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Review
. 2006 Jul;35(1):10-9.
doi: 10.1165/rcmb.2006-0080SF. Epub 2006 Mar 2.

Alveolar epithelial ion and fluid transport: recent progress

Hans G Folkesson  1 , Michael A Matthay
Affiliations
Review

Alveolar epithelial ion and fluid transport: recent progress

Hans G Folkesson et al. Am J Respir Cell Mol Biol. 2006 Jul.
No abstract available

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Figures

<b>Figure 1.</b>
Figure 1.
A section of an ARDS lung. Note the fluid-filled alveolar spaces with significant red blood cell infiltration. Insert demonstrates apical ENaC staining and basolateral Na,K-ATPase staining in lung epithelia. (Reprinted with permission from Ref. 3)
<b>Figure 2.</b>
Figure 2.
AFC rates in different animal species with and without βAR stimulation of AFC. All data are calculated as 1-h studies. (Data obtained from Refs. , , , and .)
<b>Figure 3.</b>
Figure 3.
A shows a schematic representation of the H1 promoter– driven hairpin-type siRNA-expression vector. The shRNA contains a 19-nucleotide sense strand (S), a 9-nucleotide loop (L), and an antisense strand (A), followed by an RNA polymerase III terminator. B shows a representative RT-PCR gel of αENaC mRNA in the lung after pretreatment with the pSi-0 and pSi-4 pDNAs. It is clearly shown that pSi-4 was efficient in silencing αENaC after pDNA pretreatment, as pSi-4 dramatically reduced αENaC mRNA. C shows a densitometric analysis of αENaC protein in the lung by Western blot 24 h after pretreatment with pSi-0 and pSi-4 during baseline, unstimulated conditions. pSi-4 pretreatment dramatically reduced αENaC protein expression by ∼ 80%. D shows AFC during baseline and after terbutaline stimulation 24 h after pretreatment with pSi-0 and pSi-4. pSi-4 pretreatment attenuated terbutaline-stimulated AFC and inhibited baseline AFC by ∼ 30%. (Data from Ref. .)
<b>Figure 4.</b>
Figure 4.
(A) Effect of glibenclamide inhibition of CFTR on AFC in mouse lungs with and without βAR stimulation with isoproterenol. AFC extrapolated as 1-h experiments. Glibenclamide only attenuated isoproterenol-stimulated AFC, thus providing evidence of Cl and CFTR participation in βAR stimulated AFC. (B) Effect of bumetanide inhibition of the Na,K,2Cl-cotransporter on AFC in guinea pig lungs with and without βAR stimulation with isoproterenol. AFC measured as 1-h experiments. Bumetanide only attenuated isoproterenol-stimulated AFC, thus providing evidence of Cl and the Na,K,2Cl-cotransporter participation in βAR-stimulated AFC. (Data from Refs. and .)
<b>Figure 5.</b>
Figure 5.
Percentage of patients with three categories of AFC: impaired (open bars; < 3%/h), submaximal (shaded bars; 3–14%/h), and maximal (solid bars; > 14%/h) during hydrostatic pulmonary edema and during acute lung injury–induced pulmonary edema. AFC was measured during the first 4 h after intubation and mechanical ventilation. There was a greater number of patients with submaximal-maximal AFC after hydrostatic pulmonary edema than after acute lung injury–induced pulmonary edema. In acute lung injury–induced pulmonary edema the majority of patients studied displayed an impaired AFC. (Data from Refs. and .)
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References

    1. Matthay MA, Folkesson HG, Verkman AS. Salt and water transport across alveolar and distal airway epithelium in the adult lung. Am J Physiol Lung Cell Mol Physiol 1996;270:L487–L503. - PubMed
    1. Crandall ED, Matthay MA. Alveolar epithelial transport: basic science to clinical medicine. Am J Respir Crit Care Med 2001;163:1021–1029. - PubMed
    1. Matthay MA, Folkesson HG, Clerici C. Lung epithelial fluid transport and the resolution of pulmonary edema. Physiol Rev 2002;82:569–600. - PubMed
    1. Matalon S, Lazrak A, Jain L, Eaton DC. Biophysical properties of sodium channels in lung alveolar epithelial cells. J Appl Physiol 2002;93:1852–1859. - PubMed
    1. Sznajder JI, Factor P, Ingbar DH. Lung edema clearance: role of Na+-K+-ATPase. J Appl Physiol 2002;93:1860–1866. - PubMed

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