Relationship between airway microvascular leakage, edema, and baseline airway functions

1998 ◽  
Vol 84 (1) ◽  
pp. 77-81
Author(s):  
Melissa Matheson ◽  
Ann-Christine Rynell ◽  
Melissa McClean ◽  
Norbert Berend
Keyword(s):  
Evans Blue ◽  
Airway Resistance ◽  
Respiratory Physiology ◽  
Blue Dye ◽  
Wall Area ◽  
Evans Blue Dye ◽  
Microvascular Leakage ◽  
Airway Function ◽  
Significant Difference ◽  
Before And After

Matheson, Melissa, Ann-Christine Rynell, Melissa McClean, and Norbert Berend. Relationship between airway microvascular leakage, edema, and baseline airway functions. J. Appl. Physiol. 84(1): 77–81, 1998.—This study was designed to examine the relationship among microvascular leakage, edema, and baseline airway function. Microvascular leakage was induced in the airways of anesthetized, tracheostomized New Zealand White rabbits ( n = 22) by using nebulized N-formyl-methionyl-leucyl-phenylalanine (10 mg) and was measured in the trachea by using the Evans blue dye technique. Airway wall thickness was assessed morphometrically in the right main bronchus after Formalin fixation at a pressure of 25 cmH2O. Areas calculated included the mucosal wall area, the adventitial wall area, the total wall area, and the percentage of total wall area consisting of blood vessels. A neutrophil count was also performed by analyzing numbers of cells in both the mucosal wall area and the adventitial wall area. Airway function was assessed before and 30 min after challenge with N-formyl-methionyl-leucyl-phenylalanine by determining airway resistance, functional residual capacity, specific airway resistance, and flow-volume and pressure-volume curves (after paralysis of the animals with suxamethonium). The concentration of Evans blue dye in tracheal tissue ranged from 31.3 to 131.2 μg. There was a significant correlation between this concentration and both the adventitial wall area ( P < 0.01) and mucosal neutrophil numbers ( P < 0.005). There was no correlation between Evans blue concentration and either blood vessel area or changes in respiratory physiology parameters before and after challenge. There was no significant difference between any respiratory physiology measurements before and after challenge. We conclude that an increase in microvascular leakage correlates with airway edema in the adventitia; however, these airway changes have no significant effect on airway elastic or resistive properties.

Peptidase modulation of noncholinergic vagal bronchoconstriction and airway microvascular leakage

1991 ◽  
Vol 70 (6) ◽  
pp. 2730-2735 ◽  
Author(s):  
J. O. Lotvall ◽  
K. Tokuyama ◽  
C. G. Lofdahl ◽  
A. Ullman ◽  
P. J. Barnes ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Evans Blue ◽  
Enzyme Inhibitors ◽  
Airflow Obstruction ◽  
Neutral Endopeptidase ◽  
Blue Dye ◽  
Enalapril Maleate ◽  
Evans Blue Dye ◽  
Microvascular Leakage ◽  
Degradative Enzymes

We investigated whether inhibition of neutral endopeptidase 24.11 (NEP) and/or angiotensin-converting enzyme (ACE) modifies vagally induced nonadrenergic noncholinergic (NANC) airflow obstruction and airway microvascular leakage as measured by extravasation of Evans blue dye (intravenous) in anesthetized guinea pigs. We gave phosphoramidon to inhibit NEP and enalapril maleate or captopril to inhibit ACE. Animals pretreated with inhaled phosphoramidon (7.5 or 75 nmol), enalapril maleate (87 or 870 nmol), or captopril (350 nmol) reached higher peak lung resistance (RL) values (14.3 +/- 2.7, 15.7 +/- 3.8, 16.7 +/- 3.8, 11.4 +/- 1.6, and 24.6 +/- 3.5 cmH2O.ml-1.s, respectively) than saline-treated animals (5.9 +/- 1.1; P less than 0.05) after bilateral vagus nerve stimulation (5 Hz, 10 V, 10 ms, 150 s). Intravenous phosphoramidon (1 mg/kg), but not intravenous captopril (6 mg/kg), potentiated peak RL (22.9 +/- 6.9 and 7.1 +/- 1.5 cmH2O.ml-1.s, respectively). Vagal nerve stimulation (1 and 5 Hz) increased the extravasation of Evans blue dye in tracheobronchial tissues compared with sham-stimulated animals, but this was not potentiated by inhaled enzyme inhibitors or intravenous captopril. However, intravenous phosphoramidon significantly augmented the extravasation of Evans blue dye in main bronchi and intrapulmonary airways. We conclude that degradative enzymes regulate both NANC-induced airflow obstruction and airway microvascular leakage.

Determination of plasma volume in swine by the enzyme-dilution method

1987 ◽  
Vol 252 (5) ◽  
pp. R1003-R1008
Author(s):  
M. A. Holmes ◽  
R. B. Weiskopf
Keyword(s):  
Plasma Volume ◽  
Evans Blue ◽  
Dilution Method ◽  
Blue Dye ◽  
Time Activity ◽  
Evans Blue Dye ◽  
Before And After ◽  
Concentration Curves ◽  
Alt Activity

Plasma volume of six young swine was determined by simultaneous dilution in the plasma of two purified porcine enzymes, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and Evans blue dye. Ninety-minute time-activity and time-concentration curves were obtained, and the dilution spaces of each plasma indicator at the time of injection were estimated by extrapolation of data from the first 30 min after injection. Plasma volumes estimated using the two enzymes agreed closely with each other (AST, mean 50.2 ml/kg; ALT, mean 49.8 ml/kg) and were 11% smaller than those determined using Evans blue dye (mean 56.3 ml/kg). Plasma volumes calculated from the AST and ALT activities and Evans blue dye concentration in a sample drawn 5 min after injection very closely approximated those obtained by extrapolation. These values were comparable to previously published estimates of plasma volume for swine of equivalent weight. Endogenous plasma levels of AST and ALT activity were measured in samples drawn from five swine before and after a 40% blood loss. No significant change in AST or ALT activities occurred after hemorrhage.

Brain Retractor Edema during Induced Hypotension: The Effect of the Rate of Return of Blood Pressure

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 901-906 ◽  
Author(s):  
S. Lownie ◽  
X. Wu ◽  
S. Karlik ◽  
A.W. Gelb
Keyword(s):  
Blood Pressure ◽  
Magnetic Resonance ◽  
Cerebral Edema ◽  
Evans Blue ◽  
Relaxation Times ◽  
Blue Dye ◽  
Edema Formation ◽  
Induced Hypotension ◽  
Evans Blue Dye ◽  
Significant Difference

Abstract This study evaluated the hypothesis that the postoperative formation of cerebral edema may be influenced by the rate of blood pressure return after induced hypotension in a graded brain retractor injury. Nineteen cats underwent unilateral craniotomy, isoflurane-induced hypotension to a mean of 50 mm Hg, and application of a brain retractor at 20 mm Hg of pressure for 1 hour. Blood pressure was returned to normal either within 3 minutes or over 20 minutes. The degree of cerebral edema formation was determined by Evans blue dye and coronal magnetic resonance imaging. All animals showed extravasation of Evans blue dye in the retracted hemisphere that was most marked at the periphery of the retractor. T1 relaxation times were significantly prolonged in the retracted hemispheres of both the fast return and slow return groups (18.8% and 17.8%, respectively) and more so at the Evans blue sites (42.8% and 40.8%), although not so strikingly beneath the retractor itself (6.3% and 7.8%). T2 relaxation times were similarly prolonged but to approximately half the degree of the T1 times. In the nonretracted hemisphere, drug-induced hypotension alone did not result in significant acute cerebral edema or blood-brain barrier alteration. There was no significant difference between the fast and slow groups in Evans blue extravasation or magnetic resonance changes. Thus, in a retractor-induced brain injury, restoration of arterial pressure to normal either gradually or rapidly did not influence the degree or extent of edema formation.

Airflow obstruction after substance P aerosol: contribution of airway and pulmonary edema

1990 ◽  
Vol 69 (4) ◽  
pp. 1473-1478 ◽  
Author(s):  
J. O. Lotvall ◽  
R. J. Lemen ◽  
K. P. Hui ◽  
P. J. Barnes ◽  
K. F. Chung
Keyword(s):  
Substance P ◽  
Pulmonary Edema ◽  
Evans Blue ◽  
Guinea Pigs ◽  
Airflow Obstruction ◽  
Maximum Effect ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Microvascular Leakage ◽  
Lung Resistance

We have studied the effects of aerosolized substance P (SP) in guinea pigs with reference to lung resistance and dynamic compliance changes and their recovery after hyperinflation. In addition, we have examined the concomitant formation of airway microvascular leakage and lung edema. Increasing breaths of SP (1.5 mg/ml, 1.1 mM), methacholine (0.15 mg/ml, 0.76 mM), or 0.9% saline were administered to tracheostomized and mechanically ventilated guinea pigs. Lung resistance (RL) increased dose dependently with a maximum effect of 963 +/- 85% of baseline values (mean +/- SE) after SP (60 breaths) and 1,388 +/- 357% after methacholine (60 breaths). After repeated hyperinflations, methacholine-treated animals returned to baseline, but after SP, mean RL was still raised (292 +/- 37%; P less than 0.005). Airway microvascular leakage, measured by extravasation of Evans Blue dye, occurred in the brain bronchi and intrapulmonary airways after SP but not after methacholine. There was a significant correlation between RL after hyperinflation and Evans Blue dye extravasation in intrapulmonary airways (distal: r = 0.89, P less than 0.005; proximal: r = 0.85, P less than 0.01). Examination of frozen sections for peribronchial and perivascular cuffs of edema and for alveolar flooding showed significant degrees of pulmonary edema for animals treated with SP compared with those treated with methacholine or saline. We conclude that the inability of hyperinflation to fully reverse changes in RL after SP may be due to the formation of both airway and pulmonary edema, which may also contribute to the deterioration in RL.

Thromboxane synthetase inhibition in acute focal cerebral ischemia in cats

1984 ◽  
Vol 61 (6) ◽  
pp. 1107-1112 ◽  
Author(s):  
Nazih A. Moufarrij ◽  
John R. Little ◽  
Victor Skrinska ◽  
Fred V. Lucas ◽  
John P. Latchaw ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Infarct Size ◽  
Evans Blue ◽  
Bleeding Time ◽  
Blue Dye ◽  
Sodium Fluorescein ◽  
Evans Blue Dye ◽  
Mca Occlusion ◽  
Thromboxane Synthetase ◽  
Before And After

✓ The purpose of this investigation was to study the effects of a selective thromboxane A2 (TXA2) synthetase inhibitor (TSI) upon the evolution of cerebral infarction in the cat. Adult cats, lightly anesthetized with nitrous oxide, underwent right middle cerebral artery (MCA) occlusion for 4 hours followed by a 2-hour period of reperfusion before sacrifice. Ten cats received 3 mg/kg TSI intravenously immediately before, and 10 cats received 3 mg/kg TSI intravenously immediately after MCA occlusion. Ten cats were used as controls receiving no treatment. The bleeding time was determined at baseline and at the end of each experiment. Electroencephalographic (EEG) recordings were obtained before and after MCA clipping and MCA release, and at hourly intervals thereafter. Regional cerebral blood flow (rCBF) was measured using the xenon-133 (133Xe) clearance technique before and after MCA occlusion, after MCA reopening, and before terminating each experiment. Thirty minutes before each cat was sacrificed, Evans blue dye and sodium fluorescein were given intravenously. The animals were then perfused with colloidal carbon and the brains removed and evaluated for midline shift, Evans blue dye and sodium fluorescein extravasation, carbon staining, and infarct size. The bleeding time, arterial blood pressure, rCBF changes, brain swelling, and vital dye extravasation were not statistically different between the three treatment groups. The EEG changes, carbon staining, and infarct size differences between the three groups also failed to reach statistical significance, but there was a suggestion that these parameters were adversely affected in the cats pretreated with TSI. Ten additional cats undergoing MCA occlusion and reperfusion were used for pharmacological studies. Five of them received 3 mg/kg TSI intravenously immediately after MCA occlusion, and serial drug and thromboxane B2 (TXB2) levels (a stable metabolite of TXA2) were determined. Another five cats were not treated and serial TXB2 levels were obtained. Production of TXA2 was inhibited by 95% in cats receiving TSI. In conclusion, thromboxane synthetase inhibition failed to modify favorably the evolution of cerebral infarction. When TSI was given before MCA occlusion, cerebral infarction tended to be more extensive.

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
Keyword(s):  
Evans Blue ◽  
Oxygen Mixture ◽  
Blue Dye ◽  
Mechanically Ventilated ◽  
Evans Blue Dye ◽  
Regional Deposition

scholarly journals Acoustic enhanced Evans blue dye perfusion in neurological tissues

2007 ◽  
Author(s):  
George K. Lewis Jr. ◽  
Willam L. Olbricht ◽  
George Lewis
Keyword(s):  
Evans Blue ◽  
Blue Dye ◽  
Evans Blue Dye

Flow of edema fluid into pulmonary airways

1983 ◽  
Vol 55 (4) ◽  
pp. 1262-1268 ◽  
Author(s):  
G. R. Mason ◽  
R. M. Effros
Keyword(s):  
Evans Blue ◽  
Left Atrial ◽  
Blue Dye ◽  
Edema Formation ◽  
Evans Blue Dye ◽  
Colloid Particles ◽  
Edema Fluid ◽  
Pulmonary Airways ◽  
99Mtc Sulfur Colloid

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.

A modified bioassay for heat-stable Escherichia coli enterotoxin

1977 ◽  
Vol 23 (3) ◽  
pp. 331-336 ◽  
Author(s):  
S. Stavric ◽  
D. Jeffrey
Keyword(s):  
Escherichia Coli ◽  
Body Weight ◽  
Incubation Time ◽  
Evans Blue ◽  
Room Temperature ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Heat Stable ◽  
Stomach Distention ◽  
Time Required

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.

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