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Research Article Free access | 10.1172/JCI110022

Continuous Negative External Chest Pressure Decreases Transvascular Lung Water Transport in Sheep after Pseudomonas Bacteremia

Peter Krumpe and Arnold Bernard Gorin

Department of Medicine, University of California, Davis, California 95616

Veterans Administration Medical Center, Martinez, California 94553

Find articles by Krumpe, P. in: PubMed | Google Scholar

Department of Medicine, University of California, Davis, California 95616

Veterans Administration Medical Center, Martinez, California 94553

Find articles by Gorin, A. in: PubMed | Google Scholar

Published January 1, 1981 - More info

Published in Volume 67, Issue 1 on January 1, 1981
J Clin Invest. 1981;67(1):264–273. https://doi.org/10.1172/JCI110022.
© 1981 The American Society for Clinical Investigation
Published January 1, 1981 - Version history
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Abstract

We studied the effects of continuous negative external chest pressure (CNECP) produced by a cuirass appliance on lung water and protein transport in sheep with chronic lung lymphatic fistulas. We compared data obtained during periods of mechanical ventilation (base line) to period of CNECP, using identical ventilatory support. Three groups were studied: six sheep were studied before and after application of CNECP for 1 h (control) and again after induction of a pulmonary vascular permeability defect (PVPD) by infusing live Pseudomonas bacteria (group I); another six sheep were studied under control conditions before and after prolonged application of CNECP for over 4 h (group II); 10 sheep were studied 24 h after a Pseudomonas infusion (PVPD), before and after 4 h of CNECP (group III).

Compared to base-line data, CNECP produced significant increases in functional residual capacity and decreases in pulmonary blood volume, pulmonary artery pressure, and left atrial pressure in all groups. Lung lymph flow (QL) was unchanged during the 1st h of CNECP and therefore was not significantly different from base line in group I, but after prolonged CNECP a steady-state decrease in QL as well as a decrease in lung albumin transport was found in groups II and III (P < 0.05 by paired t test). We postulate that decreased pleural pressure during CNECP produces decreased hydrostatic filtration pressures, thereby decreasing QL. Reduction of both convective forces as well as microvascular surface area available for solute exchange account for decreases in lung albumin transport. Histologic examination and gravimetric studies on four sheep failed to demonstrate increase in lung water accumulation after 4 h of CNECP. We conclude that CNECP mechanically reversed the PVPD in our group III sheep. These physiologic effects of CNECP may be of benefit in the management of patients with adult respiratory distress syndrome.

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