Pathogenesis of brain edema and hemorrhage: role of the brain capillary.
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The molecular basis of brain injury and brain edema: the role of oxygen free radicals.
This review article outlines basic concepts and pathophysiological aspects of the chemistry of oxygen free radicals in all forms of brain injury and brain edema. Recent experimental studies have demonstrated that oxygen free radicals may be important mediators of brain injury and brain edema, and pharmacological antagonism of oxygen free radicals shows beneficial therapeutic results. A number of fundamental questions need to resolved, and advanced techniques for detecting oxygen free radicals will be needed. No clinical data are available, but oxygen free radical scavengers may possibly become a critical therapeutic modality for brain injury and brain edema.
Animals↗
Surgical improvement of brain edema related to hypertensive intracerebral hemorrhage.
BACKGROUND: Patients with hypertensive intracerebral hemorrhage (ICH) are at risk for delayed neurological deterioration, especially during the second week after onset. Mass effect due to vasogenic edema caused by ICH has been shown to cause later deterioration. Control of brain edema and increased intracranial pressure (ICP) are related events that determine outcome. In this study, we compared the effects of three different treatments on brain edema caused by ICH. METHODS: Thirty-nine patients with ICH were involved in this study. Of these patients, 11 had medical therapy (group A), 15 were treated with stereotactic aspiration plus local administration of urokinase (group B), and 13 underwent conventional craniotomy and hematoma removal (group C). The intracerebral hematoma volume on admission was measured on the the brain computed tomographs (CTs), and the cerebral edema volumes surrounding the hematoma were assessed with CT scans every 5 to 7 days after symptom onset. RESULTS: The median intracerebral hematoma volumes were 23, 50 and 51 ml in groups A, B and C, respectively. Peak edema volume surrounding the hematoma was observed 5 to 15 days after symptom onset. A significant correlation (p < 0.05) was noted between peak edema and hematoma volumes in all groups. The ratio of median peak edema volume to median hematoma volume was 3.280 in group A, which was significantly higher than those in group B (0.745) and group C (0.863) (p < 0.05). CONCLUSIONS: The study revealed that brain edema induced by hypertensive ICH could be significantly ameliorated by surgical management. Stereotactic aspiration with local administration of urokinase was as effective as conventional craniotomy in reduction of brain edema volume caused by ICH and was characterized by its minimal invasiveness, easy performance, and safety.
Adult↗
Characterisation of brain edema following "controlled cortical impact injury" in rats.
Significance, origin and nature of posttraumatic brain edema are still being debated. Recently, a "controlled cortical impact injury" (CCII) was introduced to model traumatic brain injury. Purpose of this study was to investigate the development and nature of brain edema following CCII. Traumatic brain injury was applied to the intact dura of the left hemisphere in Sprague-Dawley rats (n = 52, 250-350 g b.w.). Ketamine/xylazine-anesthesia or inhalation-anesthesia were used. A pneumatic impactor with a diameter of 5 mm contused the temporo-parietal cortex with a velocity of 7 m/s and an impact depth of 2 mm. 24 hours post injury the brains were removed. Posttraumatic hemispheric swelling and water content were determined gravimetrically, Evans blue extravasation spectrophotometrically, area and volume of ischemia by staining with TTC. MRI studies were performed with T1-,T2- and diffusion-weighted sequences. Posttraumatic swelling following CCII was 14.3 +/- 3.1%. Brain water content increased to 82.5 +/- 0.5% in lesioned hemisphere compared to 79.9 +/- 0.2% in control hemisphere. Following TTC staining, the average ischemic tissue volume was 56.7 +/- 19.2 mm3. There was a moderate uptake of Evans blue into the lesioned hemisphere. MRI studies demonstrated edema in 35.4 +/- 9.5 mm3 of the lesioned hemisphere. Gd-DTPA was taken up early after trauma only. A significantly decreased ADC (apparent diffusion coefficient) indicates the cytotoxic (ischemic) component of edema in this model. In conclusion, CCII produces significant posttraumatic brain swelling and edema which is both, of vasogenic and cytotoxic nature. Thus, the CCII models the human cortical contusion more appropriately and opens new avenues for therapeutical studies focussing on cortical contusions.
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[Brain edema and aquaporin].
Aquaporin is a membrane-bound water channel and highly related to the development and resolution of brain edema. We have detected mRNA and protein expression of aquaporin-4 in ischemic and traumatic brain injury. The aquaporin-4 expression is related to the resolution of brain edema rather than the evolution of the edema. We also detected the relation of aquaporin-1 expression and the evolution of hydrocephalus. Regulation of aquaporin function may be a new venue of treatment in brain edema.
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Role of hydrodynamic processes in the pathogenesis of peritumoral brain edema in meningiomas.
OBJECT: In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema. METHODS: Gadolinium-diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood-brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (<5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema. CONCLUSIONS: The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.
Adult↗
Rapid development of an intranidal aneurysm with perifocal brain edema in an unruptured cerebral arteriovenous malformation. Case report.
The authors present the case of a 22-year-old man with an unruptured arteriovenous malformation (AVM) in which an intranidal aneurysm had grown in the course of 3 months and was complicated by perifocal brain edema. A left parietal AVM was incidentally diagnosed on magnetic resonance (MR) imaging. No aneurysms were noted on cerebral angiograms obtained simultaneously. Three months later, T2-weighted MR imaging revealed perifocal brain edema (increased signal intensity in the brain parenchyma adjacent to the nidus). An aneurysm-like signal void was demonstrated in the center of the high-signal area, but no previous hemorrhages could be detected. Angiographic studies revealed an intranidal aneurysm 4 mm in diameter projecting anterolaterally from the nidus. Surgical removal was performed without incident, and no neurological deficits or postoperative complications were observed. An MR image obtained 2 weeks postsurgery revealed complete resolution of the perifocal brain edema. To the authors' knowledge, this is the first reported case of an unruptured AVM in which an intranidal aneurysm with perifocal brain edema developed rapidly (within a few months).
Adult↗
The effect of cyclosporin A on brain edema formation following experimental cortical contusion.
Cyclosporin A (CsA) has been shown by our laboratory and others to be neuroprotective in the experimental animal model of traumatic brain injury. However, we found that the intrathecal administration resulted in a concomitant increase of brain edema. The aim of this study was to assess whether intravascular administration may also influence brain edema formation. This project includes two independent series in which different doses of CsA were intravenously given to Sprague-Dawley rats of each group. In the first series, the animals were exposed to focal brain injury by a controlled cortical impact (CCI, 6 m/sec, 3 mm depth) and randomized into the following two groups: 20 mg/kg CsA and control vehicle. In the second series, animals were also injured by CCI and randomized into 35 mg/kg CsA and control vehicle. The intravenous continuous (1 h) infusion was begun 30 minutes after the insult. All animals were sacrificed at 24 hours post injury to assess the brain water content using the gravimetric method. Intravenously-administrated CsA of either 20 or 35 mg/kg did not significantly change the brain water content. We therefore suggest that an intravascular route may be better for CsA administration because the intrathecal injection may exacerbate brain edema as found in our previous study.
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Thrombin-soaked gelatin sponge and brain edema in rats.
Previous work from this laboratory has shown that injection of thrombin into rat basal ganglia causes brain edema. This study investigates the effect on rat brain of thrombin-soaked gelatin sponge (used for intraoperative hemostasis in clinical situations) at a concentration similar to that used in humans. Three models were developed to evaluate this effect. In the first model, a gelatin sponge soaked with vehicle or thrombin (100 U/cm3) was placed on the intact pia of the right frontal lobe in rats without cortical lesions. In the second model, frontal cortex was excised (3 mm3) and the exposed brain was cauterized with electrocoagulation. Gelatin sponge was soaked with vehicle or thrombin (1000, 100, 10, or 1 U/cm3) and placed in the lesion site. In the third model, hirudin, a specific thrombin antagonist, was added to the thrombin-soaked gelatin sponge and placed in a similar cortical lesion to determine if the observed effects were specific to thrombin. The dose-response range for thrombin was determined qualitatively by magnetic resonance (MR) imaging and quantitatively by brain edema formation 24 hours after exposure. We found no edema in the cortically intact rats. The rats given cortical lesions developed significant edema when subjected to 1000, 100, and 10 U/cm3 thrombin as seen on MR imaging and at 100 and 10 U/cm3 thrombin as revealed by wet/dry weight and ion studies of brain tissue. Topical hirudin prevented thrombin-induced edema. It is concluded that thrombin-soaked gelatin sponges cause or enhance significant brain edema in rats at concentrations typically used for human neurosurgery.
Administration, Topical↗
Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils.
Previous studies have demonstrated that a green tea polyphenol, (-)-epigallocatechine gallate (EGCG), has a potent free radical scavenging and antioxidant effect. Glutamate leads to excitotoxicity and oxidative stress, which are important pathophysiologic responses to cerebral ischemia resulting in brain edema and neuronal damage. We investigated the effect of EGCG on excitotoxic neuronal damage in a culture system and the effect on brain edema formation and lesion after unilateral cerebral ischemia in gerbils. In vitro, excitotoxicity was induced by 24-hr incubation with N-methyl-D-aspartate (NMDA; 10 microM), AMPA (10 microM), or kainate (20 microM). EGCG (5 microM) was added to the culture media alone or with excitotoxins. We examined malondialdehyde (MDA) level and neuronal viability to evaluate the effect of EGCG. In vivo, unilateral cerebral ischemia was induced by occlusion of the right common carotid artery for 30, 60, or 90 min and followed by reperfusion of 24 hr. Brain edema, MDA, and infarction were examined to evaluate the protective effect of EGCG. EGCG (25 or 50 mg/kg, intraperitoneally) was administered twice, at 30 min before and immediately after ischemia. EGCG reduced excitotoxin-induced MDA production and neuronal damage in the culture system. In the in vivo study, treatment of gerbils with the lower EGCG dose failed to show neuroprotective effects; however, the higher EGCG dose attenuated the increase in MDA level caused by cerebral ischemia. EGCG also reduced the formation of postischemic brain edema and infarct volume. These results demonstrate EGCG may have future possibilities as a neuroprotective agent against excitotoxicity-related neurologic disorders such as brain ischemia.
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[Effect of dipfluzine on acute ischemic brain edema in gerbils].
OBJECTIVE: To examine the effect of dipfluzine (Dip), a novel calcium channel blocker first developed in China, on acute ischemic brain edema. METHODS: One hundred and thirty gerbils, 65 males and 65 females, weighing 68 +/- 10 g, were used. Eighty gerbils randomly divided into four groups of 20 animals: sham operation group, Dip 25 mg/kg group, and Dip 50 mg/kg group. All of the 120 gerbils were injected with solution or Dip at different concentrations intraperitoneally. The skin of neck was incised one hour after injection. Except in the sham operation group, bilateral carotid artery ligation (BCAL) was performed in the other 70 gerbils to cause brain edema. Another 10 gerbils were used as normal controls without undergoing injection and operation. One hour after the operation, all of the animals were killed and the whole brain tissue was taken to detect the water and Na(+) and K(+) contents. The brain tissues of other 50 gerbils were used to produce homogenate to determine the Na(+), K(+)-ATPase activity. RESULTS: The water and Na(+) contents in hippocampus of model control group were 77.4% and 279 +/- 22 micro mol/g dry tissue respectively, significantly higher than those in sham operation group (74.8% and 220 +/- 22 micro mol/g dry tissue). The K(+) content in the hippocampus of the model control group was 381 +/- 28 micro mol/g dry tissue respectively, significantly lower than that in the sham operation group (430 +/- 30 micro mol/g dry tissue). The Na(+), K(+)-ATPase activity in the plasmalemma of brain cells in model control group was 179 +/- 62 micro mol pi/mg protein/min, significantly lower than that in sham operation group (1006 +/- 130 micro mol pi/mg protein/min, P < 0.01). The water contents of hippocampus in Dip 25 mg/kg group and Dip 50 mg/kg group were 75.4 +/- 0.5% and 74.8 +/- 0.9% respectively, significantly lower than that in model control group (all P < 0.01). The Na(+) contents in hippocampus of Dip 25 mg/kg group and Dip 50 mg/kg group were 235 +/- 39 micro mol/g dry tissue and 223 +/- 36 micro mol/g dry tissue respectively, significantly lower than that in model control group (279 +/- 22 micro mol/g dry tissue, all P < 0.01). The K(+) content in hippocampus of Dip 25 mg/kg group and Dip 50 mg/kg group were 427 +/- 32 micro mol/g dry tissue and 434 +/- 29 micro mol/g dry tissue respectively, significantly higher than that in model control group (P < 0.05 and P < 0.01). The Na(+), K(+)-ATPase activity in the plasmalemma of brain cells in Dip 25 mg/kg group and Dip 50 mg/kg group was 649 +/- 45 and 1 198 +/- 218 micro mol pi/mg protein/min respectively, significantly higher than that in model control group (r = 0.9981, P < 0.01). The correlation between brain water content and Na(+), K(+)-ATPase activity was significant (r = -0.999 7, P < 0.01). CONCLUSION: Dip attenuates dose-dependently the increased H(2)O and Na(+) contents, prevents the decrease in potassium level, and accelerates the restoration of lowered Na(+), K(+)-ATPase activity resulted from cerebral ischemia, thus preventing ischemic brain edema.
Acute Disease↗
[Involvement of arachidonic acid cascade in brain edema and cerebral energy metabolism after reperfusion].
The involvements of arachidonic acid metabolites in the development of ischemic brain edema and cerebral energy metabolism were investigated on the experimental ischemia and reperfusion model. The level of arachidonic acid in brain tissue increases especially on the ischemic insult, which is rapidly converted to prostaglandins and leukotrienes after the reperfusion. The drugs which modify the arachidonic acid metabolism were administrated to clarify the effect on ischemic brain edema and cerebral energy metabolism. Male stroke resistant spontaneously hypertensive rats (SHRSR) were subjected to incomplete ischemia for two hours by occlusion of both common carotid arteries with vascular clips, and reperfused for two hours. The drugs used are dexamethasone, indomethacin, trapidil and OKY-046. Indomethacin inhibits cyclooxygenase. Dexamethasone inhibits phospholipases by the production of lipocortin. OKY-046 inhibits thromboxane A2 synthetase. Trapidil inhibits thromboxane A2 synthetase and increases the level of 6-keto-PGF1 alpha. These drugs were administered 18 hours before, just after clipping on (1/2) and off (1/2). Brain water content, cerebral ATP and lactic acid levels were examined. In the saline treated group, the cerebral water content was increased after the reperfusion and reached its maximal level after two hours of the reperfusion. The development of brain edema was prevented by the administration of dexamethasone or trapidil, but not by indomethacin and OKY-046. Administration of trapidil or dexamethasone was found to prevent the decrease in ATP and the increase of lactic acid. In the indomethacin administrated group, only the increase of lactic acid was prevented. 6-keto-PGF1 alpha was high in the trapidil administrated group and low in the indomethacin administrated group.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗
[Effect of benzodiazepine and GABA derivatives on the energy metabolism indices in brain edema].
The development of toxic and traumatic brain edema in rats is accompanied by a decrease in the ATP level, in the total amount of adenyl nucleotides, the magnitude of the energy charge in the ATP-ADP-AMP system, and by an elevation in the content of AMP. Diazepam (0.5 mg/kg) and phenibut (50 mg/kg) that exert an antiedematous action reduce the amplitude of bioenergetic shifts during edema. As for piracetam (1000 mg/kg) it exhibits an insignificant effect. It is assumed that positive action of diazepam and phenibut on brain bioenergetics in edema is realized via the GABA-ergic system.
Animals↗
Effect of magnesium given 1 hour after head trauma on brain edema and neurological outcome.
Excitatory amino acids (EAA), mainly glutamate and aspartate, are released in excessive amounts from terminals of ischemic or traumatically injured neurons. These excessive levels of EAAs initiate a cascade of events believed to lead to secondary delayed damage to the surrounding brain. The N-methyl-D-aspartate receptor antagonists MK-801 and ketamine are reported to suppress excessive EAA release and to attenuate the development of focal brain edema following neuronal injury. Magnesium is also reported to work at the postsynaptic receptor to reduce the neurotoxic effect of glutamate. The present study was undertaken to examine the effect of postinjury treatment with Mg++ on brain edema and neurological outcome after traumatic brain injury. Sixty-nine rats that survived halothane anesthesia and closed head trauma (CHT) were randomly assigned to one of seven experimental groups: sham, CHT, and CHT with administration of Mg++ 1 hour postinjury. At 48 hours, brain tissue Mg++ concentration (calculated from optical density using a standard curve) was significantly increased compared to baseline levels (10.06 +/- 2.44 mg/g vs. 6.83 +/- 0.81 mg/g, p < 0.01 calculated by one-way analysis of variance). Also at 48 hours postinjury, brain tissue specific gravity in the contused hemisphere of Mg(++)-treated rats was significantly greater than that in the contused hemisphere of untreated rats, indicating attenuation of brain edema formation by Mg++. The neurological severity score (NSS) of rats treated with Mg++ improved significantly at both 18 and 48 hours, compared to baseline values obtained 1 hour after CHT but prior to administration of Mg++ (11.2 +/- 2.5 vs. 15.2 +/- 4.1, p = 0.03; and 12.3 +/- 6.1 vs. 17.3 +/- 3.6, p = 0.004, respectively). In the untreated groups, the NSS at 18 and 48 hours was not significantly different from baseline values (that is, no neurological improvement). The present study indicates that postinjury treatment with Mg++ attenuates brain edema formation and improves neurological outcome after experimental CHT.
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Effects of venom defibrase on brain edema after intracerebral hemorrhage in rats.
We evaluated the effects of defibrase DF-521 batroxobin on reducing brain edema formation and the expression of ICAM-1, complement C3d and C9 in the perihematomal area after intracerebral hemorrhage (ICH) in rats. A rat ICH model, involving infusion of autologous blood into the right basal ganglia, were used in this study. The animals were sacrificed at 24 and 72 hours after ICH to determine the water content of the brain tissue with wet/dry weight measurement. While the expression of ICAM-1 and complement C3d was detected using immuno-histochemistry, and C9 was detected semi-quantitatively with Western blot analysis in the perihematomal area. Perihematomal brain edema was reduced after intraperitoneally injection of DF-521 batroxobin 24 and 72 hours after intracerebral hemorrhage. Immunohistochemistry showed that there were less ICAM-I positive cells were found around the hematoma after intraperitoneally injection of DF-521 batroxobin 24 and 72 hours after ICH. Immuno-histochemistry also showed that C3d deposition reduced significantly, and the Western blot analysis also showed the content of C9 protein declined around the hematoma in DF-521 batroxobin treatment group at 72 hours after ICH. Defibrase DF-521 batroxobin down-regulate ICAM-1 and complement C3d and C9 expression in the perihematomal area, and attenuate brain edema formation in ICH rats.
Animals↗
Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability.
The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
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Brain edema after intracerebral hemorrhage: the effects of systemic complement depletion.
The complement cascade is activated after experimental intracerebral hemorrhage (ICH) and may play an important, role in edema formation. This study investigated the effects of systemic complement depletion on brain edema formation following ICH. Thirty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) while controls received an equal volume of saline injection (i.p.). In both treatment and control rats, autologous blood (100-microL) was infused stereotactically into the right basal ganglia. Rats were sacrificed one and three days later for brain water and ion content measurements and immunohistochemical studies. Immunohistochemistry was used to detect complement C3d, C5a, and C9. Western blot analysis was applied for C9 semiquantitation. Perihematomal brain edema was reduced by systemic complement depletion at one and three days. The water content of the cerebellum (a tissue distant from the hematoma site) was unaffected by complement depletion. Immunocytochemistry found complement depletion significantly reduced perihematomal C9 deposition, C3d production, and C5a positive cell accumulation. In conclusion, complement depletion by CVF attenuates brain edema in ICH perhaps by inhibiting the inflammatory response and membrane attack complex (MAC) formation.
Animals↗
Duration of ischemia influences the development and resolution of ischemic brain edema.
The influence of the duration of ischemia on the development and resolution of post-ischemic brain edema (SG method) was studied in anesthetized rats. Edema developed during ischemia and the amount of edema was related to the duration of ischemia (r = 0.843, p less than 0.001). With recirculation to three hours, the major determinant of the amount of edema was still the duration of the preceding ischemia (p less than 0.001). Resolution of brain edema only occurred following fifteen minutes ischemia. Post-ischemic blood-brain barrier breakdown (14C-AIB, EB albumin) was greatest following longer ischemia. Where present, the BBB leakage was simultaneously to large and small molecules.
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