HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Guest Access | Sign In via User Name/Password

This Article Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Effros, R.M. Articles by Presberg, K. Search for Related Content PubMed PubMed Citation Articles by Effros, R.M. Articles by Presberg, K.

Increasing Airway Pressures Can Promote Transvascular Edema Reabsorption^*

^* From the Pulmonary/Critical Care Division, Medical College of Wisconsin, Milwaukee, WI. Supported by grants NIH HL 18606 and VA 7731-05.

Correspondence to: Richard Effros, MD, FCCP, Chief of Pulmonary and Crit Care Med, Medical College of Wisconsin, 9200 W Wisconsin Ave, Milwaukee, WI 53226-3522

Considerable controversy persists concerning the mechanisms of edema reabsorption from the lung and the effect of mechanical ventilation on this process. Lymphatic drainage probably plays a relatively minor role in reabsorbing excess fluid, and it has not been possible to show that increasing serum protein concentrations enhance dehydration of the interstitium. Simultaneous increases in airspace and pleural pressure (PA and Ppl) at constant lung volumes should increase interstitial pressure, and this would result in the reabsorption of fluid in accordance with Starling principles if interstitial pressures rise above pressures in the vasculature. However, increases in PA and Ppl above pressures in the vasculature also compress septal vessels, preventing fluid reabsorption.

We have recently completed studies that suggest that the lungs are protected from edema formation by the unique capacity of nonseptal vessels to remain open even when lung tissues are compressed at high PA and Ppl. Transvascular movement of fluid was studied by following changes in concentration of a vascular indicator (fluorescein isothiocyanate-dextran 71,000 or 2,000,000 molecular weight) in the perfusate of isolated rat lungs. To magnify changes in dextran concentration, flow was stopped for 10 min and the fluid that was in the lungs was then flushed out. Albumin concentrations in the perfusate were kept low (0.5 g/dL) to minimize protein oncotic pressure effects. No fluid reabsorption was noted when PA = 5 and Ppl = 0 cm H₂O during the stop interval. However, increasing PA to 25 and Ppl to 20 (same lung volume) resulted in the reabsorption of 0.119 ± 0.030 mL from lungs, which weighed approximately 2 g. No reabsorption was observed in atelectatic lungs (PA = 0, Ppl = 20 cm H₂O). Additional stop-flow experiments indicated that some filtration occurred through venous but not arterial vessels. These studies suggest that increases in PAs can favor fluid reabsorption through venous vessels by keeping airspaces and associated nonseptal (corner and extra-alveolar) vessels open and increasing interstitial pressure above venous pressures.

This Article Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Effros, R.M. Articles by Presberg, K. Search for Related Content PubMed PubMed Citation Articles by Effros, R.M. Articles by Presberg, K.