scholarly journals Inactivation of Exogenous Surfactant by Pulmonary Edema Fluid

1991 ◽  
Vol 29 (4) ◽  
pp. 353-356 ◽  
Author(s):  
Tsutomu Kobayashi ◽  
Keiko Nitta ◽  
Masaya Ganzuka ◽  
Sachiko Inui ◽  
Gertie Grossmann ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Exogenous Surfactant ◽  
Edema Fluid

scholarly journals The Role of Alveolar Edema in COVID-19

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1897
Author(s):  
Shu Yuan ◽  
Si-Cong Jiang ◽  
Zhong-Wei Zhang ◽  
Yu-Fan Fu ◽  
Jing Hu ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Fluid Management ◽  
Exogenous Surfactant ◽  
Small Airways ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Edema Fluid ◽  
One Year ◽  
Alveolar Edema

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threateninghypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation–perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (conservative fluid management, exogenous surfactant replacementsand ethanol–oxygen vapor therapyhypothetically) may be greatly helpful for reducingthe occurrences of severe cases. Given that late mechanical ventilation may causemucus (edema fluid) to be blown deep intothe small airways,oxygentherapy should be given at the early stages. Theoptimaltimeand blood oxygen saturation (SpO2) thresholdforoxygentherapy are also discussed.

Neuropeptides in pulmonary edema fluid of adult respiratory distress syndrome

Inflammation ◽  
1992 ◽  
Vol 16 (5) ◽  
pp. 509-517 ◽  
Author(s):  
Roger F. Espiritu ◽  
Jean -Francois Pittet ◽  
Michael A. Matthay ◽  
Edward J. Goetzl
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Adult Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Edema Fluid

Edema Fluid and Coagulation Changes During Fulminant Pulmonary Edema

CHEST Journal ◽  
1981 ◽  
Vol 79 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Richard W. Carlson ◽  
Richard C. Schaeffer ◽  
Moises Carpio ◽  
Max Harry Weil
Keyword(s):  
Pulmonary Edema ◽  
Edema Fluid

Alveolar epithelial fluid transport and the resolution of clinically severe hydrostatic pulmonary edema

1999 ◽  
Vol 87 (4) ◽  
pp. 1301-1312 ◽  
Author(s):  
G. M. Verghese ◽  
L. B. Ware ◽  
B. A. Matthay ◽  
M. A. Matthay
Keyword(s):  
Pulmonary Edema ◽  
Fluid Transport ◽  
Simplified Acute Physiology Score ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Alveolar Fluid Clearance ◽  
Ventricular Ejection Fraction ◽  
Mechanically Ventilated ◽  
Alveolar Epithelial ◽  
Edema Fluid

To characterize the rate and regulation of alveolar fluid clearance in the uninjured human lung, pulmonary edema fluid and plasma were sampled within the first 4 h after tracheal intubation in 65 mechanically ventilated patients with severe hydrostatic pulmonary edema. Alveolar fluid clearance was calculated from the change in pulmonary edema fluid protein concentration over time. Overall, 75% of patients had intact alveolar fluid clearance (≥3%/h). Maximal alveolar fluid clearance (≥14%/h) was present in 38% of patients, with a mean rate of 25 ± 12%/h. Hemodynamic factors (including pulmonary arterial wedge pressure and left ventricular ejection fraction) and plasma epinephrine levels did not correlate with impaired or intact alveolar fluid clearance. Impaired alveolar fluid clearance was associated with a lower arterial pH and a higher Simplified Acute Physiology Score II. These factors may be markers of systemic hypoperfusion, which has been reported to impair alveolar fluid clearance by oxidant-mediated mechanisms. Finally, intact alveolar fluid clearance was associated with a greater improvement in oxygenation at 24 h along with a trend toward shorter duration of mechanical ventilation and an 18% lower hospital mortality. In summary, alveolar fluid clearance in humans may be rapid in the absence of alveolar epithelial injury. Catecholamine-independent factors are important in the regulation of alveolar fluid clearance in patients with severe hydrostatic pulmonary edema.

scholarly journals Profiling of ARDS pulmonary edema fluid identifies a metabolically distinct subset

2017 ◽  
Vol 312 (5) ◽  
pp. L703-L709 ◽  
Author(s):  
Angela J. Rogers ◽  
Kévin Contrepois ◽  
Manhong Wu ◽  
Ming Zheng ◽  
Gary Peltz ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Metabolic Profiling ◽  
Metabolic Profile ◽  
Principal Component ◽  
Distinct Group ◽  
Multivariate Statistical ◽  
Clinical Criteria ◽  
Edema Fluid ◽  
Biological Heterogeneity ◽  
Physiological Heterogeneity

There is considerable biological and physiological heterogeneity among patients who meet standard clinical criteria for acute respiratory distress syndrome (ARDS). In this study, we tested the hypothesis that there exists a subgroup of ARDS patients who exhibit a metabolically distinct profile. We examined undiluted pulmonary edema fluid obtained at the time of endotracheal intubation from 16 clinically phenotyped ARDS patients and 13 control patients with hydrostatic pulmonary edema. Nontargeted metabolic profiling was carried out on the undiluted edema fluid. Univariate and multivariate statistical analyses including principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) were conducted to find discriminant metabolites. Seven-hundred and sixty unique metabolites were identified in the pulmonary edema fluid of these 29 patients. We found that a subset of ARDS patients (6/16, 38%) presented a distinct metabolic profile with the overrepresentation of 235 metabolites compared with edema fluid from the other 10 ARDS patients, whose edema fluid metabolic profile was indistinguishable from those of the 13 control patients with hydrostatic edema. This “high metabolite” endotype was characterized by higher concentrations of metabolites belonging to all of the main metabolic classes including lipids, amino acids, and carbohydrates. This distinct group with high metabolite levels in the edema fluid was also associated with a higher mortality rate. Thus metabolic profiling of the edema fluid of ARDS patients supports the hypothesis that there is considerable biological heterogeneity among ARDS patients who meet standard clinical and physiological criteria for ARDS.

Pulmonary Edema Fluid Clearance Pathways

Physiology ◽  
1995 ◽  
Vol 10 (3) ◽  
pp. 107-111
Author(s):  
R. E. Drake ◽  
J. C. Gabel
Keyword(s):  
Pulmonary Edema ◽  
Lung Tissue ◽  
Lymphatic Vessels ◽  
Edema Fluid

Lymphatic vessels normally remove excess fluid from the lung tissue and thus prevent pulmonary edema. However, when lungs do become edematous, the edema fluid may be cleared via several pathways. Each clearance pathway has unique properties, and recent studies have helped to define those properties.

scholarly journals Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury

2006 ◽  
Vol 291 (3) ◽  
pp. L354-L361 ◽  
Author(s):  
Michael T. Ganter ◽  
Lorraine B. Ware ◽  
Marybeth Howard ◽  
Jérémie Roux ◽  
Brandi Gartland ◽  
...  
Keyword(s):  
Heat Shock ◽  
Pulmonary Edema ◽  
Stress Protein ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial ◽  
Edema Fluid ◽  
Protein Response ◽  
Alveolar Edema

Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The second objective was to determine whether activation of the stress protein response (SPR) caused the release of Hsp72 into the extracellular space in vivo and in vitro and to determine whether SPR activation and/or eHsp72 itself would prevent the IL-1β-mediated inhibition of the vectorial fluid transport across alveolar type II cells. We found that eHsp72 was present in plasma and pulmonary edema fluid of ALI patients and that eHsp72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, SPR activation in vivo in mice and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of Hsp72. Finally, SPR activation, but not eHsp72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1β. Thus SPR may protect the alveolar epithelium against oxidative stress associated with experimental ALI, and eHsp72 may serve as a marker of SPR activation in the distal air spaces of patients with ALI.

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