Correlations between the apparent diffusion coefficient, water content, and ultrastructure after induction of vasogenic brain edema in cats

1999 ◽  
Vol 90 (3) ◽  
pp. 499-503 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Tsukasa Nagaoka ◽  
Masato Ueki ◽  
Ichiro Yamada ◽  
Naoyuki Miyasaka ◽  
...  
Keyword(s):  
White Matter ◽  
Water Content ◽  
Brain Edema ◽  
Nerve Fibers ◽  
Tissue Water ◽  
Content Type ◽  
Deep White Matter ◽  
Vasogenic Brain Edema ◽  
Apparent Diffusion ◽  
Fine Print

Object. The authors examined the correlation between changes in the apparent diffusion coefficient, regional water content, and tissue ultrastructure after vasogenic brain edema.Methods. Vasogenic edema was induced in the white matter of six cats by cortical cold lesioning. The trace of diffusion tensor (Trace[D]) obtained from magnetic resonance imaging to measure the orientationally averaged water diffusibility was compared with the corresponding tissue water content determined by gravimetric studies and with ultrastructural water localization. Edema fluid had spread to the subcortical and deep white matter by 4.5 hours postlesioning. The increase in Trace(D) showed a significant linear correlation with the increase in tissue water content, both in the subcortical and deep white matter as follows: y = 45.5x − 2367 (r = 0.94) and y = 37.0x − 1769 (r = 0.93), respectively, where x is the water content (gram water/gram tissue) and y the Trace(D) (× 10−6 mm2/second). On histological examination, nerve fibers were found to be dissociated in the white matter and the extracellular space was markedly enlarged with protein-rich fluid. No noticeable hydropic swelling of the cellular components was observed.Conclusions. A linear correlation was observed between increases in Trace(D) and increases in extracellular water volume in in vivo vasogenic brain edema. A similar correlation between the subcortical and deep white matter showing different arrangements of nerve fibers (parallel compared with intermingled, respectively) indicated that measurement of Trace(D) is a suitable parameter for the evaluation of vasogenic brain edema.

The kallikrein-kinin system as mediator in vasogenic brain edema

1984 ◽  
Vol 61 (1) ◽  
pp. 87-96 ◽  
Author(s):  
Andreas Unterberg ◽  
Alexander J. Baethmann
Keyword(s):  
White Matter ◽  
Water Content ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Vasogenic Edema ◽  
Ventricular System ◽  
Periventricular White Matter ◽  
Content Type ◽  
Vasogenic Brain Edema ◽  
Fine Print

✓ Plasma and bradykinin were perfused into the ventricular system of mongrel dogs to investigate whether either or both induce brain edema. Formation of cerebral edema was determined by measurement of cerebral water and electrolytes in periventricular white matter, cerebral cortex, and caudate nucleus. The response of cerebral tissue to exposure to bradykinin or to plasma, as a carrier of kininogens, was analyzed by assessment of the perfusate composition after ventricle passage. The authors report that cerebral administration of bradykinin induces cerebral edema. Ventricular perfusion with plasma also led to an increase of cerebral water content which was restricted to the white matter, but involved all brain tissue areas, if bradykinin was used. Ventricular perfusion with plasma was associated with consumption of the kinin precursor (kininogens) indicative of formation of kinins. Significant consumption of the precursor was found in five out of nine animals subjected to plasma perfusion of the ventricular system. In these animals a close correlation between the increase of white matter water content and kininogen-consumption as a measure of kinin-formation was obtained. Marked kinin-degrading activity was observed during ventricular perfusion with bradykinin as concluded from a considerable decrease of bradykinin concentration in the cisternal effluent compared to the inflowing perfusate concentration. Ventricular perfusion with plasma was associated with a decrease of K+ clearance capacity with continued duration, and in two animals with a release of glutamate into the plasma perfusate, suggesting an involvement of cytotoxic mechanisms. These findings provide support for the hypothesis of a mediator function of the kallikrein-kinin (KK) system in vasogenic brain edema. The next question that needs to be answered to complete the picture — does spontaneous activation of the KK system occur in conditions leading to vasogenic edema? — is studied in a subsequent report.

A simple gravimetric technique for measurement of cerebral edema

1978 ◽  
Vol 49 (4) ◽  
pp. 530-537 ◽  
Author(s):  
Anthony Marmarou ◽  
Werner Poll ◽  
Kenneth Shulman ◽  
Hemmige Bhagavan
Keyword(s):  
White Matter ◽  
Specific Gravity ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Tissue Water ◽  
Simple Method ◽  
Content Type ◽  
Adult Cats ◽  
Automated Technique ◽  
Fine Print

✓ A simple method was developed for the laboratory preparation of gradient columns of specific gravity used in measurement of brain-tissue water. By this automated technique, virtually linear and repeatable density gradients were obtained from which values of tissue specific gravity could be determined. The specific gravity of both solid and fresh cortex and white matter from adult cats was measured and converted to units of percent water per gram tissue using conversion factors derived for this purpose and applicable to studies of brain edema.

Influence of the rate of ventricular enlargement on the white matter water content in progressive feline hydrocephalus

1987 ◽  
Vol 66 (4) ◽  
pp. 577-583 ◽  
Author(s):  
Futoshi Takei ◽  
Kenneth Shapiro ◽  
Ira Kohn
Keyword(s):  
White Matter ◽  
Water Content ◽  
Progressive Increase ◽  
Central Canal ◽  
Ventricular Enlargement ◽  
Ventricular Size ◽  
Content Type ◽  
Wet Weight ◽  
Dural Opening ◽  
Fine Print

✓ The effectiveness of transependymal absorption of cerebrospinal fluid in hydrocephalus was studied by correlating the measured water content of feline hydrocephalic white matter with the rate of enlargement of the ventricles. Two groups of cats were subjected to opening of either the calvaria or the calvaria and dura before the intracisternal injection of kaolin to obtain two profiles of ventricular enlargement. The water content 1, 2, and 3 mm from the lateral ventricles was measured in each group using the dry/wet weight and microgravimetric techniques after sacrificing the animals in each group at 2, 3, or 6 weeks after inducing hydrocephalus. In the animals with both calvarial and dural opening, the ventricles enlarged rapidly in the first 2 to 3 weeks and then continued to increase but at a slower rate. Concomitant with this early increase of ventricular size was a progressive increase in white matter water content both adjacent to and remote from the ventricles, which continued through 6 weeks. When only the calvaria was opened, ventricular size increased gradually, but continued to increase at a constant rate throughout the 6 weeks. Water content adjacent to the ventricle did not increase until the 3rd week, with little spread to adjacent areas by the 6th week. The central canals of the spinal cord were enlarged in both groups at all sampling levels. Neither increased periventricular water nor dilatation of the central canal was associated with stabilization of ventricular size in these studies. The authors conclude that these pathways are not sufficient to arrest the hydrocephalic process in these models.

Composition of isolated edema fluid in cold-induced brain edema

1979 ◽  
Vol 51 (1) ◽  
pp. 70-77 ◽  
Author(s):  
Jurjen Gazendam ◽  
K. Gwan Go ◽  
Annie K. van Zanten
Keyword(s):  
Cerebrospinal Fluid ◽  
White Matter ◽  
Brain Edema ◽  
Vasogenic Edema ◽  
Colloid Osmotic Pressure ◽  
Freezing Damage ◽  
Content Type ◽  
Edema Fluid ◽  
The Brain ◽  
Fine Print

✓ Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients

2000 ◽  
Vol 93 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Anthony Marmarou ◽  
Panos P. Fatouros ◽  
Pal Barzó ◽  
Gennarina Portella ◽  
Masaaki Yoshihara ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Tissue ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Brain Swelling ◽  
Tissue Water ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling.Methods. Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (± standard deviation) percentage of swelling due to water was 9.37 ± 8.7%, whereas that due to blood was −0.8 ± 1.32%.Conclusions. The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.

Focal brain edema associated with acute arterial hypertension

1986 ◽  
Vol 64 (4) ◽  
pp. 643-649 ◽  
Author(s):  
Shizuo Hatashita ◽  
Julian T. Hoff ◽  
Shozo Ishii
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Water Content ◽  
Brain Edema ◽  
Evans Blue ◽  
Blue Dye ◽  
Boundary Zone ◽  
Tissue Pressure ◽  
Content Type ◽  
Fine Print

✓ Acute arterial hypertension was studied in normal cats to determine its role in the formation of brain edema. Arterial hypertension was induced for 30 minutes by inflation of a balloon catheter situated in the descending aorta. Cerebral edema was evaluated by gross and microscopic observations, tissue water content by wet/dry weights, and blood-brain barrier (BBB) permeability by extravasation of horseradish peroxidase (HRP) and Evans blue dye. For 1 hour after the hypertensive insult, tissue pressure and regional cerebral blood flow (rCBF) were measured from the arterial boundary zone and from a non-boundary region, and intracranial pressure was recorded from the lateral ventricle as ventricular fluid pressure. Focal lesions with increased BBB permeability to Evans blue dye or HRP were usually located symmetrically in the cortex, corresponding to the occipitoparietal parts of the arterial boundary zones. The increase in water content was found only in areas of increased permeability. Tissue pressure increased simultaneously with the abrupt rise in blood pressure, and an increase in rCBF paralleled the elevation of blood pressure. Tissue pressure and rCBF returned to a steady state when blood pressure returned to normal. There were no differences in tissue pressure or rCBF between the arterial boundary zone and the non-boundary zone, even during arterial hypertension. In cerebral hemispheres examined 48 hours after the hypertensive challenge, brain edema had not continued to develop. The data indicate that acute arterial hypertension may produce focal brain edema with increased permeability of the BBB in the cortex of normal brain, particularly in the arterial boundary zones. The authors postulate that increased cerebral blood volume, high intraluminal pressure, and breakthrough of autoregulation play an important role in the formation of hypertensive brain edema.

The effects of cold-induced brain edema and white-matter ischemia on the somatosensory evoked response

1980 ◽  
Vol 53 (2) ◽  
pp. 180-184 ◽  
Author(s):  
Leslie N. Sutton ◽  
Derek A. Bruce ◽  
Frank Welsh
Keyword(s):  
White Matter ◽  
Brain Edema ◽  
Vasogenic Edema ◽  
Evoked Response ◽  
Content Type ◽  
Cold Lesion ◽  
Somatosensory Evoked Response ◽  
Electrophysiological Effects ◽  
Fine Print ◽  
Cortical Waves

✓ The electrophysiological effects of cold-lesion edema and white-matter ischemia were studied in cats by reference to the short-latency somatosensory evoked response. The primary cortical waves were found to be considerably delayed following a period of white-matter ischemia; however, cold-lesion edema appeared to have no significant effect on the evoked response. The authors conclude that vasogenic edema does not interfere with axonal functioning by an ischemic mechanism.

Evidence against leukotrienes as mediators of brain edema

1991 ◽  
Vol 74 (5) ◽  
pp. 773-780 ◽  
Author(s):  
Andreas Unterberg ◽  
Walter Schmidt ◽  
Michael Wahl ◽  
Earl F. Ellis ◽  
Anthony Marmarou ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Brain Edema ◽  
Parietal Cortex ◽  
Brain Slices ◽  
Control Group ◽  
Tissue Water ◽  
Content Type ◽  
Cranial Window ◽  
Fine Print

✓ Leukotrienes are powerful metabolites of arachidonic acid which are known to increase the permeability of peripheral blood vessels. These substances are found in brain tissue in association with cerebral ischemia, and in brain tumors. Therefore, it has been proposed that leukotrienes have a mediator function in brain edema. This hypothesis was subjected to further experimental analysis in this study, in which the authors investigated whether: 1) superfusion of the exposed brain surface with leukotrienes increases the permeability of extraparenchymal blood vessels in vivo; 2) intraparenchymal infusion of leukotrienes induces brain edema; and 3) pharmacological inhibition of leukotriene formation by BW755C, an inhibitor of leukotriene synthesis, reduces formation of brain edema from a standardized traumatic insult. The pial vessels of the parietal cortex of cats were examined by fluorescence microscopy during cerebral superfusion with the leukotrienes C4 (LTC4), D4 (LTD4), or E4 (LTE4) by using an open cranial window preparation. Intravenous Na+-fluorescein served as an in vivo blood-brain barrier (BBB) indicator. Superfusion of the pia with leukotrienes (up to 2 µM) did not open the barrier to fluorescein, but was associated with a significant constriction (up to 25%) of arterial and venous vessels. In experiments with slow infusion of leukotriene B4 (LTB4) or LTC4 into the white matter of feline brain, the tissue water content was subsequently determined in serial brain slices using the specific gravity method. Tissue water profiles obtained after a 15- µM infusion of either LTB4 or LTC4 were virtually identical with those of control animals infused with mock cerebrospinal fluid. Thus, neither LTB4 nor LTC4 led to an augmentation of infusion-induced brain edema. In a final series, a cold lesion of the left parietal cortex was induced in rabbits. Twenty-four hours later, swelling of the exposed hemisphere was quantified by gravimetrical comparison of its weight with that of the contralateral nontraumatized hemisphere. Eight animals received BW755C intravenously prior to and after trauma to inhibit formation of leukotrienes. Seven rabbits were infused with an equivalent volume of saline as a control study. The resulting hemispheric swelling was 7.7% ± 0.6% (mean ± standard error of the mean) 24 hours later in animals receiving BW755C and 7.8% ± 1.2% in the control group, indicating that inhibition of leukotrienes was ineffective in preventing formation of vasogenic brain edema. The findings demonstrate that leukotrienes administered to the brain in concentrations occurring under pathological conditions do not open the BBB nor do they induce brain edema. Moreover, formation of brain edema from a standard insult was not therapeutically influenced by inhibition of leukotriene synthesis. Thus, the current findings taken together do not support a role of leukotrienes as mediators in brain edema.

Microgravimetric analysis of human brain tissue Correlation with computerized tomography scanning

1981 ◽  
Vol 54 (6) ◽  
pp. 797-801 ◽  
Author(s):  
Hiroshi Takagi ◽  
Kenneth Shapiro ◽  
Anthony Marmarou ◽  
Hugh Wisoff
Keyword(s):  
White Matter ◽  
Arteriovenous Malformation ◽  
Water Content ◽  
Computerized Tomography ◽  
Attenuation Coefficient ◽  
Human Brain Tissue ◽  
Content Type ◽  
Ct Attenuation ◽  
Elevated Water ◽  
Fine Print

✓ Microgravimetric technique was used to measure the water content of tumors and adjacent brain. Multiple 1-cu mm samples were obtained from 17 patients with neurosurgical lesions. The site of each sample was located on the appropriate computerized tomography (CT) slice, and the water content correlated with the CT attenuation coefficient. The water content of peritumor white matter in 11 patients with glioblastomas was 5% to 8% H2O/gm tissue greater than the water content of white matter measured in three normal control individuals. These areas corresponded to low CT attenuation coefficients (8 to 15 EMI units). There were no statistically significant differences between the water content of tumors and adjacent white matter, even though the CT attenuation coefficient of the tumor was often of higher value. Low CT attenuation coefficient areas surrounding meningioma, metastasis, and lymphoma always correlated with elevated water content. The greatest water content (84.7% H2O/gm tissue) was found in the white matter surrounding an arteriovenous malformation. There was no correlation between the CT attenuation coefficient of this tissue and the water content in the arteriovenous malformation. This study shows that areas of low CT attenuation coefficient may correlate with measurements of the water content of tissue, but that increased water content may exist without demonstrable changes in the CT attenuation coefficient.

Cerebral blood flow and glucose metabolism in experimental brain edema

1989 ◽  
Vol 71 (6) ◽  
pp. 868-874 ◽  
Author(s):  
Leslie N. Sutton ◽  
David Barranco ◽  
Joel Greenberg ◽  
Stephen Dante ◽  
Sandra Florin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Vasogenic Edema ◽  
Tissue Water ◽  
Content Type ◽  
Control Value ◽  
Experimental Brain Edema ◽  
Fine Print ◽  
Edematous Brain

✓ The relationship between cerebral blood flow (CBF) and cerebral metabolic rate of glucose (CMR gl) in the white matter was studied in a plasma infusion model of vasogenic edema in cats. Local CBF, as determined by iodoantipyrine testing, was found to be significantly decreased in edematous white matter (mean ± standard error of the mean: 17.3 ± 1.5 ml/100 gm/min) when compared with CBF in the contralateral control white matter (24.8 ± 1.8 ml/100 gm/min). When the values for edematous brain were corrected for dilution, however, the local CBF averaged 25.3 ± 1.7 ml/100 gm/min, which was similar to the control value. Local CMRgl was found to be significantly increased in plasma-infused white matter (16.3 ± 2.2 µmol/100 gm/min) compared with that in control white matter (10.7 ± 1.3 µmol/100 gm/min). This difference remained, despite correction for dilution and recalculation of local CMRgl values based on altered kinetic constants found in edematous brain. A similar increase in local CMRgl was noted with saline-infusion edema. It is concluded that the increased tissue water level does not alter CBF, but does induce an increase in anaerobic metabolism.

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