scholarly journals Pulmonary oedema fluid induces non‐α‐ENaC‐dependent Na + transport and fluid absorption in the distal lung

2002 ◽  
Vol 544 (2) ◽  
pp. 537-548 ◽  
Author(s):  
Bijan Rafii ◽  
Daniel J. Gillie ◽  
Chris Sulowski ◽  
Vicky Hannam ◽  
Tony Cheung ◽  
...  
Keyword(s):  
Pulmonary Oedema ◽  
Fluid Absorption ◽  
Na Transport ◽  
Distal Lung ◽  
Oedema Fluid

Absence of Lipoprotein in Pulmonary Œdema Fluid produced by Cytotoxic Antibody

Nature ◽  
1964 ◽  
Vol 201 (4925) ◽  
pp. 1237-1238 ◽  
Author(s):  
L. S. KIND ◽  
A. T. SMITH ◽  
P. ELLMAN
Keyword(s):  
Pulmonary Oedema ◽  
Cytotoxic Antibody ◽  
Oedema Fluid

scholarly journals Determining the aetiology of pulmonary oedema by the oedema fluid-to-plasma protein ratio

2009 ◽  
Vol 35 (2) ◽  
pp. 331-337 ◽  
Author(s):  
L. B. Ware ◽  
R. D. Fremont ◽  
J. A. Bastarache ◽  
C. S. Calfee ◽  
M. A. Matthay
Keyword(s):  
Pulmonary Oedema ◽  
Plasma Protein ◽  
Protein Ratio ◽  
Oedema Fluid

Electrolyte and fluid transport across the mature alveolar epithelium

1993 ◽  
Vol 74 (1) ◽  
pp. 1-15 ◽  
Author(s):  
G. Saumon ◽  
G. Basset
Keyword(s):  
Fluid Transport ◽  
Basolateral Membrane ◽  
Adult Life ◽  
Alveolar Epithelium ◽  
Epithelial Lining ◽  
Fluid Absorption ◽  
Na Transport ◽  
Alveolar Cells ◽  
Epithelial Lining Fluid ◽  
Transepithelial Na Transport

The lungs must be kept "dry" for efficient gas exchange. The mechanisms that contribute to clear alveoli from fetal lung fluid at birth are still present during adult life and allow recovery from alveolar flooding. It has recently been shown with the use of different approaches in vitro, as well as in vivo, that alveolar epithelium performs solute-coupled fluid transport. Fluid absorption from alveoli occurs chiefly as a result of active transepithelial Na+ transport. The mechanisms of Na+ transport have been partly elucidated; Na+ enters alveolar cells through apical Na+ channels and Na(+)-coupled solute transporters and is pumped out at the basolateral membrane by a Na(+)-K(+)-adenosinetriphosphatase (ATPase). Transepithelial Na+ transport and fluid absorption are stimulated by beta-adrenergic agonists, with adenosine 3',5'-cyclic monophosphate being the likely intracellular second messenger. K+ is probably secreted into alveoli because its concentration in the epithelial lining fluid is larger than expected for passive distribution. K+ channels have been described that, in conjunction with Na(+)-K(+)-ATP-ase, might provide pathways for active transport. Active proton secretion or bicarbonate absorption have been reported, which may explain the low pH of the alveolar epithelial lining fluid. It is probable that active solute transports are the main determinants of epithelial lining fluid depth and composition. A challenge for the future is to understand how this homeostasis is achieved.

scholarly journals Assessment of a Novel Method for Non-invasive Sampling of the Distal Airspace in Acute Respiratory Distress Syndrome Patients Receiving Inhaled Sedation with Sevoflurane: the ANAISS Study Protocol

2020 ◽  
Author(s):  
Pierre-Antoine Tronche ◽  
Robin Lalande ◽  
Raiko Blondonnet ◽  
Laurence Roszyk ◽  
Ruoyang Zhai ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Oedema ◽  
Study Protocol ◽  
Distress Syndrome ◽  
Non Invasive ◽  
Tnf Α ◽  
Distal Airspace ◽  
Oedema Fluid

ABSTRACTIntroductionRecently, fluid collected from the heat-and-moisture-exchange filters, which are commonly used in most mechanically ventilated patients under intravenous sedation, has been reported as a potential surrogate for fluid in the distal airspace. Therefore, collection of this fluid represents a promising, non-invasive method for sampling the distal airspace in patients with acute respiratory distress syndrome (ARDS) and for facilitating a mechanistic understanding of this devastating disease. The current study protocol was constructed to assess whether this fluid could be sampled from a dedicated device (Anaesthetic Conserving Device [AnaConDa-S], Sedana Medical, Danderyd, Sweden) used to deliver inhaled sevoflurane for sedation in patients with ARDS.Methods and analysisA total of 30 adult patients within 24 hours of meeting the Berlin criteria for moderate-severe ARDS and receiving inhaled sevoflurane as standard sedation in participating centres will be eligible for inclusion into this investigator-initiated, exploratory, prospective, bicentre study. After at least 12 h of inhaled sedation, a sample of directly aspirated, undiluted pulmonary oedema fluid will be collected concurrently with fluid from the AnaConDa-S device. Levels of proinflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α and sTNFr-1) and markers of lung endothelial (Ang-2) and epithelial (sRAGE) injury will be measured in both fluids by Multiplex. The primary endpoint is the correlation between protein markers (IL-1β, IL-6, IL-8, TNF-α, sTNFr-1, Ang-2 and sRAGE) measured in the undiluted pulmonary oedema fluid versus the AnaConDa-S fluid.Ethics and disseminationThe study was approved by the appropriate ethics committee (CPP Est I). Informed consent is required. The fluid collection from the AnaConDa-S has potential to foster our understanding of the potential effects of inhaled sedation in clinical ARDS and to open up novel perspectives for prognostic and predictive enrichment in future trials. The results will be published in a peer-reviewed journal.Registration numberNCT03964155.

scholarly journals Oxygen‐evoked Na + transport in rat fetal distal lung epithelial cells

2001 ◽  
Vol 532 (1) ◽  
pp. 105-113 ◽  
Author(s):  
D. L. Baines ◽  
S. J. Ramminger ◽  
A. Collett ◽  
J. J. E. Haddad ◽  
O. G. Best ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Na Transport ◽  
Lung Epithelial ◽  
Distal Lung

Endotoxin-stimulated alveolar macrophages impair lung epithelial Na+ transport by an L-Arg-dependent mechanism

1994 ◽  
Vol 266 (5) ◽  
pp. C1330-C1341 ◽  
Author(s):  
C. G. Compeau ◽  
O. D. Rotstein ◽  
H. Tohda ◽  
Y. Marunaka ◽  
B. Rafii ◽  
...  
Keyword(s):  
Ion Transport ◽  
Alveolar Macrophages ◽  
Single Channel ◽  
Short Circuit ◽  
Na Transport ◽  
Epithelial Ion Transport ◽  
Lung Epithelial ◽  
Air Space ◽  
Distal Lung ◽  
Dependent Mechanism

The Na+ transport function of alveolar epithelium represents an important mechanism for air space fluid clearance after acute lung injury. We studied the effect of endotoxin-stimulated rat alveolar macrophages on lung epithelial ion transport and permeability in vitro. Cultured rat distal lung (alveolar) epithelial monolayers incubated with both endotoxin and macrophages demonstrated a 75% decline in transepithelial resistance and a selective 60% reduction in amiloride-sensitive short-circuit current (Isc). Single-channel patch-clamp analysis demonstrated a 60% decrease in the density of 25-pS nonselective cation (NSC) channels on the apical membrane of epithelium exposed to both endotoxin and macrophages. A concurrent reduction in epithelial F-actin content suggested a role for actin depolymerization in mediating this effect. Incubation of cocultures with the methylated L-arginine (Arg) derivative NG-monomethyl-L-arginine prevented the reduction in epithelial Isc, as did substitution of L-Arg with D-Arg or incubation in L-Arg-free medium. Furthermore, the stable and products of Arg metabolism were found to have no effect on epithelial ion transport. These studies show that endotoxin-stimulated alveolar macrophages impair distal lung epithelial ion transport by an L-Arg-dependent mechanism by inactivating amiloride-sensitive 25-pS NSC channels. This may represent a novel mechanism whereby local inflammatory cells regulate lung epithelial ion transport. This could affect the ability of the lung to clear fluid from the air space.

The role of α-, β-, and γ-ENaC subunits in distal lung epithelial fluid absorption induced by pulmonary edema fluid

2007 ◽  
Vol 293 (3) ◽  
pp. L537-L545 ◽  
Author(s):  
Nael Elias ◽  
Bijan Rafii ◽  
Muhammad Rahman ◽  
Gail Otulakowski ◽  
Ernest Cutz ◽  
...  
Keyword(s):  
Lamellar Body ◽  
Fetal Lung ◽  
Mouse Lung ◽  
Maximal Effect ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Fluid Absorption ◽  
Edema Fluid ◽  
Distal Lung

Edema fluid (EF) increases epithelial Na+ transport by rat fetal distal lung epithelia (FDLE) and induces net lung fluid absorption in fetal mouse lung explants [Rafii B, Gillie DJ, Sulowski C, Hannam V, Cheung T, Otulakowski G, Barker PM, O'Brodovich H. J Physiol (Lond) 544: 537–548, 2002]. We now show that EF increases fluid absorption across monolayers of rat FDLE in a dose-dependent manner. To study the role of subunits of the epithelial Na+ channel (ENaC) in the phenomena, we cultured explants from the distal lungs of 16-day gestational age wild-type (WT) or α-, β-, or γ-ENaC knockout or heterozygote (HT) mice. WT explants cultured in media continuously expanded over time as a result of net fluid secretion. In contrast, when explants were exposed to EF for 24 h, net fluid absorption occurred. EF-exposed explants had normal histology, but marked changes were seen after Triton X-100 or staurosporine exposure. Transmission electron microscopy showed EF promoted lamellar body formation and abundant surfactant in the explants' lumens. EF-induced changes in explant size were similar in α-ENaC knockout, WT, and HT littermate fetal lung explants ( P > 0.05). In contrast, EF's effect was attenuated in β- and γ-ENaC knockouts ( P < 0.05) vs. WT and HT littermate fetal lung explants. EF exposure slightly decreased or had no effect on mRNA levels for α-ENaC in various mouse genotypes but decreased expression of β- and γ-ENaC subunit mRNAs ( P < 0.01) across all genotype groups. We conclude that β- and γ-, but not α-, ENaC subunits are essential for EF to exert its maximal effect on net fluid absorption by distal lung epithelia.

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