Pulmonary edema.

Staub, Norman C.

doi:10.1152/physrev.1974.54.3.678

Cited by 699 publications

(258 citation statements)

References 0 publications

Supporting

Mentioning

238

Contrasting

Unclassified

Order By: Relevance

“…The reaction is dose-related and reproducible for up to three studies in a given sheep (1). There is a sizeable body of data supporting the assumption that lung lymph flow and protein concentrations under steady-state conditions reflect the flow and protein concentration oftransmicrovascular filtrate in the lung (17)(18)(19). Therefore the high flow ofprotein rich lymph seen during the steadystate late phase of the endotoxin reaction is interpreted as increased lung vascular permeability to fluid and protein (1).…”

Section: Discussionmentioning

confidence: 81%

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Heflin¹,

Brigham²

1981

J. Clin. Invest.

394

116

View full text Add to dashboard Cite

A B S T R A C T To see whether circulating granulocytes are necessary for the lung vascular reaction to endotoxin, we measured the endotoxin response in chronically instrumented sheep before and after granulocyte depletion with hydroxyurea. Granulocyte depletion did not affect the pulmonary hypertension caused by endotoxin (peak mean pulmonary artery pressures = 38+2 cm H20 before depletion and 42+2 after depletion, P = NS). The late phase increase in lung lymph flow after endotoxin was significantly lower in the granulocytopenic animals as reflected by lung lymph flow (mean steady state lymph flow before depletion = 30.6+2.0 SE ml/h; mean steady state lymph flow after granulocyte depletion = 15.4+1.0; P < 0.01) even though late phase pulmonary vascular pressures were similar before and after granulocyte depletion. Lung lymph protein clearance (lymph flow x lymph/plasma protein concentration) was also significantly lower after granulocyte depletion (mean steady state before depletion = 21.4 + 1.4 SE ml/h; and after depletion = 10.4+ 1.0; P < 0.01). We conclude that circulating granulocytes are necessary for the development of increased lung vascular permeability to fluid and protein following endotoxin. The pulmonary vasopressor effects of endotoxin in sheep are independent of granulocytes.

show abstract

Section: Discussionmentioning

confidence: 81%

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Heflin¹,

Brigham²

1981

J. Clin. Invest.

394

116

View full text Add to dashboard Cite

show abstract

“…9,21,22,41 Physiopathologically cardiogenic pulmonary edema presents initially as an exudative effusion in the perivascular and peribronchial interstitial spaces, easily drained at the hilum at first and later involving interlobular septa, intralobular interstitial space, and finally alveoli. 42,43 On the basis of what was proposed above, pure septal syndrome would represent the initial phase of this pathologic process (at times actually the only phase present), soon being replaced by interstitial alveolar syndrome from panlobular involvement. Edema in ALI/ARDS never appears as a pure septal syndrome because the lesion is born as intralobular and intra-alveolar, so that predominant aspects are confluent ULCs and white lung with some normal areas, all showing primitively alveolar dyshomogeneous imbibition.…”

Section: Discussionmentioning

confidence: 97%

Sonographic Interstitial Syndrome

Soldati¹,

Copetti

Sher

2009

Journal of Ultrasound in Medicine

225

172

View full text Add to dashboard Cite

Objective. Ultrasound lung comets (ULCs) now have an acknowledged correlation with extravascular lung water, but they present in different orders and numbers in different pathologic pulmonary entities. How these artifacts are created is not yet known, and the literature gives discordant hypotheses. Understanding their formation is the first step in understanding lung disease. The purpose of this study was to show the morphologic and genetic variability of interstitial lung disease studied with echography and thus to propose a unitary mechanism for the formation of ULCs. Methods. This study included 3 parts: (1) a retrospective analysis of echographic lung images of patients with interstitial syndrome; (2) an analysis of the literature for definitions of the size of the pulmonary lobule; and (3) an experimental model of different air-water interfaces scanned with varying ultrasonic frequencies.Results. The retrospective analysis of echographic lung images included 176 patients with diffuse ULCs: 118 patients had acute pulmonary edema; 18 had acute lung injury/acute respiratory distress syndrome; and 40 were premature neonates with respiratory distress syndrome. Experimental models permitted us to discover that ring-down artifacts are produced only by single and double layers of bubbles in specific structural settings. Conclusions. Reverberation between bubbles with a critical radius seems to be at the origin of ring-down artifacts. Echographic manifestations of interstitial lung disease, whose genesis lies in the partial air loss of lobes and segments, are acoustic phenomena originating from variations in the tissue-fluid relationship of the lung. A correlation between anatomopathologic characteristics and structures of sonographic artifacts could allow more rapid and noninvasive diagnoses.

show abstract

“…Also, until the early 1980s, there were no satisfactory animal models to study the resolution of alveolar edema, and the isolation and culture of alveolar epithelial type II cells was just becoming a useful experimental method. Although the removal of interstitial pulmonary edema by lung lymphatics and the lung microcirculation was discussed by Staub in 1974 in his review of pulmonary edema (333), there was no information on how pulmonary edema was removed from the distal airspaces of the lung.…”

Section: Introductionmentioning

confidence: 99%

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Matthay

Folkesson²,

Clérici³

2002

Physiological Reviews

611

649

View full text Add to dashboard Cite

The discovery of mechanisms that regulate salt and water transport by the alveolar and distal airway epithelium of the lung has generated new insights into the regulation of lung fluid balance under both normal and pathological conditions. There is convincing evidence that active sodium and chloride transporters are expressed in the distal lung epithelium and are responsible for the ability of the lung to remove alveolar fluid at the time of birth as well as in the mature lung when pathological conditions lead to the development of pulmonary edema. Currently, the best described molecular transporters are the epithelial sodium channel, the cystic fibrosis transmembrane conductance regulator, Na+-K+-ATPase, and several aquaporin water channels. Both catecholamine-dependent and -independent mechanisms can upregulate isosmolar fluid transport across the distal lung epithelium. Experimental and clinical studies have made it possible to examine the role of these transporters in the resolution of pulmonary edema.

show abstract

Pulmonary edema.

Cited by 699 publications

References 0 publications

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Sonographic Interstitial Syndrome

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Contact Info

Product

Resources

About