scholarly journals Central Role of Maladapted Astrocytic Plasticity in Ischemic Brain Edema Formation

2016 ◽  
Vol 10 ◽  
Author(s):  
Yu-Feng Wang ◽  
Vladimir Parpura
Keyword(s):  
Brain Edema ◽  
Edema Formation ◽  
Ischemic Brain ◽  
Ischemic Brain Edema ◽  
Brain Edema Formation

Attenuation of Ischemic Brain EDEMA and Cerebrovascular Injury after Ischemic Preconditioning in the Rat

2001 ◽  
Vol 21 (1) ◽  
pp. 22-33 ◽  
Author(s):  
Tetsuya Masada ◽  
Ya Hua ◽  
Guohua Xi ◽  
Steven R. Ennis ◽  
Richard F. Keep
Keyword(s):  
Brain Edema ◽  
Blood Brain Barrier ◽  
Vascular Injury ◽  
Ischemic Preconditioning ◽  
Dry Weight ◽  
Sham Operation ◽  
Edema Formation ◽  
Ischemic Brain ◽  
Ischemic Brain Edema ◽  
Brain Edema Formation

Ischemic preconditioning (IPC) induces neuroprotection to subsequent severe ischemia, but its effect on the cerebrovasculature has not been studied extensively. This study evaluated the effects of IPC on brain edema formation and endothelial cell damage that follows subsequent permanent focal cerebral ischemia in the rat. Transient (15 minute) middle cerebral artery occlusion (MCAO) was used for IPC. Three days after IPC or a sham operation, permanent MCAO was induced. Twenty-four hours after permanent MCAO, neurologic deficit, infarction volume, and water and ion content were evaluated. Six hours post-ischemia, blood–brain barrier (BBB) permeability was examined using [3H]-inulin. Water, ion contents, and BBB permeability were assessed in three zones (core, intermediate, and outer) depending on their relation to the MCA territory. Heat shock protein 70 (HSP70) was also examined as a potential marker of vascular injury. The model of IPC significantly reduced brain infarction and neurologic deficit. Compared with a sham operation, IPC also significantly attenuated brain edema formation in the intermediate (sham and IPC water contents: 5.99 ± 0.65 vs. 4.99 ± 0.81 g/g dry weight; P < 0.01) and outer zones (5.02 ± 0.48 vs. 4.37 ± 0.42 g/g dry weight; P < 0.01) of the ipsilateral hemisphere but not in the core zone. Blood–brain barrier disruption assessed by [3H]-inulin was significantly attenuated in the IPC group and the number of blood vessels that displayed HSP70 immunoreactivity was also reduced. Thus, IPC significantly attenuates ischemic brain edema formation, BBB disruption, and, as assessed by HSP70, vascular injury. Understanding the mechanisms involved in IPC may provide insight into methods for preserving cerebrovascular function during ischemia.

Possible involvement of interleukin-1 in ischemic brain edema formation

1992 ◽  
Vol 142 (1) ◽  
pp. 45-47 ◽  
Author(s):  
Yasundo Yamasaki ◽  
Takashi Suzuki ◽  
Hidetoshi Yamaya ◽  
Naosuke Matsuura ◽  
Hiroshi Onodera ◽  
...  
Keyword(s):  
Brain Edema ◽  
Interleukin 1 ◽  
Edema Formation ◽  
Ischemic Brain ◽  
Ischemic Brain Edema ◽  
Brain Edema Formation

Blood—Brain Barrier Permeability and Brain Concentration of Sodium, Potassium, and Chloride during Focal Ischemia

1994 ◽  
Vol 14 (1) ◽  
pp. 29-37 ◽  
Author(s):  
A. Lorris Betz ◽  
Richard F. Keep ◽  
Mary E. Beer ◽  
Xiao-Dan Ren
Keyword(s):  
Cerebral Ischemia ◽  
Brain Edema ◽  
Relative Permeability ◽  
Sodium Transport ◽  
Focal Ischemia ◽  
Edema Formation ◽  
Ischemic Brain ◽  
Early Stages ◽  
Brain Edema Formation ◽  
Rate Of Accumulation

Brain edema formation during the early stages of focal cerebral ischemia is associated with an increase in both sodium content and blood–brain barrier (BBB) sodium transport. The goals of this study were to determine whether chloride is the principal anion that accumulates in ischemic brain, how the rate of BBB transport of chloride compares with its rate of accumulation, and whether the stimulation seen in BBB sodium transport is also seen with other cations. Focal ischemia was produced by occlusion of the middle cerebral artery (MCAO) in anesthetized rats. Over the first 6 h after MCAO, the amount of brain water in the center of the ischemic cortex increased progressively at a rate of 0.15 ± 0.02 (SE) g/g dry wt/h. This was accompanied by a net increase in brain sodium (48 ± 12 μmol/g dry wt/h) and a loss of potassium (34 ± 7 μmol/g dry wt/h). The net rate of chloride accumulation (16 ± 1 μmol/g dry wt/h) approximated the net rate of increase of cations. Three hours after MCAO, the BBB permeability to three ions (22Na, 36Cl, and 86Rb) and two passive permeability tracers {[3H]α-aminoisobutyric acid (3H]AIB) and [14C]urea} was determined. Permeability to either passive tracer was not increased, indicating that the BBB was intact. The rate of 36Cl influx was 3 times greater and the rate of 22Na influx 1.8 times greater than their respective net rates of accumulation in ischemic brain. The BBB permeability to 22Na relative to that of [3H]AIB was significantly increased in the ischemic cortex, the relative permeability to 86Rb was significantly decreased, and the relative permeability to 36Cl was unchanged. These results indicate that the stimulation in BBB sodium transport is specific for sodium. Further, chloride accumulates with sodium in brain during the early stages of ischemia; however, its rate of accumulation is low compared with its rate of transport from blood to brain. Therefore, inhibition of BBB sodium transport is more likely to reduce edema formation than is inhibition of BBB chloride transport. This study demonstrates that chloride is the principal anion that accompanies the accumulation of sodium in ischemic brain, but its rate of accumulation in brain is much less than its rate of movement into brain, and therefore inhibition of chloride uptake would have little effect on brain edema formation. There is a specific acceleration of blood-to-brain sodium transport during ischemia that is not seen with another positively charged ion, 86Rb. This is consistent with stimulation of brain capillary Na,K-ATPase activity in response to the elevated extracellular potassium concentration. Inhibition of potassium influx across the BBB would probably be more successful in lessening edema formation than accelerating potassium efflux. However, inhibition of blood-to-brain sodium transport is likely to be a more effective approach to reducing brain edema formation during the early stages of cerebral ischemia.

The Role of Catecholamine-Induced Lipid Peroxidation and Histamine in Ischemic Brain Edema

1989 ◽  
pp. 818-820 ◽  
Author(s):  
H. Morooka ◽  
H. Sasayama ◽  
K. Sakai ◽  
S. Namba ◽  
A. Nishimoto
Keyword(s):  
Lipid Peroxidation ◽  
Brain Edema ◽  
Ischemic Brain ◽  
Ischemic Brain Edema

Role of Arginine Vasopressin V1 and V2 Receptors for Brain Damage After Transient Focal Cerebral Ischemia

2005 ◽  
Vol 25 (8) ◽  
pp. 1012-1019 ◽  
Author(s):  
Abedin Vakili ◽  
Hiroharu Kataoka ◽  
Nikolaus Plesnila
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Brain Damage ◽  
Arginine Vasopressin ◽  
Focal Cerebral Ischemia ◽  
Edema Formation ◽  
Transient Focal Cerebral Ischemia ◽  
Brain Edema Formation

Brain edema formation is one of the most important mechanisms responsible for brain damage after ischemic stroke. Despite considerable efforts, no specific therapy is available yet. Arginine vasopressin (AVP) regulates cerebral water homeostasis and has been involved in brain edema formation. In the current study, we investigated the role of AVP V1 and V2 receptors on brain damage, brain edema formation, and functional outcome after transient focal cerebral ischemia, a condition comparable with that of stroke patients undergoing thrombolysis. C57/BL6 mice were subjected to 60-min middle cerebral artery occlusion (MCAO) followed by 23 h of reperfusion. Five minutes after MCAO, 100 or 500 ng of [deamino-Pen(1), O-Me-Tyr(2), Arg(8)]-vasopressin (AVP V1 receptor antagonist) or [adamantaneacetyl(1), O-Et-d-Tyr(2), Val(4), Abu(6), Arg(8,9)]-vasopressin (AVP V2 receptor antagonist) were injected into the left ventricle. Inhibition of AVP V1 receptors reduced infarct volume in a dose-dependent manner by 54% and 70% (to 29±13 and 19±10 mm3 versus 63±17 mm3 in controls; P<0.001), brain edema formation by 67% (to 80.4%±1.0% versus 82.7%±1.2% in controls; P<0.001), blood-brain barrier disruption by 75% ( P<0.001), and functional deficits 24 h after ischemia, while V2 receptor inhibition had no effect. The current findings indicate that AVP V1 but not V2 receptors are involved in the pathophysiology of secondary brain damage after focal cerebral ischemia. Although further studies are needed to clarify the mechanisms of neuroprotection, AVP V1 receptors seem to be promising targets for the treatment of ischemic stroke.

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