Relationship of ultrafiltration and anastomotic flow in isolated rat lungs

When arterial and venous pressures are increased to equal values in "stop-flow" studies, perfusate continues to enter the pulmonary vasculature from the arterial and venous reservoirs. Losses of fluid from the pulmonary vasculature are due to ultrafiltration and flow through disrupted anastomotic (bronchial) vessels. This study compared the relative sites of ultrafiltration and anastomotic flows at low and high intravascular pressures.

Isolated rat lungs were perfused for 10 minutes with FITC-dextran, which was used to detect ultrafiltration. Arterial and venous catheters were then connected to reservoirs containing radioactively labeled dextrans at 20 or 30 cm H2O for 10 minutes. The vasculature was subsequently flushed into serial vials, and ultrafiltration and vascular filling during the equal-pressure interval were calculated.

Ultrafiltration equaled 0.43 +/- 0.11 mL at 20 cm H2O and was similar to the volume of fresh arterial and venous perfusate which entered and remained in the pulmonary vasculature during the equal-pressure interval (0.45 +/- 0.10 mL). At 30 cm H2O, 0.80 +/- 0.23 mL entered and remained in the vasculature during the equal-pressure interval, replacing the original perfusate, and calculated transudation (0.56 +/- 0.09 mL) was not significantly more than at 20 cm H2O. Fluid also entered the airspaces at 30 cm H2O but not at 20 cm H2O.

At 20 cm H2O, flow through anastomotic vessels occurs at sites that are at the arterial and venous ends of the microcirculation. Flow in exchange vessels remains minimal, permitting measurements of ultrafiltration and exchange. Losses of perfusate from the pulmonary vessels complicate measurements of ultrafiltration at 30 cm H2O.