A B S T R A C T In awake sheep, we compared the responses of lung lymph flow and lymph and plasma protein concentrations to steady state elevations of pulmonary vascular pressures made by inflating a left atrial balloon with those after an intravenous infusion of 10W-10°Pseudomonas 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 presssure and lymph flow and decreased left atrial pressure and lymph protein concentration. 3-5 h 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 state 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 h 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 h. 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

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In 20 unanesthetized sheep, we measured lung lymph flow and lymph and plasma protein concentrations during steady-state base-line conditions and during steady-state elevations of pulmonary microvascular hydrostatic pressure (range 3 to 23 cm H2O). In every sheep there was a base-line lung lymph flow (average 5.7 +/- 2.5 (SD) ml/hour), demonstrating that net fluid filtration occurred. The base-line lymph-plasma total protein ratio averaged 0.69 +/- 0.05, indicating a high protein osmotic pressure in the interstitial fluid at the filtration site. Lymph flow increased and lymph protein concentration decreased approximately linearly whenever hydrostatic pressure rose. A new steady-state condition was reached in 1-2 hours. The difference in plasma-to-lymph protein osmotic pressure increased by half the hydrostatic pressure increment (50% negative feedback regulation). Extravascular lung water content, measured post-mortem, did not change significantly until microvascular hydrostatic pressure more than doubled, indicating a large safety factor that protects the lungs against fluid accumulation normally. The major contributions to the safety factor appeared to be a sensitive and efficient lymph pump coupled to a washout of interstitial protein. The fluid filtration coefficient, whose calculation required many assumptions, averaged 1.64 +/- 2.65 ml/(cm H2O times hour) in the base-line condition and did not change significantly over the pressure range studied.

SUMMARY We studied the effect of 10 cm H 2 O of continuous positive airway pressure breathing (CPAPB) on steady state lung fluid balance. In 9 of 20 chronically instrumented, unanesthetized sheep, we measured lung lymph flow, pulmonary vascular pressure, cardiac output, pleura! pressure, and lymph and plasma protein concentration during a 2-hour baseline period and 3-4 hours of CPAPB. In eight sheep, we measured the same variables after increasing average left atrial pressure by 18 cm H,O to cause mild interstitial edema. At the end of the final experiment, we anesthetized the sheep, removed the lungs, and measured their water content. During CPAPB, pleural and left atrial pressures increased by 5 cm H,O, whereas puhnonary artery pressure increased by 7-10 cm H 2 O. Lung lymph flow as well as lymph and plasma protein concentrations did not change significantly. In six sheep, postmortem lung water content was increased above that predicted but was within the predicted range for the group as a whole. We conclude that moderate CPAPB does not measurably affect the steady state lung fluid balance. More important, however, the rise in puhnonary vascular pressure must have been balanced by a rise in perimicrovascular interstitial fluid pressure since filtration did not change. It appears that the fraction of increased alveolar pressure transmitted to the microvessels was via the perimicrovascular fluid rather than through solid tissue contact.THE IMPROVED arterial blood oxygenation obtained by increasing airway pressure in patients or experimental animals with pulmonary edema is attributed to two mechanisms. The first, and well established one, is by reinflation of collapsed or fluid-filled alveoli. found that positive pressure ventilation markedly increased right lymph duct flow, at least transiently, in anesthetized dogs with acute pulmonary edema. Several other workers, however, found that positive pressure breathing does not reduce lung water content or the rate of fluid accumulation under edemogenic conditions."*" 16 Bo and associates 17 have demonstrated that, at constant vascular pressures, in isolated, perfused rabbit lungs increased alveolar pressure and lung volume sometimes increase fluid filtration. They have analyzed the separate effects of the increased alveolar pressure and the increased lung volume.The importance of having unequivocal data on the effects of positive alveolar pressure in lung fluid balance is important, not only for establishing the rationale for this clinical maneuver, but also because it may aid in establishing the role of interstitial hydrostatic forces which are not directly accessible for measurement. -Kcr(nmv -ripmv), where K is the endothelial fluid conductance, a is the protein reflection coefficient, P is the hydrostatic pressure, and FI is the protein osmotic pressure in the microvascular (mv) and perimicrovascular (pmv) fluids, respectively.We used unanesthetized sheep with chronic lung lymph fistulas 22 to determine the effect of continuous positive pressure airway breathing ...

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