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PubMed1995

Intracerebral infusion of thrombin as a cause of brain edema.

Purified thrombin from an exogenous source is a hemostatic agent commonly used in neurosurgical procedures. The toxicity of thrombin in the brain, however, has not been examined. This study was performed to assess the effect of thrombin on brain parenchyma, using the formation of brain edema as an indicator of injury. Ten microliters of test solution was infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later, and the extent of brain edema and ion content were measured. Concentrations of human thrombin as low as 1 U/microliter resulted in a significant increase in brain water content. Rats receiving 10 U/microliters had a mortality rate of 33% compared to no mortality in the groups receiving smaller doses. Thrombin-induced brain edema was inhibited by a specific and potent thrombin inhibitor, hirudin. A medical grade of bovine thrombin commonly used in surgery also caused brain edema when injected at a concentration of 2 U/microliters. Edema formation was prevented by another highly specific thrombin inhibitor, N alpha-(2-Naphthalenesulfonylglycyl)-4-DL-phenylalaninepiperidid e (alpha-NAPAP). Thrombin-induced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Changes in brain ions were inhibited by both hirudin and alpha-NAPAP, corresponding to the inhibition of brain water accumulation. This study shows that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/microliter, an amount within the range of concentrations used for topical hemostasis in neurosurgery.

Animals↗
PubMed1992

Attenuated development of ischemic brain edema in vasopressin-deficient rats.

Brain edema formation was investigated in the vasopressin-deficient Brattleboro rat using a middle cerebral artery occlusion model of early ischemic injury. Water and sodium accumulation after 4 h of ischemia were attenuated 36 and 20%, respectively, in the Brattleboro strain as compared to the control Long-Evans strain. This effect was independent of differences in animal size and state of hydration. In addition, measurements of cerebral blood flow indicated that Brattleboro and Long-Evans rats had equal levels of ischemia following middle cerebral artery occlusion. Systemic treatment of Brattleboro rats with vasopressin normalized their serum electrolyte concentrations and osmolarity but did not alter sodium or water accumulation in the ischemic brain. In contrast, intraventricular administration of vasopressin in Brattleboro rats increased edema formation to that seen in control rats. The reduced water and sodium accumulation in Brattleboro rats subjected to middle cerebral artery occlusion may be related to alterations in blood-brain barrier permeability since the blood-to-brain sodium flux was 36% less in the ischemic tissue of the Brattleboro as compared to the Long-Evans strain. These results support the hypothesis that central vasopressin is a regulator of brain volume and electrolyte homeostasis. Furthermore, our findings suggest a role for central vasopressin in the development of ischemic brain edema.

Aminoisobutyric Acids↗
PubMed2002

Peritumoral brain edema in intracranial meningiomas evaluated by dynamic perfusion-weighted MR imaging: a preliminary study.

Our objective was to semi-quantitatively evaluate the cerebral perfusion in the peritumoral brain edema of meningiomas using dynamic perfusion-weighted MR imaging. Six patients with intracranial meningiomas accompanied by peritumoral brain edema were prospectively examined by perfusion-weighted MR imaging. One patient was examined twice, once before and once 5 months after the surgical resection. The relative regional cerebral blood volume (rrCBV), the relative regional cerebral blood flow (rrCBF), and the relative regional mean transit time (rrMTT) were calculated for peritumoral brain edema and the contralateral white matter. These parameters were compared between peritumoral brain edema and the contralateral white matter. The time-concentration curve of the peritumoral brain edema was less prominent than that of the contralateral white matter, resulting in a significantly lower rrCBV (mean 46%) and rrCBF (mean 45%) in peritumoral brain edema than those of contralateral white matter. The serial perfusion-weighted MR imaging also demonstrated the recovery of these parameters after the removal of meningioma by means of surgical resection. Perfusion-weighted MR imaging can demonstrate significantly decreased rrCBV and rrCBF in peritumoral brain edema compared with those in normal white matter.

Aged↗
PubMed2003

[Macrophotographic measurement of brain surface area for evaluating brain edema after focal cerebral ischemia in mice].

OBJECTIVE: To establish a new macrophotographic measurement of brain surface area to evaluate brain edema after focal cerebral ischemia in mice. METHODS: Permanent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice. The brains were removed 10,30 min,1,3,6,12 and 24 h after MCAO, and photographed in dorsal and lateral views by a digital camera. Then, 6 coronal slices of 1 mm thick were cut and photographed. Finally, the water content of brain tissue was measured by heating at 110 degrees C for 24 h. The left and right hemisphere areas of the brains and the brain slices were analyzed and calculated by MedBrain 2 imaging analyzer to evaluate brain edema. RESULT: The macrophotographic measurement showed that the ischemic hemisphere areas significantly increased from 1 h after focal cerebral ischmia, which was similar to the measurement of water content. This measurement for brain edema correlated well with those of water content and brain slice volume. CONCLUSION: The macrophotographic measurement is an objective and quantitative method for evaluating brain edema after focal cerebral ischemia.

Animals↗
PubMed2000

LF16-0687 a novel non-peptide bradykinin B2 receptor antagonist reduces vasogenic brain edema from a focal lesion in rats.

Head injury world wide is still the most frequent cause of morbidity and mortality among the population under 45 years. Approximately 50% of patients dying from severe head injury have a therapy refractory intracranial pressure rise (Baethmann 1998). Traumatic brain edema, e.g. resulting from disruption of the blood-brain barrier is viewed as an important factor of the increased intracranial pressure. Bradykinin, an active peptide of the kallikrein-kinin system is considered to enhance brain edema formation which is attributed to its permeabilizing effect on the blood-brain barrier and on dilation of arterial blood vessels in the brain mediated by B2-receptors facilitating extravasation. Currently, LF16-0687, a novel non-peptide bradykinin B2 receptor antagonist was experimentally tested as to its therapeutical potential on vasogenic brain edema from a cortical focal lesion. Following trephination of the skull in anaesthesia, male Sprague-Dawley rats were subjected to a focal cold injury of the left parietal cortex. Animals of two experimental groups were receiving either LF16-0687 as high or low dose, whereas one group of untreated animals with trauma was treated with 0.9% NaCl as continuous infusion beginning 10 min before until 24 h after lesion. 24 h after trauma the brain was removed from the skull, and the cerebral hemispheres were separated in the median plane for gravimetric assessment of hemispheric swelling. No significant reduction of hemispheric brain swelling (+7.4 +/- 2.9%) was found in animals receiving high-dose LF16-0687 as compared to the untreated controls. Brain swelling, however was significantly attenuated by the low-dose treatment, i.e. to +6.4 +/- 1.3%; vs. +9.3 +/- 1.1% found in the controls, (p < 0.05). The current data confirm that blocking of bradykinin B2-receptors by LF16-0687 is significantly attenuating vasogenic brain edema from a focal cold lesion. The therapeutical properties of the antagonist on brain edema formation cannot be attributed to a lowering of the blood pressure. Rather, specific blocking effects of B2-receptors in the brain appear to be involved. In conclusion, the understanding of secondary brain damage including brain edema in head injury has been markedly enhanced by the discovery of pathophysiologically active mediator compounds playing a role in its various manifestations. The current data confirm a pathophysiological function of bradykinin in vasogenic brain edema mediated by activation of B2-receptors. Currently it is studied whether LF16-0687 also reduces brain swelling when given after an insult.

Animals↗
PubMed1987

Protective effects of liposome-entrapped superoxide dismutase on posttraumatic brain edema.

Oxygen-derived free radicals and membrane lipid peroxidation have been postulated to be involved in brain edema and cell death, secondary to ischemia and traumatic injury. Using a model of brain edema induced by cold-induced injury, we have demonstrated an early elevation of superoxide radicals followed by permeability changes in the blood-brain barrier and development of edema in injured brain. Intravenous injection of liposome-entrapped copper-zinc-superoxide dismutase 5 minutes before the injury-enhanced entry of the enzyme into endothelial cells of the blood-brain barrier of injured brain reduced the brain level of superoxide radicals and ameliorated blood-brain barrier permeability changes and brain edema. Identical treatment 5 minutes after injury was also effective. These data demonstrate that superoxide radicals play an important role in the delayed development of vasogenic brain edema following brain injury.

Animals↗
PubMed2003

[Role of free radicals in brain edema induced by endotoxin in infant rats and the therapeutic effect of dexamethasone and IVIG].

OBJECTIVE: Glucocorticoid is considered as an effective drug for prevention and treatment of brain edema and reducing the blood-brain barrier (BBB) permeability. Intravenous immunoglobulin (IVIG) is frequently used to treat neurological diseases with immune abnormality, its function and potential mechanism on brain edema have not been reported. In this study, the roles of the total hydrosulfide group (TSH), non-protein hydrosulfide group (NPSH) and malondialdehyde (MDA) in etiology of the endotoxin brain edema in infant rats and the interfering effects of dexamethasone (DEX) and IVIG were investigated. METHODS: In 35 infant rats, 10 mg/kg lipopolysaccharide (LPS) was intraperitoneally injected. The same volume of normal saline was injected to 24 control rats. Ten mg/kg DEX and 400 mg/kg IVIG were intravenously injected respectively to 36 and 24 infant rats instantly following LPS injection. The TSH, NPSH and MDA concentrations and the brain Evans blue contents were detected at different time in the brain tissue. The brain water content was measured by drying method. RESULTS: The brain water, EB and MDA contents after endotoxin injection were significantly higher than those of control group, while the brain TSH, NPSH content were significantly lower than those of control group (P < 0.05 or P < 0.01); After treatment with DEX or IVIG, the brain EB, MDA and water content significantly decreased with the peak at 6 h (P < 0.05 or P < 0.01), TSH and NPSH significantly increased compared with LPS group. However, the NPSH content in IVIG treatment group did not change significantly (P > 0.05). CONCLUSION: Free radicals play a role in the brain edema induced by LPS in infant rats. The primary results suggested that DEX and IVIG have therapeutic effect for the endotoxin-induced brain edema by affecting the free radicals.

Animals↗
PubMedDate not supplied

[Effect of diazepam and phenazepam on Leao's depression in brain edema].

Experiments on rats with brain edema under water intoxication were made to examine the effect of the benzodiazepine tranquilizers diazepam and phenazepam on the time course of the recovery of brain electrical activity after passing the spreading Leao's depression wave. It was found that the drugs indicated possess antiedematous properties and improve brain function under these conditions. It is assumed that the drug action on the spreading depression is linked with their effect on metabolic processes in the brain and antiedematous properties.

Animals↗
PubMed1991

Evidence against leukotrienes as mediators of brain edema.

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 microM) 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-microM 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.(ABSTRACT TRUNCATED AT 400 WORDS)

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2002

[Comparative study of the image observation of earlypostburn brain edema in severely burned dogs].

OBJECTIVE: To explore the diagnostic value of MRI and SPECT in early postburn brain edema in severely burned dogs. METHODS: Twenty-six mongrel dogs were randomized into control (n = 6) and burned groups in which every 5 dogs were allotted to each of following time points: 6, 12, 18 and 24 postburn hours (PBHs). The dogs in burn groups were inflicted with 50% TBSA of III degree skin burn and were infused with 5% glucose solution after 6 PBHs, so that severe early postburn brain edema was produced. MRI and SPECT were employed to observe dynamically the brain of dogs in all groups. The results were collected and compared with one another. RESULTS: The results indicated that with MRI brain morphological change of early brain edema could be shown as early as within 12 PBH and diffuse brain edema became more obvious with elapse of time. The changes might be difficult to be found by MRI when T(1)WISIR decreased below 10%. T(2)WI SIR increased by 8.29% at 24 PBH with blurred demarcation between the brain gray and white matters. There was diffused and progressive nuclide ((99)TCm-ECD) concentration in the brain tissue as shown by SPECT at 6 PBH. The radio-nuclide taking ratio increased significantly after 12 PBH, especially at 24 PBH (P < 0.01) when compared with that before burn. CONCLUSION: Combined application of MRI and SPECT could evidently increase sensitivity and specificity in the diagnosis of early postburn brain edema.

Animals↗
PubMed1989

Blood-brain barrier sodium transport limits development of brain edema during partial ischemia in gerbils.

Sodium derived from the blood is known to accumulate in brain tissue during the early stages of incomplete ischemia. Our present studies were undertaken to determine the relation between blood-brain barrier sodium transport and the development of ischemic brain edema. Incomplete cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. Following recovery from the anesthetic, the gerbis were evaluated for the presence of neurologic symptoms and were divided into symptomatic (n = 77) and asymptomatic (n = 94) groups. Tissue water, sodium, and potassium contents, tissue plasma volume, and brain uptake of 22Na were measured in both groups 1.5, 3, 6, 12, and 24 hours after carotid ligation. There was a progressive accumulation of sodium and water in the ipsilateral cerebral cortex of the symptomatic group compared with either the corresponding contralateral cortex of the same gerbils or with the asymptomatic group. Net changes in brain sodium and potassium concentrations appeared to be the main determinants of fluid accumulation. Brain edema was not due to opening of the blood-brain barrier because the unidirectional transport of 22Na remained low and was even reduced by 35-55% in the ischemic cortex. Nevertheless, this sodium transport activity appeared to be rate-limiting in the development of brain edema during the first 3 hours of ischemia because the rate of sodium accumulation in the tissue was the same as the rate of 22Na transport from the blood to the brain. We conclude that blood-brain barrier sodium transport is an important factor in the formation of ischemic brain edema.

Animals↗
PubMed1990

Proton relaxation in acute and subacute ischemic brain edema.

The relation between regional ischemic brain edema and tissue proton relaxation rates (R1 = 1/T1; R2 = 1/T2) were studied in 16 macaque monkeys subjected to MCA occlusion. In vivo R2 measurements were obtained from multiple spin-echo (eight echoes) images taken at 2-, 3-, 4-, and 72-hr postischemia. In vitro R1 and R2 values were determined for corresponding regions after sacrifice at 4 hr (n = 8) or at 72-hr postischemia in seven surviving animals. The water content of the white and gray matter tissue samples was measured by the wet/dry method. Four animals (25%) showed ipsilateral regions of increased signal intensity as early as 2 hr after MCA occlusion. All seven animals imaged at 72 hr displayed such regions. Despite the absence of measured changes in tissue water content, significant decreases in R2, but not in R1, occurred at 4 hr. At this stage, R2 values correlated more closely than R1 with individual variations in water content. At 72 hr, marked decreases in both R1 and R2 were measured in ischemic deep gray matter and white matter. Cortical gray matter was unchanged. In edematous gray and white matter, both R1 and R2 correlated closely with tissue water content, but R2 was consistently 10 to 20 times more sensitive than R1. Biexponential R2 decay was observed at 4 and 72 hr, but only in the white matter region that became severely edematous at 72 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1999

Albumin or hetastarch improves neurological outcome and decreases volume of brain tissue necrosis but not brain edema following closed-head trauma in rats.

The present study examined whether hemodilution with 20% human serum albumin (HSA) or 10% hydroxyethyl starch (HES) improved the outcome from closed-head trauma (CHT) in rats. Rats anesthetized with halothane were given one of three hemodilution solutions (i.e., 20% HSA, 10% HES, or control [0.9% saline]) after CHT or sham surgery. CHT was delivered using a weight drop impact of 0.5 J onto the closed cranium. The hemodilution solution (volume = 1% of body weight) was given just after determining the neurological severity score (NSS) at 1 hour following CHT. The NSS was determined again at 24, 48, and 72 hours following CHT. At 72 hours, brains were removed, and brain edema and brain tissue necrosis volume were determined. Solutions of 20% HSA and 10% HES significantly improved brain tissue necrosis volume (143 +/- 72 mm3 and 104 +/- 53 mm3 as compared to 271 +/- 65 mm3 in controls, mean +/- SD) and NSS (12 +/- 2 and 9 +/- 2 as compared to 15 +/- 2 in controls at 72 hours, median +/- range) but not brain edema. The hematocrit decreased similarly in all groups during hemodilution. Hemodilution with 20% HSA and 10% HES following CHT in rats did not decrease brain edema but did decrease brain tissue necrosis volume and NSS (improved neurological function), suggesting that the beneficial effect of hemodilution resulted not from decreased edema formation but rather from effects not measured in this study such as improved perfusion of the salvageable brain tissue surrounding the core injury.

Animals↗
PubMed1989

Protective effect of the iron chelator deferoxamine on cold-induced brain edema.

Oxygen free radicals such as superoxide radical and iron-catalyzed hydroxyl radical generated by the superoxide system have been implicated in the genesis of brain edema. Therefore, deferoxamine (DFO), an iron chelator, could potentially be used to treat brain edema. To examine this hypothesis, vasogenic brain edema was produced in 48 cats by a cortical freezing lesion. The animals were separated into three groups: Group 1 comprised 14 cats that received no DFO and were sacrificed at 6 or 24 hours; Group 2 consisted of 12 cats that were treated with DFO (50 mg/kg/ml, intravenously) at 15 minutes before the lesion was made and 60 minutes later and were sacrificed at 6 or 24 hours; and Group 3 included 12 cats that were treated with DFO (50 mg/kg/ml, intravenously) at 15 minutes after the lesion was produced and 60 minutes later and were sacrificed at 6 or 24 hours. The effect of DFO on arterial blood pressure was also studied in the remaining 10 cats. Brain water content in eight sampling areas was measured by the specific gravity method. Blood-brain barrier disruption was assessed by spread of Evans blue dye with planimetry. Specific gravity values at 6 and 24 hours were significantly higher in Group 2 than in Group 1 animals. Areas of Evans blue dye extravasation at 6 and 24 hours were significantly reduced in Group 2 relative to Group 1. Group 3 cats showed improvement in specific gravity values and Evans blue extravasation at 6 hours, but not at 24 hours. The iron chelator DFO prevented early development of brain edema; thus, this oxygen free radical scavenger may provide a foundation for a new therapy for brain edema.

Animals↗
PubMedDate not supplied

[Brain edema as a cause of critical states in neurosurgical patients].

The results of the studies in 120 patients after resection of tumours located in cranial fossa (40 cases), basal-diencephalic area (45 cases), hemispheres (35 cases) have shown the role of brain edema in the onset of critical conditions after neurosurgery (with consideration of a new concept concerning the mechanisms of brain edema development). It has been demonstrated that brain edema at its early stages is a biologically expedient adaptation response to any damage and is manifested in hyperhydration of all the tissues, most marked in the affected focus. Specific (neurogenic, neurohumoral) and non-specific (biochemical, autoimmune, mechanical, etc.) factors of brain edema onset have been identified. It turned out that the location of the affected focus determines the differences in neurogenic and neurohumoral mechanisms of the edema onset. The nearer the affected focus to the stem and diencephalic structures, the more marked the effect of neurogenic and neurohumoral factors and the more distinct the tendency towards edema generalization. Brain edema may be a cause of critical conditions and lethal outcomes only when it leads to dislocation and strangulation of them brain structures, and disturbances of brain metabolism and blood flow.

Brain Edema↗
PubMed1980

[Brain edema evolution (author's transl)].

Brain edema of the vasogenic type is being discussed in its subsequent stages of exudation, spreading and resolution; and particularly the pathophysiological mechanisms which are involved in these stages.

Blood Pressure↗
PubMed2006

Inhibition of the Na+ -K+ -2Cl- -cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage.

The present study was aimed to elucidate the possible role of Na+ -K+ -2Cl- -cotransporter (NKCC1) on traumatic brain injury-induced brain edema, cerebral contusion and neuronal death by using traumatic brain injury animal model. Contusion volume was verified by 2,3,5,-triphenyltetrazolium chloride monohydrate staining. NKCC1 mRNA expression was detected by RT-PCR and the protein expression of NKCC1 was measured by Western blot. We found that the expression of NKCC1 RNA and protein were up-regulated in choroid plexus apical membrane from 2 h after traumatic brain injury, peaked at 8 h, and lasted for 24 h. Rats in the experimental group displayed severe brain edema (water content: 81.45 +/- 0.32% compared with 78.38 +/- 0.62% of sham group) and contusion volume significantly increased 8 h after traumatic brain injury (864.14 +/- 28.07 mm3). Administration of the NKCC1 inhibitor bumetanide (15 mg/kg, I.V.) significantly attenuated the contusion volume (464.03 +/- 23.62 mm3) and brain edema (water content: 79.12 +/- 0.28%) after traumatic brain injury. Our study demonstrates that NKCC1 contributes to traumatic brain injury-induced brain edema and neuronal damage.

Animals↗