway fluid was evident in all lobes by 0.5 h after infusion. The wet-to-dry weight ratio was higher in group III than group II. In the near absence of blood, massive edema developed rapidly following OA. Thus normal blood components, such as platelets, leukocytes, and fibrin do not appear to be essential mediators of OA-induced permeability edema. OA appears to increase vascular permeability either by injuring the lung directly or by releasing mediators endogenous to lung tissue.