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 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

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.

Long-term mild jogging increases insulin action despite no influence on body mass index or VO2 max

1989 ◽  
Vol 66 (5) ◽  
pp. 2206-2210 ◽  
Author(s):  
Y. Oshida ◽  
K. Yamanouchi ◽  
S. Hayamizu ◽  
Y. Sato
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Clearance Rate ◽  
Insulin Action ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Before And After ◽  
Plasma Insulin Levels ◽  
Improve Glucose Tolerance

Physical training has been shown to improve glucose tolerance and insulin sensitivity. In the present study, insulin action was determined using the euglycemic clamp technique in six untrained nonobese subjects before, during, and after long-term mild regular jogging. After 1 yr of jogging, steady-state plasma insulin levels (I) decreased significantly, and the metabolic clearance rate of insulin was increased by 87%, although insulin infusion rate during the clamp was constant for each individual. The amount of glucose infused (glucose metabolism, M) tended to increase from 6.16 +/- 0.94 to 8.15 +/- 1.94 mg.kg-1.min-1 after regular jogging for 1 yr, although that was not statistically significant. However, M/I increases significantly from 0.060 +/- 0.012 to 0.184 +/- 0.056 (P less than 0.05) after 1 yr. The concentrations of plasma free fatty acids during the hyperinsulinemic clamp decreased more significantly after 1 yr of jogging (P less than 0.05). The concentrations of plasma glycerol decreased gradually before and after long-term regular jogging, showing only a 50–60% reduction in 120 min. Therefore, long-term mild regular jogging, which did not influence either body mass index or maximal O2 uptake, appears to improve insulin action in both carbohydrate and lipid metabolism and to increase the metabolic clearance rate of insulin.

scholarly journals Combined Effect of Infiltration, Capillary Barrier and Sloping Layered Soil on Flow and Solute Transfer in a Heterogeneous Lysimeter

2013 ◽  
Vol 03 (03) ◽  
pp. 138-153 ◽  
Author(s):  
Le Binh Bien ◽  
Dieuseul Predelus ◽  
Laurent Lassabatere ◽  
Thierry Winiarski ◽  
Rafael Angulo-Jaramillo
Keyword(s):  
Layered Soil ◽  
Combined Effect ◽  
Capillary Barrier ◽  
Solute Transfer

scholarly journals Average molecular weight of surfactants in aerosols

2007 ◽  
Vol 7 (5) ◽  
pp. 13805-13838 ◽  
Author(s):  
M. T. Latif ◽  
P. Brimblecombe
Keyword(s):  
Molecular Weight ◽  
Surface Tension ◽  
Atmospheric Aerosols ◽  
Average Molecular Weight ◽  
Molecular Size ◽  
Weight Fraction ◽  
Ozone Exposure ◽  
Before And After ◽  
Fine Mode ◽  
Active Substances

Abstract. Surfactants in atmospheric aerosols determined as methylene blue active substances (MBAS) and ethyl violet active substances (EVAS). The MBAS and EVAS concentrations can be correlated with surface tension as determined by pendant drop analysis. The effect of surface tension was more clearly indicated in fine mode aerosol extracts. The concentration of MBAS and EVAS was determined before and after ultrafiltration analysis using AMICON centrifuge tubes that define a 5000 Da (5 K Da) nominal molecular weight fraction. Overall, MBAS and to a greater extent EVAS predominates in fraction with molecular weight below 5 K Da. In case of aerosols collected in Malaysia the higher molecular fractions tended to be a more predominant. The MBAS and EVAS are correlated with yellow to brown colours in aerosol extracts. Further experiments showed possible sources of surfactants (e.g. petrol soot, diesel soot) in atmospheric aerosols to yield material having molecular size below 5 K Da except for humic acid. The concentration of surfactants from these sources increased after ozone exposure and for humic acids it also general included smaller molecular weight surfactants.

The Two Doctors Fick

2011 ◽  
pp. 94-100
Author(s):  
James R. Munis
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Transfer Rate ◽  
Dialysis Membrane ◽  
Solute Transfer ◽  
Fick Principle ◽  
Capillary Membrane ◽  
The Difference ◽  
Physical Laws ◽  
Alveolar Capillary

We often confuse the ‘Fick principle’ with ‘Fick's law of diffusion.’ They are not the same. Ironically, Fick borrowed heavily from already known physical laws when he first described both his law of diffusion and his principle. Borrowing from Ohm's law of electricity, Fick applied concepts of diffusion and transfer across a resistance to formulate a law of diffusion that could be applied to gas or solute transfer across a membrane. Whether we are talking about transfer across the alveolar-capillary membrane or across a dialysis membrane, the concept is the same. The concept is similar to electricity—you have a transfer rate, resistance, and a gradient. Now let's consider the Fick principle. On the basis of another physical law he understood that, in the steady state, the difference between the amount of oxygen going into a tissue bed minus that leaving the tissue bed must be equal to the oxygen consumed. With a little reworking, this became the Fick principle: Cardiac output = O2 consumption / (arterial O2 - venous O2).

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.

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