scholarly journals Solute permeability of the alveolar capillary barrier.

Thorax ◽  
1987 ◽  
Vol 42 (1) ◽  
pp. 1-10 ◽  
Author(s):  
M P Barrowcliffe ◽  
J G Jones
Keyword(s):  
Capillary Barrier ◽  
Solute Permeability ◽  
Alveolar Capillary

Clearance of charged and uncharged dextrans from normal and injured lungs

1990 ◽  
Vol 68 (1) ◽  
pp. 341-347 ◽  
Author(s):  
M. P. Barrowcliffe ◽  
G. D. Zanelli ◽  
D. Ellison ◽  
J. G. Jones
Keyword(s):  
Clearance Rate ◽  
Dextran Sulfate ◽  
Molecular Size ◽  
Confidence Limits ◽  
Half Time ◽  
Capillary Barrier ◽  
Solute Transfer ◽  
Molecular Charge ◽  
Before And After ◽  
Alveolar Capillary

To examine how molecular charge affects the transfer of molecules across the alveolar-capillary barrier, we prepared the following dextrans of equivalent molecular size (mol wt 10,000) but varying molecular charge: neutral dextran, cationic DEAE dextran, and anionic dextran sulfate. These were labeled with 99mTc. The lungs of three groups of anesthetized rabbits were insufflated with dextran aerosols, with six rabbits receiving each type, and the half-time pulmonary clearance (t1/2) was measured. Control t1/2's (95% confidence limits) were 95 (74-120), 227 (192-268), and 291 (246-345) min for neutral, cationic, and anionic dextrans, respectively. One week later, when the same animals were restudied 4 h after 3 micrograms/kg iv endotoxin, t1/2's were 102 (75-139), 167 (149-187), and 126 (102-154) min, respectively. After 30 min during this repeat study, animals were ventilated with 20 breaths of cigarette smoke, which acutely increased the clearance rate to 34 (26-46), 25 (20-31), and 13 (7-24) min, respectively. Mean carboxyhemoglobin levels were not significantly different in the three groups: 13.6, 12.7, and 11.1%, respectively. These results demonstrated that neutral dextrans showed the same clearance rate before and after endotoxin, whereas the charged dextrans had a significantly faster clearance after endotoxin. After smoke exposure the anionic dextran left the lung more rapidly than the neutral dextran. Thus molecular charge affects solute transfer across the alveolar-capillary barrier in both normal and injured lungs, and an effect of endotoxin on the lung can be detected with charged dextrans but not with neutral dextran.

scholarly journals Early disruption of the alveolar-capillary barrier in a ricin-induced ARDS mouse model: neutrophil-dependent and -independent impairment of junction proteins

2019 ◽  
Vol 316 (1) ◽  
pp. L255-L268 ◽  
Author(s):  
Anita Sapoznikov ◽  
Yoav Gal ◽  
Reut Falach ◽  
Irit Sagi ◽  
Sharon Ehrlich ◽  
...  
Keyword(s):  
Connexin 43 ◽  
Early Stage ◽  
Capillary Barrier ◽  
Edema Formation ◽  
Pulmonary Tissue ◽  
Time To Death ◽  
Pulmonary Exposure ◽  
Junction Protein ◽  
Alveolar Capillary ◽  
Junction Proteins

Irrespective of its diverse etiologies, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) leads to increased permeability of the alveolar-capillary barrier, which in turn promotes edema formation and respiratory failure. We investigated the mechanism of ALI/ARDS lung hyperpermeability triggered by pulmonary exposure of mice to the highly toxic plant-derived toxin ricin. One prominent hallmark of ricin-mediated pulmonary intoxication is the rapid and massive influx of neutrophils to the lungs, where they contribute to the developing inflammation yet may also cause tissue damage, thereby promoting ricin-mediated morbidity. Here we show that pulmonary exposure of mice to ricin results in the rapid diminution of the junction proteins VE-cadherin, claudin 5, and connexin 43, belonging, respectively, to the adherens, tight, and gap junction protein families. Depletion of neutrophils in ricin-intoxicated mice attenuated the damage caused to these junction proteins, alleviated pulmonary edema, and significantly postponed the time to death of the intoxicated mice. Inhibition of matrix metalloproteinase (MMP) activity recapitulated the response to neutrophil depletion observed in ricin-intoxicated mice and was associated with decreased insult to the junction proteins and alveolar-capillary barrier. However, neutrophil-mediated MMP activity was not the sole mechanism responsible for pulmonary hyperpermeability, as exemplified by the ricin-mediated disruption of claudin 18, via a neutrophil-independent mechanism involving tyrosine phosphorylation. This in-depth study of the early stage mechanisms governing pulmonary tissue integrity during ALI/ARDS is expected to facilitate the tailoring of novel therapeutic approaches for the treatment of these diseases.

scholarly journals Catching Common Cold Virus with a Net: Pyridostatin Forms Filaments in Tris Buffer That Trap Viruses—A Novel Antiviral Strategy?

Viruses ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 723
Author(s):  
Antonio Real-Hohn ◽  
Rong Zhu ◽  
Haleh Ganjian ◽  
Nahla Ibrahim ◽  
Peter Hinterdorfer ◽  
...  
Keyword(s):  
Host Defense ◽  
Common Cold ◽  
Respiratory Virus ◽  
Tris Buffer ◽  
Neutrophil Extracellular Trap ◽  
Dependent Manner ◽  
Capillary Barrier ◽  
Concentration Dependent Manner ◽  
Virus Inhibition ◽  
Alveolar Capillary

The neutrophil extracellular trap (ET) is a eukaryotic host defense machinery that operates by capturing and concentrating pathogens in a filamentous network manufactured by neutrophils and made of DNA, histones, and many other components. Respiratory virus-induced ETs are involved in tissue damage and impairment of the alveolar–capillary barrier, but they also aid in fending off infection. We found that the small organic compound pyridostatin (PDS) forms somewhat similar fibrillary structures in Tris buffer in a concentration-dependent manner. Common cold viruses promote this process and become entrapped in the network, decreasing their infectivity by about 70% in tissue culture. We propose studying this novel mechanism of virus inhibition for its utility in preventing viral infection.

scholarly journals Rhodiola crenulataExtract Alleviates Hypoxic Pulmonary Edema in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Shih-Yu Lee ◽  
Min-Hui Li ◽  
Li-Shian Shi ◽  
Hsin Chu ◽  
Cheng-Wen Ho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Capillary Barrier ◽  
Lung Water ◽  
Stress Markers ◽  
Rhodiola Crenulata ◽  
High Altitude Illness ◽  
Alveolar Capillary

Sudden exposure of nonacclimatized individuals to high altitude can easily lead to high altitude illnesses. High altitude pulmonary edema (HAPE) is the most lethal form of high altitude illness. The present study was designed to investigate the ability ofRhodiola crenulataextract (RCE), an herbal medicine traditionally used as an antiacute mountain sickness remedy, to attenuate hypoxia-induced pulmonary injury. Exposure of animals to hypobaric hypoxia led to a significant increase in pathological indicators for pulmonary edema, including the lung water content, disruption of the alveolar-capillary barrier, and protein-rich fluid in the lungs. In addition, hypobaric hypoxia also increased oxidative stress markers, including (ROS) production, (MDA) level, and (MPO) activity. Furthermore, overexpression of plasma (ET-1), (VEGF) in (BALF), and (HIF-1α) in lung tissue was also found. However, pretreatment with RCE relieved the HAPE findings by curtailing all of the hypoxia-induced lung injury parameters. These findings suggest that RCE confers effective protection for maintaining the integrity of the alveolar-capillary barrier by alleviating the elevated ET-1 and VEGF levels; it does so by reducing hypoxia-induced oxidative stress. Our results offer substantial evidence to support arguments in favor of traditional applications ofRhodiola crenulatafor antihigh altitude illness.

scholarly journals Flotillin-involved uptake of silica nanoparticles and responses of an alveolar-capillary barrier in vitro

2013 ◽  
Vol 84 (2) ◽  
pp. 275-287 ◽  
Author(s):  
Jennifer Kasper ◽  
Maria I Hermanns ◽  
Christoph Bantz ◽  
Stefanie Utech ◽  
Olga Koshkina ◽  
...  
Keyword(s):  
Silica Nanoparticles ◽  
Capillary Barrier ◽  
Alveolar Capillary

The Effect of Surgery with Cardiopulmonary Bypass on Alveolar-Capillary Barrier Function in Human Beings

1985 ◽  
Vol 40 (2) ◽  
pp. 139-143 ◽  
Author(s):  
David Royston ◽  
Barbara D. Minty ◽  
M.I. Biol ◽  
Tim W. Higenbottam ◽  
John Wallwork ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Barrier Function ◽  
Human Beings ◽  
Capillary Barrier ◽  
Alveolar Capillary

Tyrosol attenuates lipopolysaccharide-induced acute lung injury by inhibiting the inflammatory response and maintaining the alveolar capillary barrier

2017 ◽  
Vol 109 ◽  
pp. 526-533 ◽  
Author(s):  
Yeon-Yong Kim ◽  
Soyoung Lee ◽  
Min-Jong Kim ◽  
Byeong-Cheol Kang ◽  
Hima Dhakal ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Capillary Barrier ◽  
Alveolar Capillary

Accuracy of Cell Mechanical Measurements Using Oscillating Optical Tweezers: A Computational Study

2008 ◽  
Author(s):  
Laura M. Ricles ◽  
Hannah L. Dailey ◽  
Samir N. Ghadiali
Keyword(s):  
Optical Tweezers ◽  
Computational Study ◽  
Capillary Barrier ◽  
Mechanically Ventilated ◽  
Deformation Response ◽  
Ventilator Induced Lung Injury ◽  
Hydrodynamic Stresses ◽  
Airway Walls ◽  
Alveolar Capillary

The accurate characterization of living cell micro-mechanical properties is a clinically important problem since several disease pathologies depend on the deformation response of cells to applied mechanical loads. For example, the acute respiratory distress syndrome (ARDS) is characterized by an increase in the permeability of the alveolar-capillary barrier, resulting in an influx of edema fluid into the lung. Due to the surfactant inactivation and decreased gas exchange, ARDS patients must be mechanically ventilated [1,3]. However, hydrodynamic stresses exerted on the epithelial cells (EpC) that line airway walls during the reopening of the collapsed or fluid-filled airways can lead to further injury known as ventilator-induced lung injury [1].

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