Regional Deposition of Inhaled Evans Blue Dye in Mechanically Ventilated Rabbits with Air or Helium Oxygen Mixture

1998 ◽  
Vol 24 (2) ◽  
pp. 159-172 ◽  
Author(s):  
Magnus Svartengren ◽  
Patrik Skogward ◽  
Ola Nerbrink ◽  
Magnus Dahlbäck
2007 ◽  
Author(s):  
George K. Lewis Jr. ◽  
Willam L. Olbricht ◽  
George Lewis
Keyword(s):  
Blue Dye ◽  

1983 ◽  
Vol 55 (4) ◽  
pp. 1262-1268 ◽  
Author(s):  
G. R. Mason ◽  
R. M. Effros

An in situ rabbit preparation was used to characterize the manner in which edema fluid enters the airways when left atrial pressures are elevated. The airways were initially filled with fluid to minimize retrograde flow of edema fluid into the alveoli. The airway solution contained 125I-albumin and in some studies [14C]sucrose, and the lungs were perfused with a comparable solution which contained albumin labeled with Evans blue dye and 99mTc-diethylenetriaminepentaacetate (DTPA) or 99mTc-sulfur-colloid particles (0.4-1.7 micron diam). After 30 min of perfusion, fluid was pumped from the airways into serial tubes. When left atrial pressures were low, there was very little transfer of labels detectable between the airway and perfusate solutions. However when left atrial pressures were increased to either 15 or 22 cmH2O, fluid entered the airways containing approximately the same concentrations of Evans blue dye and 99mTc-DTPA as those present in the perfusate. In contrast, the concentration of colloid particles averaged less than 5% perfusate concentrations, indicating that the fluid had not escaped through a tear in the barriers separating the vascular and airway compartments. Concentrations of the perfusate fluid and indicators were highest in the initial samples pumped from the airways. These observations suggest that some of the fluid entering the airways may be derived from peribronchial cuffs or that there are marked regional differences in edema formation from alveoli.


1977 ◽  
Vol 23 (3) ◽  
pp. 331-336 ◽  
Author(s):  
S. Stavric ◽  
D. Jeffrey

Infant mice were injected orally with preparations containing Escherichia coli heat-stable enterotoxin (ST) and Evans blue dye, and incubated at 22 °C. With enterotoxin-positive samples, the stomach was distended and contained essentially all of the dye. With enterotoxin-negative samples, the stomach remained normal in size and the dye passed freely into the intestines. The time required to obtain the maximum ratio of gut weight to body weight varied from 30 to 90 min and was dependent upon the concentration of enterotoxin. Heat-labile enterotoxin (LT) had no effect during this period.Based on these findings, the mouse incubation time was reduced from 4 h to 90 min, and the heating of test samples was retained only for confirmation of ST. The location of the dye and stomach distention served as an indicator of positive responses to ST. Incubation of the mice at room temperature (22 °C) was found satisfactory.


2006 ◽  
Vol 34 (3) ◽  
pp. 264-271 ◽  
Author(s):  
Q-H Ke ◽  
T-B Liang ◽  
J Yu ◽  
S-S Zheng

The development of central pontine myelinolysis was studied in rats. Severe hyponatraemia was induced using vasopressin tannate and 2.5% dextrose in water and then rapidly corrected with hypertonic saline alone, hypertonic saline and dexamethasone simultaneously, or hypertonic saline plus dexamethasone 24 h later. The permeability of the blood-brain barrier was evaluated using the extravasation of Evans blue dye and the expression of inducible nitric oxide synthase (iNOS) in the brain was examined using Western blot analysis. Histological sections were examined for demyelinating lesions. In rats receiving hypertonic saline alone, Evans blue dye content and expression of iNOS began to increase 6 and 3 h, respectively, after rapid correction of hyponatraemia and demyelinating lesions were seen. When dexamethasone was given simultaneously with hypertonic saline, these increases were inhibited and demyelinating lesions were absent. These effects were lost if dexamethasone injection was delayed. Disruption of the blood-brain barrier and increased iNOS expression may be involved in the pathogenesis of central pontine myelinolysis, and early treatment with dexamethasone may help prevent the development of central pontine myelinolysis.


1982 ◽  
Vol 38 (3) ◽  
pp. 932-937 ◽  
Author(s):  
A J Crowle ◽  
M H May
Keyword(s):  
Blue Dye ◽  

2006 ◽  
Vol 13 (5) ◽  
pp. 692-700 ◽  
Author(s):  
Chris Tsopelas ◽  
Elaine Bevington ◽  
James Kollias ◽  
Sabah Shibli ◽  
Gelareh Farshid ◽  
...  

Animals ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 38 ◽  
Author(s):  
Majid Shakeri ◽  
Jeremy James Cottrell ◽  
Stuart Wilkinson ◽  
Weicheng Zhao ◽  
Hieu Huu Le ◽  
...  

In a 2 × 2 factorial design, 60 male Ross-308 broilers were fed either a control or 1 g/kg betaine diet and housed under thermoneutral (TN) or heat stress (HS) conditions. Broilers were acclimated to diets for 1 week under TN (25 °C), then either kept at TN or HS, where the temperature increased 8 h/day at 33 °C and 16 h/day at 25 °C for up to 10 days. Respiration rate (RR) was measured at four time points, and on each of 1, 2, 3, 7 and 10 days of HS, 12 broilers were injected with 0.5 mg/kg of Evans Blue Dye (EBD) solution to quantify regional changes in tissue damage. Betaine was quantified in tissues, and ileal damage was assessed via morphometry and transepithelial resistance (TER). Heat stress elevated RR (p < 0.001) and resulted in reduced villous height (p = 0.009) and TER (p < 0.001), while dietary betaine lowered RR during HS (p < 0.001), increased betaine distribution into tissues, and improved ileal villous height (p < 0.001) and TER (p = 0.006). Heat stress increased EBD in the muscle and kidney of chickens fed the control diet but not in those receiving betaine. Overall, these data indicate that supplemented betaine is distributed to vital organs and the gastrointestinal tract, where it is associated with improved tolerance of HS. Furthermore, EBD markers help reveal the effects of HS on organs dysfunction.


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