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Brain Water Content (brain + water_content)
Selected AbstractsMagnesium sulphate treatment decreases blood,brain barrier permeability during acute hypertension in pregnant ratsEXPERIMENTAL PHYSIOLOGY, Issue 2 2008Anna G. Euser Eclampsia is associated with increased blood,brain barrier (BBB) permeability and formation of cerebral oedema. Magnesium sulphate is used to treat eclampsia despite an unclear mechanism of action. This study was to determine the effect of magnesium sulphate on in vivo BBB permeability and formation of cerebral oedema during acute hypertension and on brain aquaporin-4 (AQP4) protein expression. An in vivo model of hypertensive encephalopathy was used in late-pregnant (LP) rats following magnesium sulphate treatment, 270 mg kg,1i.p. injection every 4 h for 24 h. Permeability of the BBB was determined by in situ brain perfusion of Evan's Blue (EB) and sodium fluorescein (NaFl), and dye clearance determined by fluorescence spectrophotometry. Cerebral oedema was determined following acute hypertension by measuring brain water content. The effect of magnesium treatment on AQP4 expression was determined by Western blot analysis. Acute hypertension with autoregulatory breakthrough increased BBB permeability to EB in both brain regions studied (P < 0.05). Magnesium attenuated BBB permeability to EB during acute hypertension by 41% in the posterior cerebrum (P < 0.05) but had no effect in the anterior cerebrum (P > 0.05). Treatment with magnesium did not change NaFl permeability, cerebral oedema formation or AQP4 expression. In summary, BBB permeability to Evan's Blue was increased by acute hypertension in LP rats, and this was attenuated by treatment with magnesium sulphate. The greatest effect on BBB permeability to EB was in the posterior cerebrum, an area particularly susceptible to oedema formation during eclampsia. [source] Neurovascular and neuronal protection by E64d after focal cerebral ischemia in ratsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2006Tamiji Tsubokawa Abstract Calpains and cathepsins are two families of proteases that play an important role in ischemic cell death. In this study, we investigated the effect of E64d, a ,-calpain and cathepsin B inhibitor, in the prevention of neuronal and endothelial apoptotic cell death after focal cerebral ischemia in rats. Rats underwent 2 hr of transient focal ischemia from middle cerebral artery occlusion (MCAO) and were sacrificed 24 hr later. E64d (5 mg/ kg intraperitoneally) was administered 30 min before MCAO. Assessment included neurological function, infarction volume, brain water content, blood,brain barrier permeability, histology, and immunohistochemistry. The E64d-treated rats had significant brain protection against ischemic damage. We observed a reduction of infarction volume, brain edema, and improved neurological scores in E64d-treated rats compared with the nontreated control. Furthermore, there was a remarkable reduction in both proteases and caspase-3 activation and apoptotic changes in both neurons and endothelial cells in E64d-treated rats. These results suggest that E64d protects the brain against ischemic/reperfusion injury by attenuating neuronal and endothelial apoptosis. © 2006 Wiley-Liss, Inc. [source] Melatonin reduces experimental subarachnoid hemorrhage-induced oxidative brain damage and neurological symptomsJOURNAL OF PINEAL RESEARCH, Issue 3 2009Mehmet Ersahin Abstract:, Oxidative stress has detrimental effects in several models of neurodegenerative diseases, including subarachnoid hemorrhage (SAH). This study investigated the putative neuroprotective effect of melatonin, a powerful antioxidant, in a rat model of SAH. Male Wistar albino rats were divided as control, vehicle-treated SAH, and melatonin-treated (10 mg/kg, i.p.) SAH groups. To induce SAH, 0.3 mL blood was injected into cisterna magna of rats. Forty-eight hours after SAH induction, neurological examination scores were measured and the rats were decapitated. Brain tissue samples were taken for blood,brain barrier (BBB) permeability, brain water content, histological examination, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+ -K+ -ATPase activities. Formation of reactive oxygen species in brain tissue samples was monitored by using a chemiluminescence (CL) technique. The neurological examination scores were increased in SAH groups on the second day of SAH induction and SAH caused a significant decrease in brain GSH content and Na+ -K+ -ATPase activity, which was accompanied with significant increases in CL, MDA levels, and MPO activity. On the other hand, melatonin treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations, while increased brain water content and impaired BBB were also reversed by melatonin treatment. This study suggests that melatonin, which can easily cross BBB, alleviates SAH-induced oxidative stress and exerts neuroprotection by preserving BBB permeability and by reducing brain edema. [source] Cerebral oedema in minimal hepatic encephalopathy due to extrahepatic portal venous obstructionLIVER INTERNATIONAL, Issue 8 2010Amit Goel Abstract Background: Minimal hepatic encephalopathy (MHE) has recently been reported in patients with extrahepatic portal venous obstruction (EHPVO). Aims: To evaluate brain changes by magnetic resonance studies in EHPVO patients. Methods: Blood ammonia level, critical flicker frequency (CFF), brain metabolites on 1H-magnetic resonance (MR) spectroscopy and brain water content on diffusion tensor imaging and magnetization transfer ratio (MTR) were studied in 31 EHPVO patients with and without MHE, as determined by neuropsychological tests. CFF and magnetic resonance imaging studies were also performed in 23 controls. Results: Fourteen patients (14/31, 45%) had MHE. Blood ammonia level was elevated in all, being significantly higher in the MHE than no MHE group. CFF was abnormal in 13% (4/31) with EHPVO and in 21% (3/14) with MHE. On 1H-MR spectroscopy, increased Glx/Cr, decreased mIns/Cr, and no change in Cho/Cr were noted in patients with MHE compared with controls. Significantly increased mean diffusivity (MD) and decreased (MTR) were observed in the MHE group, suggesting presence of interstitial cerebral oedema (ICE). MD correlated positively with blood ammonia level (r=0.65, P=0.003) and Glx (r=0.60, P=0.003). Discussion: MHE was detected in 45% of patients with EHPVO while CFF was abnormal in only 13%. ICE was present in 7/10 brain regions examined, particularly in those with MHE. Hyperammonaemia elevated cerebral Glx levels correlated well with ICE. Conclusions: MHE was common in EHPVO; CFF could identify it only in a minority. ICE was present in EHPVO, particularly in those with MHE. It correlated with blood ammonia and Glx/Cr levels. Hyperammonaemia seems to contribute to ICE in EHPVO. [source] | ||||||||||