• BMB Reports
• /
• v.48 no.6
• /
• pp.348-353
• /
• 2015

In the present study, we investigated the characteristics of drug efflux transporter expressions following status epilepticus (SE). In the hippocampus and piriform cortex (PC), vasogenic edema peaked 3-4 days after SE. The expression of breast cancer resistance protein (BCRP), multidrug resistance protein-4 (MRP4), and p-glycoprotein (p-GP) were decreased 4 days after SE when vasogenic edema was peaked, but subsequently increased 4 weeks after SE. Multidrug resistance protein-1 (MRP1) expression gradually decreased in endothelial cells until 4 weeks after SE. These findings indicate that SE-induced vasogenic edema formation transiently reduced drug efflux pump expressions in endothelial cells. Subsequently, during recovery of vasogenic edema drug efflux pump expressions were differentially upregulated in astrocytes, neuropils, and endothelial cells. Therefore, we suggest that vasogenic edema formation may be a risk factor in pharmacoresistent epilepsy. [BMB Reports 2015; 48(6): 348-353]

• Journal of Korean Neurosurgical Society
• /
• v.49 no.2
• /
• pp.112-115
• /
• 2011

The intra-arterial administration of nimodipine (IAN) is commonly used for cerebral vasospasm refractory to medical treatments. We report two cases of vasogenic edema after IAN. Our patients with aneurismal subarachnoid hemorrhage presented with vasospasm, which was treated by IAN. Consequently, vasogenic edema developed in the basal ganglia. Reperfusion following IAN for vasospasm may have the potential for inciting vasogenic edema in the ischemic brain.

• Biomedical Science Letters
• /
• v.11 no.1
• /
• pp.31-36
• /
• 2005

To evaluate the magnetic resonance imaging and electron microscopic findings of the hyperacute stage of cerebral fat embolism in cats and the time needed for the development of vasogenic edema. Magnetic resonance imaging was performed at 30 minutes (group 1, n=9) and at 30 minutes and 1, 2, 4, and 6 hours after embolization with triolein (group 2, n= 10). As a control for group 2, the same acquisition was obtained after embolization with polyvinyl alcohol particles (group 3, n=5). Electron microscopic examination was done in all cats. In group 1, the lesions were iso- or slightly hyperintense on T2-weighted (T2W) and diffusion-weighted (DWIs) images, hypointense on the apparent diffusion coefficient (ADC) map image, and markedly enhanced on the gadolinium-enhanced T1-weighted images (Gd-T1WIs). In group 2 at 30 minutes, the lesions were similar to those in group 1. Thereafter, the lesions became more hyperintense on T2WIs and DWIs and more hypoinfense on the ADC map image. In group 3, the lesions showed mild hyperintensity on T2WIs at 6 hours but hypointensity on the ADC map image from 30 minutes, with a tendency toward a greater decrease over time. Electron microscopic findings revealed discontinuity of the capillary endothelial wall, perivascular and interstitial edema, and swelling of glial and neuronal cells in groups 1 and 2. The lesions were hyperintense on T2WIs and DWIs, hypointense on the ADC map image, and enhanced on Gd-T1WIs. On electron microscopy, the lesions showed cytotoxic and vasogenic edema with disruption of the blood-brain barrier.

• BMB Reports
• /
• v.48 no.9
• /
• pp.507-512
• /
• 2015

In the present study, we addressed the question of whether treatment with mannitol, an osmotic diuretic, affects astrogliovascular responses to status epilepticus (SE). In saline-treated animals, astrocytes exhibited reactive astrogliosis in the CA1-3 regions 2-4 days after SE. In the mannitol-treated animals, a large astroglial empty zone was observed in the CA1 region 2 days after SE. This astroglial loss was unrelated to vasogenic edema formation. There was no difference in SE-induced neuronal loss between saline- and mannitol-treated animals. Furthermore, mannitol treatment did not affect astroglial loss and vasogenic edema formation in the dentate gyrus and the piriform cortex. These findings suggest that mannitol treatment induces selective astroglial loss in the CA1 region independent of vasogenic edema formation following SE. These findings support the hypothesis that the susceptibility of astrocytes to SE is most likely due to the distinctive heterogeneity of astrocytes independent of hemodynamics. [BMB Reports 2015; 48(9): 507-512]

• Proceedings of the KSMRM Conference
• /
• 2004.09a
• /
• pp.39-39
• /
• 2004

• Journal of Korean Neurosurgical Society
• /
• v.47 no.3
• /
• pp.203-209
• /
• 2010

Objective : The purpose of study was to evaluate the feasibility of brain magnetic resonance (MR) images of the rat obtained using a 1.5T MR machine in several blood-brain barrier (BBB) experiments. Methods : Male Sprague-Dawley rats were used. MR images were obtained using a clinical 1.5T MR machine. A microcatheter was introduced via the femoral artery to the carotid artery. Normal saline (group 1, n = 4), clotted autologous blood (group 2, n = 4), triolein emulsion (group 3, n = 4), and oleic acid emulsion (group 4, n = 4) were infused into the carotid artery through a microcatheter. Conventional and diffusion-weighted images, the apparent coefficient map, perfusion-weighted images, and contrast-enhanced MR images were obtained. Brain tissue was obtained and triphenyltetrazolium chloride (TTC) staining was performed in group 2. Fluorescein isothiocyanate (FITC)-labeled dextran images and endothelial barrier antigen (EBA) studies were performed in group 4. Results : The MR images in group 1 were of good quality. The MR images in group 2 revealed typical findings of acute cerebral infarction. Perfusion defects were noted on the perfusion-weighted images. The MR images in group 3 showed vasogenic edema and contrast enhancement, representing vascular damage. The rats in group 4 had vasogenic edema on the MR images and leakage of dextran on the FITC-labeled dextran image, representing increased vascular permeability. The immune reaction was decreased on the EBA study. Conclusion : Clinical 1.5T MR images using a rat depicted many informative results in the present study. These results can be used in further researches of the BBB using combined clinical MR machines and immunohistochemical examinations.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.23 no.4
• /
• pp.866-871
• /
• 2009

Brain edema is a major importance in the pathophysiology of CNS injuries including stroke. Ischemic brain edema results from both cytotoxic edema, which is severe in astrocytes at early stage, and vasogenic edema caused by excessive blood-brain barrier (BBB) permeability. The present study was performed to determine the effect of Rhei Rhizoma on brain edema induced by middle cerebral artery occlusion (MCAO) in the rats. The neurological symptom, total infarct volume and edema index caused by MCAO were measured. The changes of Matrix Metalloproteinase-9 (MMP-9) and inducible nitric oxide synthase (iNOS) immunoreactivities were also observed. We found that Rhei Rhizoma extract improved the neurological symptom and attenuated the total infarct volume and brain edema caused by ischemic insult. Rhei Rhizoma extract also attenuated the expression of MMP-9 and iNOS. This results suggest that Rhei Rhizoma has a protective effect on the brain edema caused by ischemic insult.

• Journal of Korean Neurosurgical Society
• /
• v.54 no.2
• /
• pp.139-141
• /
• 2013

Presented here is a 36-year-old male with arterial hypertension who developed brainstem edema and intracranial hemorrhage. Magnetic resonance scan revealed diffuse brainstem hyperintensity in T2-weighted and fluid-attenuated inversion-recovery images, with an increase in apparent diffusion coefficient values. After a reduction in blood pressure, rapid resolution of the brainstem edema was observed on follow-up. The patient's condition was thus interpreted as hypertensive brainstem encephalopathy. While many consider this a vasogenic phenomenon, induced by sudden, severe hypertension, the precise mechanism remains unclear. Prompt recognition and aggressive antihypertensive treatment in such patients are essential to prevent permanent or life-threatening neurologic injury.

• Journal of Korean Neurosurgical Society
• /
• v.37 no.1
• /
• pp.1-7
• /
• 2005

Objective: Peritumoral brain edema(PTBE) accounts for approximately 60% of meningiomas. It has not been identified why vasogenic edema, frequently shown in intra-axial tumors is also developed in extra-axial tumor such as meningiomas. Therefore, the authors assess the peritumoral brain edema of meningiomas with a focus on the angiographic pattern and expression of MIB-1 to clarify their correlation. Methods: A total 32 cases of meningioma was studied. The authors attempted to identify 1) the location of PTBE and the edema index (EI), 2) the location and dominancy of pial supply compared with meningeal supply, 3) the biological activity of meningiomas indicated by the MIB-1 LI (labeling index), 4) their interaction. Results: No PTBE was observed in the meningiomas without pial arterial supplement from internal carotid artery (ICA) and vertebral artery (VA). The PTBE of meningiomas with pial supply was developed intensely along the pial arterial supplement, and increased statistically in proportion to the extent of pial supply from ICA or VA rather than meningeal supply. Also, the MIB-1 LI in meningiomas tended to be larger in the tumors of the larger EI and the dominancy of pial supply. Conclusion: A strong correlation is found between the extent of PTBE in meningiomas and the dominancy of pial supply. The MIB-1 LI also tend to be associated with the PTBE. Therefore, the MIB-1 LI in benign meningiomas may represent not only the proliferative potential of the tumor, but also the biological activity like angiogenesis.

• Biomedical Science Letters
• /
• v.10 no.2
• /
• pp.115-120
• /
• 2004

To investigate the correlation between the magnetic resonance imaging (MRI) of cerebral fat embolism that is induced by injecting oleic acid into 10 cats, and a pathologic diagnosis. Using a microcatheter, 30 ${mu}ell$ of oleic acid was injected into the internal carotid artery of 10 cats. MR T2-weighted image (T2WI), diffusion-weighted image (DWI) and Gadolinium-enhanced T1-weighted image (Gd-enhanced T1WI) were obtained after 30 minutes and 2 hours of embolization. After 30 minutes of the embolization, lesions of very high signal intensity were detected by T2WI in 6 cats, and of slightly high signal intensity in 2 cats; in the remaining 2 cats, signal intensity was normal. DWI showed lesions of very high intensity in 9 cats and of slightly high intensity in one cat. According to the findings of light microscopic examination, infarcted lesions mainly involved the gray matter, but also some white matter. A magnetic resonance imaging diagnosis for cerebral fat embolism that was induced by oleic acid through the internal carotid artery in cats showed high signal intensity on the T2WI and the DWI within an initial 2 hours, and with a well enhancement on the Gd-enhanced T1WI. Considering cellular edema, cerebrovascular injury and extracellular space widening, we assumed pathologically that cytotoxic and vasogenic edema exists at the same time.