Increased sheep lung vascular permeability caused by Pseudomonas bacteremia

Abstract

In awake sheep, the responses of lung lymph flow and lymph and plasma protein concentrations were compared to steady state elevations of pulmonary vascular pressures made by inflating a left atrial balloon with those after an intravenous infusion of P. aeruginosa. Lymph flow increased when pressure was increased, but lymph plasma protein concentration ratios always fell and lymph protein flow (lymph flow X lymph protein concentration) increased only slightly. After Pseudomonas, sheep had transient chills, fever, leukopenia, hypoxemia, increased pulmonary artery pressure and lymph flow and decreased left atrial pressure and lymph protein concentration. 3-5 hr after Pseudomonas, when vascular pressures and lymph protein concentrations had returned to near base line, lymph flow increased further to 3-10 times base line and remained at a steady level for many hours. During this steady period, lymph plasma protein concentration ratios were similar to base line and lymph protein flow was higher than in the increased pressure studies. Two sheep died of pulmonary edema 7 and 9 hr after Pseudomonas, but in 16 studies, five other sheep appeared well during the period of highest lymph flow and all variables returned to base line in 24-72 hr. Six serial indicator dilution lung water studies in five sheep changed insignificantly from base line after Pseudomonas. Postmortem lung water was high in the two sheep dead of pulmonary edema and one other, but six sheep killed 1-6 hr after Pseudomonas had normal lung water. Because of the clear difference between the effects of increased pressure and Pseudomonas on lymph plasma protein concentration ratios and lymph protein flow, it is concluded that Pseudomonas causes a prolonged increase in lung vessel permeability to protein. Because lung lymph flow was seen as high as 10 times base line without pulmonary edema, it is concluded that lung lymphatics are a sensitive high capacity mechanism for removing excess filtered fluid. An equivalent pore model of sheep lung vessels suggests that the changes seen after Pseudomonas could result from small changes in the structure of exchanging vessel walls.