Brain vasogenic

Papadopoulos, M. C., Manley, G. T., Krishna, S. and Verkman, A. S. Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema. FASEB J. 18 1291-1293, 2004. 

Fig. 5 Aquaporin-4 deletion increases brain swelling in vasogenic edema, a Increased ICP in AQP4-null mice in response to intraparenchymal fluid infusion. Left representative ICP traces from two wildtype and AQP4 null mice. Right, increased ICP at 60 min in response to isotonic fluid infusion (0.5 p.l/min). Data shown for individual mice and mean SE. b Increased ICP and in AQP4 null mice with melanoma brain tumor. Top, site of injection of melanoma cells. Bottom., tumor size at 4 and 7 days after implantation showing similar-sized tumors in wildtype and AQP4 null mice, c ICP measured 7 days after tumor implantation. From Papadopoulos et al. (2004)...

MRI Changes Corresponding to Vasogenic Edema after Experimental Brain Ischemia 137... 

MRI can provide valuable information on the progression of vasogenic edema and necrosis in the living organism. Free and bound water (e.g., water in the ventricles vs. water bound to cellular structures) can be discriminated based on different T1 and T2 relaxation times (Bakay et al. 1975 Naruse et al. 1982). Typical T1 and T2 relaxation times of normal rat brain at 4.7 T are 869+145 ms and 72+2 ms (caudate putamen) and 928 117 ms and 73 2 ms (cortex), while more liquid structures such as edematous tissue, cysts or CSF will lead to significantly elevated T1 and T2 relaxation times (Hoehn-Berlage et al. 1995). 

Related to the post-traumatic microvascular damage is the pathophysiological process of vasogenic brain edema that represents a disruption of blood-brain barrier integrity, resulting in sodium and protein accumulation and osmotic fluid expansion of the brain extracellular space. Clinically, this is reflected by an increase in intracranial pressure which, if unchecked, can cause secondary compressive injury to vital brain structures. 

The precise mechanism of post-traumatic vasogenic edema is unknown, but Chan and colleagues [51] have provided data suggesting an important role for an arachidonic-acid-derived oxygen-radical-mediated process. In initial in vitro experiments, it has been discovered that when rat-brain cortical slices are... 

Coincident with the reduction in brain level of hydroxyl radicals, U-74006F administered at 5 minutes post-injury also acts to reduce post-traumatic opening of the blood-brain barrier (i.e. decreased brain uptake of 14C-albumin) [56]. This effect of U-74006F to close the barrier may be related to the attenuation of hydroxyl-radical levels or an antagonism of the effects of free radicals on the barrier endothelium (i.e. decreased membrane-lipid peroxidation). Indeed, free radicals are known to increase barrier permeability [57]. Consistent with this reduction in post-traumatic opening of the blood-brain barrier which would lead to vasogenic brain edema, U-74006F has been shown to attenuate post-traumatic brain edema in a rat model of fluid percussion head injury [58]. 

Hall, E.D. and Travis, M.A. (1988) Inhibition of arachidonic acid-induced vasogenic brain edema by the non-glucocorticoid 21-aminosteroid U74006F, Brain Res. 451, 350-352. 

Cerebral ischemia causes not only reversible and then irreversible loss of brain function, but also cerebral edema (Symon et al. 1979 Hossman 1983). Ischemic edema is partly cytotoxic and partly vasogenic. Cytotoxic edema starts early, within minutes of stroke onset, and affects the gray more than the white matter, where damaged cell membranes allow intracellular water to accumulate. Vasogenic edema, which starts rather later, within hours of stroke onset, affects the white matter more, where the damaged blood-brain barrier allows plasma constituents to enter the extracellular space. Ischemic cerebral edema reaches its maximum in two to four days and then subsides over a week or two. 

One to two days after stroke onset, the infarcted area appears as an ill-defined hypodense area as vasogenic edema becomes predominant. Within two or three days, the attenuation values become lower, the ischemic area is better demarcated and there may be evidence of mass effect (Figs. 5.1 and 11.3). Later, there may be ipsilateral ventricular dilatation owing to loss of brain substance. Hemorrhagic transformation usually occurs a few days after stroke onset in large infarcts, but it may develop within hours and result in appearances very similar to primary intracerebral hemorrhage (Fig. 16.1) (Bogousslavsky 1991). 

Keywords Vasogenic edema Neurovascular unit teinases Aquaporins Blood-brain barrier Imaging... 

Brain edema is defined as an abnormal accumulation of fluid associated with volumetric enlargement of the brain (Klatzo, 1967). Excess fluid can accumulate in the intracellular or extracellular spaces. Two types of brain edema have been defined based on the site of damage and where the fluid accumulates. Cytotoxic edema results in intracellular swelling without alterations in vascular permeability. Vasogenic edema is associated with damage to the BBB leading to flow of water and plasma constituents into the brain. These types of edema rarely exist in isolation typically, one type of edema dominates the other, but both co-exist. 

Several recent reviews have been published on MMPs in brain injury (Ning et al., 2008 Candelario-Jalil et al., 2009 Rosenberg, 2009). This section focuses only on their role in BBB disruption and formation of vasogenic edema. 

Doczi et al., 1984 Laszlo et al., 1999), and cold-induced vasogenic edema (Ikeda et al., 1997b Bemana and Nagao, 1999). There is a relationship between AVP and AQP in the kidney, but the interaction between AVP and water channels in the brain remains to be elucidated. 

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