Pulmonary interstitial compartments and tissue resistance to fluid flux.

We have produced interstitial fluid exchange in six isolated plasma-perfused canine lobes by introducing small increases in microvascular hydrostatic pressure. We measured early fast fluid exchange with a colorimetric technique and used weight changes to follow slow exchange. The observed biphasic time course suggested fluid flux across the microvascular membrane into two interstitial compartments in series (perimicrovascular and central). We related the initial rate of fluid flux into each compartment to the applied hydrostatic pressure change to obtain membrane (Kf1) and tissue conductances (Kf2) and to the exchanged volume to determine perimicrovascular (C1) and central (C2) interstitial compliances. C2 (0.25 +/- 0.193) was twice C1 (0.10 +/- 0.031 ml X cmH2O-1 X g DW-1, where DW represents dry weight. C2 increased significantly with hydration (C2 = 0.06 X WW/DW - 0.15) ml X cmH2O-1 X g DW-1 (WW/DW, wet-to-dry weight ratio), whereas C1 did not. Kf1 (0.26 +/- 0.17) was one order of magnitude larger than Kf2 (0.027 +/- 0.014 ml X min-1 X cmH2O-1 X g DW-1). Kf2 increased with hydration (Kf2 = 0.005 X WW/DW - 0.007) ml X min-1 X cmH2O-1 X g DW-1, whereas Kf1 did not. Our data point to the tissues and not the microvascular membranes as the major rate-limiting structure. Our data suggest an interstitium composed of a smaller rigid perimicrovascular space which communicates to a larger looser downstream space by a high-resistance pathway. As hydration increases, fluid accumulation becomes easier because tissue resistance to fluid flux drops and the compliance of the downstream compartment doubles.