Brain edema cells

Mokri B (2001) The Monro-Kellie hypothesis applications in CSF volume depletion. Neurology 56 1746-1748 Naruse S, Horikawa Y, Tanaka C, Hirakawa K, Nishikawa H, Yoshizaki K (1982) Proton nuclear magnetic resonance studies on brain edema. J Neurosurg 56 747-752 Nedergaard M, Vorstrup S, Astrup J (1986) Cell density in the borderzone around old small human brain infarcts. Stroke 17 1129-1137... 

These include mannitol and sorbitol which act mainly in the proximal tubules to prevent reabsorption of water. These polyhydric alcohols cannot be absorbed and therefore bind a corresponding volume of water. Since body cells lack transport mechanisms for these substances (structure on p.175), they also cannot be absorbed through the intestinal epithelium and thus need to be given by intravenous infusion. The result of osmotic diuresis is a large volume of dilute urine, as in decompensated diabetes melli-tus. Osmotic diuretics are indicated in the prophylaxis of renal hypovolemic failure, the mobilization of brain edema, and the treatment of acute glaucoma attacks (p. 346). 

Cerebral tissue acidosis following ischemia or flaumatic brain injury contributes to cytotoxic brain edema formation. In vitro lactacidosis induces swelling of glial cells by intracellular Na" - and Cl accumulation by the Na" /H+-antiporter, Cr/HCOs antiporters, and the Na -K -2C1 cotransport (Staub et al., 1990 Ringel et al., 2006a). 

Experimental evidence indicates that COX modulates BBB permeability in neuroinflammatory conditions, ischemia, and hemorrhage. The COX inhibitor, KBT-3022, prevented brain edema induced by bilateral carotid occlusion and recirculation in gerbils (Yamamoto et al., 1996). In the collagenase model of intracerebral hemorrhage, the brain water content of rats treated with the COX-2 inhibitor, celecoxib, decreased both in lesioned and nonlesioned hemispheres in a dose-dependent manner, which was accompanied with reduced perihematomal cell death (Chu et al., 2004). Delayed damage to the BBB and vasogenic edema, which follow ischemic stroke, were significantly diminished by administration of... 

Chi OZ, Hunter C, Liu X, Weiss HR (2007) Effects of anti-VEGF antibody on blood-brain barrier disruption in focal cerebral ischemia. Exp Neurol 204 283-287 Chu K, Jeong SW, Jung KH, Han SY, Lee ST, Kim M, Roh JK (2004) Celecoxib induces fimctional recovery after intracerebral hemorrhage with reduction of brain edema and perihematomal cell death. J Cereb Blood Flow Metab 24 926-933... 

Fischer S, Wobben M, Marti HH, Renz D, Schaper W (2002) Hypoxia-induced hyperpermeability in brain microvessel endothelial cells involves VEGF-mediated changes in the expression of zonula occludens-1. Microvasc Res 63 70-80 Fishman RA (1975) Brain edema. N Engl J Med 293 706-711... 

It was observed that rats with a transient MCA occlusion have a larger brain infarction when recombinant human IL-1 P is injected into the lateral ventricle immediately after reperfusion [7,41]. Similar results have been obtained in rats with a permanent MCA occlusion [7,42]. The intraventricular injection of recombinant human IL-1 p also enhances the formation of brain edema and increases both the number of neutrophils in ischemic areas and neutrophil-endothelial cell adhesion. The most widely recognized functions of IL-1 appear to be the induction of endothelial cell adhesion molecule expression and the promotion of neutrophil tissue infiltration [7,41]. These observations suggest that IL-1 may play a deleterious role in cerebral ischemia. Studies showing a reduction in infarct size after the administration of IL-1 antagonists or inhibitors provide further evidence of the importance of IL-1 in cerebral ischemia [41,43-49]. The possible harmful mechanisms induced or activated by IL-1 include fever, increased heart rate and arterial blood pressure, enhancement of N-methyl-D-aspartate-mediated injury, proliferation of microglia, release of arachidonic acid, and stimulation of NO synthesis [7,50]. 

Sharma, H.S., Westman, J., Cervos-Navarro, J., and Nyberg, F., Role of neurochemicals in brain edema and cell changes following hyperthermic brain injury in the rat, Acta Neurochir. Suppl, 70, 269, 1997. 

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