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.

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.

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.

The Influence of the Calcium Antagonist Nimodipine and Induced Hypertension on the Behavior of the Cerebral Pial Arteries, the Blood-Brain Barrier, Cerebral Edema, and Cerebral Infarction in Cats with One-Hour Occlusion of the Middle Cerebral Artery

Neurosurgery ◽  
1991 ◽  
Vol 28 (2) ◽  
pp. 267-272 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Shigeru Tsunoda ◽  
Tetsuya Morimoto
Keyword(s):  
Middle Cerebral Artery ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Cerebral Edema ◽  
Evans Blue ◽  
Control Group ◽  
Blue Dye ◽  
Pial Arteries ◽  
Evans Blue Dye ◽  
Induced Hypertension

Abstract Thirty anesthetized cats were randomly assigned to one of three groups of 10 cats each: nimodipine treatment, nimodipine treatment combined with induced hypertension, or a control group. The behavior of the cerebral pial arteries was measured by means of microscopic observation through a cranial window. The middle cerebral artery of each cat was clipped for 1 hour via the transorbital approach. Five hours after circulation was reestablished in the middle cerebral artery. Evans blue dye was injected intravenously: 30 minutes later, the animal was killed. Administration of nimodipine or saline in the treated or control group was started 5 minutes before the middle cerebral artery was clipped and maintained until the end of the experiment. Induced hypertension was produced by administration of dopamine during the occlusion. Damage to the blood-brain barrier (BBB) was judged by extravasation of Evans blue dye. Cerebral edema and infarction were evaluated from histological findings. They were most prominent in the control group; the extent of the hemisphere affected was as follows (mean ± standard error): extravasation. 40.5 ± 8.8%: edema, 43.2 ± 5.7%: infarction, 35.5 ± 9.6%. On the other hand, the extravasation of Evans blue dye and cerebral edema were significantly more extensive in the group treated with nimodipine and induced hypertension (extravasation, 28.2 ± 9.6% of the hemisphere; edema, 30.3 ± 7.1%) than in the group treated with nimodipine alone (extravasation. 18.5 ± 8.7% of the hemisphere; edema, 19.4 ± 6.3%). but the infarction size was similar in both groups (16.6 ± 4.9% of the hemisphere in the former; 17.0 ± 6.2 in the latter). Based on these results, we arc cautious in combining calcium entry blocking agents such as nimodipine with induced hypertension in patients with acute cerebral ischemia.

The influence of systemic arterial pressure and intracranial pressure on the development of cerebral vasogenic edema

1983 ◽  
Vol 59 (5) ◽  
pp. 803-809 ◽  
Author(s):  
Quentin J. Durward ◽  
Rolando F. Del Maestro ◽  
A. Loren Amacher ◽  
J. Keith Farrar
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Vasogenic Edema ◽  
Brain Barrier ◽  
Blue Dye ◽  
Content Type ◽  
Evans Blue Dye ◽  
Fine Print

✓ The influence of intracranial pressure (ICP), systemic arterial pressure (SAP), and cerebral perfusion pressure (CPP) upon the development of vasogenic cerebral edema is largely unknown. To study their relationship, the authors have produced an osmotic disruption of the blood-brain barrier unilaterally in rabbits by injecting 1 cc/kg of 2M NaCl into the left internal carotid artery. The amount of vasogenic edema produced was assessed by quantitation of the extravasation of Evans blue dye into the area of maximum blood-brain barrier breakdown by means of optical densitometry following formamide extraction. The ICP was measured using a cisterna magna catheter into which mock cerebrospinal fluid could be infused at a predetermined pressure. The SAP was controlled by exsanguination from a femoral artery catheter. In 18 animals in which blood pressure was not controlled, no significant relationship between the ICP and the degree of Evans blue dye extravasation was noted. In these animals, however, a direct relationship between CPP (defined as mean arterial pressure minus mean ICP) and extravasation of Evans blue dye was found (correlation coefficient 0.630; p < 0.001). When ICP was held constant at 0 to 5 mm Hg in another group of 16 animals and different levels of blood pressure were produced by exsanguination, a significant direct relationship between extravasation of Evans blue dye and the SAP was found (correlation coefficient 0.786; p < 0.001). In a third group of 20 animals, the blood pressure was held constant at 90 to 100 mm Hg and the ICP was varied between 0 and 75 mm Hg. There was a highly significant result indicating increasing Evans blue dye extravasation with lower levels of ICP (p < 0.001). Cerebral blood flow determinations by the hydrogen clearance method indicated loss of autoregulation in all animals in the areas of brain injured by intracarotid hypertonic saline. These results indicate that high SAP and low ICP (that is, a large CPP) promote Evans blue dye extravasation in this model of blood-brain barrier disruption. This finding has implications for the management of patients with vasogenic edema.

scholarly journals Cardiac Output in Pregnancy: Correlation Between Evans Blue Dye and Blood Pressure Methods

1955 ◽  
Vol 3 (5) ◽  
pp. 506-509 ◽  
Author(s):  
CHARLES H. HENDRICKS ◽  
EDWARD J. QUILLIGAN
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Evans Blue ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
In Pregnancy

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

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.

scholarly journals A Study of the Pathogenesis and Prevention of Central Pontine Myelinolysis in a Rat Model

2006 ◽  
Vol 34 (3) ◽  
pp. 264-271 ◽  
Author(s):  
Q-H Ke ◽  
T-B Liang ◽  
J Yu ◽  
S-S Zheng
Keyword(s):  
Hypertonic Saline ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Central Pontine Myelinolysis ◽  
Brain Barrier ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Pontine Myelinolysis ◽  
Demyelinating Lesions ◽  
Central Pontine

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.

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