Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Jul 30;6(3):e0025. doi: 10.5041/RMMJ.10210

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright: © 2015 Azzam and Sznajder.

This is an open-access article. All its content, except where otherwise noted, is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

A: The rate of alveolar fluid clearance (AFC) was modulated following therapeutic interventions: catecholamines, vasopressin, and gene therapy upregulated AFC; however, the administration of endothelin, angiotensin, amiloride, ouabain, or colchicine inhibited active sodium transport and thus AFC. The data were adapted from references 13, 27, 28, 31, 33, 36, 37.

B: Alveolar fluid clearance (AFC) was decreased in the various states of acute lung injury, such as sepsis, hyperoxia, hypercapnia, and ventilation-induced lung injury. Moreover, in rats exposed to acutely increased left atrial pressure (e.g. acute left heart failure) AFC was inhibited; whereas AFC was significantly upregulated in chronic heart failure rats. The data were adapted from references 34, 40–43.

The bars represent mean ± SEM. Alfa2, α2-subunit of Na,K-ATPase; Ami, amiloride; beta1, β1-subunit of Na,K-ATPase; beta2 adr, β2 adrenergic receptor; CT, control; Ouab, ouabain; VILI, ventilation-induced lung injury.