Brain edema fluid

Laterra, L. and Goldstein, G.W., Ventricular organization of cerebral spinal fluid blood-brain barrier, brain edema, and hydrocephalus, in Principles of Neuroscience, 4th ed., Kandel, E.R., Schwartz, J.H., and Jessell, T.M., Eds., McGraw-Hill, New York, 2000, appendix B. 

Milhorat, T. H. (ed.), Cerebrospinal Fluid and the Brain Edemas. New York Neuroscience Society of New York, 1987. 

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. 

AQP-4 Cerebrospinal fluid reabsorption in central nervous system regulation of brain edema... 

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. 

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]. 

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. 

Rosenberg GA, Kyner WT, Estrada E (1980) Bulk flow of brain interstitial fluid under normal and hyperosmolar conditions. Am J Physiol 238 F42-F49 Rosenberg GA, NavratU M (1997) MetaUoproteinase inhibition blocks edema in intracerebral hemorrhage in the rat. Neurology 48 921-926... 

Rose, C., Michalak, A., Rama Rao, K.V., Quack, G., Kircheis, G., Butterworth, R.F. L-ornithine-L-aspartate lowers plasma and cerebrospinal fluid ammonia and prevents brain edema in rats with acute liver failure. Hepatology 1999 30 636—640... 

The encephalopathy induced by lead toxicity is most hkely due to a compromise in the blood-brain barrier. Brain edema occurs in the interstitial area and appears due to compromised blood vessels integrity. The brain capillaries and blood vessels have endothelial cells that contain tight junctions and act as a seal or carrier that excludes many plasma proteins and organic molecules and impedes Na and K exchange. Elevated lead levels disrupt these vessels, and plasma proteins such as albumin enter the interstitial spaces, as do some ions. This increases osmotic pressure, and water accumulates in response. The increased interstitial fluid flows into the cerebrospinal fluid. The edema causes in an increase in intracranial pressure and restricts blood flow to the brain. The direct mechanisms by which the blood-brain barrier and blood vessels that compose the barrier may be compromised may be due to astrocytes appearing to be vulnerable to the toxic effects of lead. The astrocytes cover the walls of the brain blood vessels, and lead can injure these structures. 

A delicate balance of normal pressure is maintained in the brain and spinal cord by brain, blood, and cerebrospinal fluid (CSF) volume. Since the brain is contained within a confined space (skull), any foreign mass contained within that space causes adverse sequelae. This results in either destruction or displacement of normal brain tissue with associated edema. Most brain metastases occur through hematogenous spread of the primary tumor, and around 80% of patients will have multiple sites of metastases within the brain. 

Postmortem lesions include excessive fluid in the sac surrounding the heart (hydropericardium) in the chest cavity (hydrothorax) pulmonary edema hemorrhage in the abomasum and intestine hemorrhagic gastroenteritis enlarged liver, spleen, and lymph nodes and edema and hemorrhage of the brain. 

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)...

Weakness, dizziness, insomnia, headache, and nausea can occur in mountain travelers who rapidly ascend above 3000 m. The symptoms are usually mild and last for a few days. In more serious cases, rapidly progressing pulmonary or cerebral edema can be life-threatening. By decreasing cerebrospinal fluid formation and by decreasing the pH of the cerebrospinal fluid and brain, acetazolamide can increase ventilation and diminish symptoms of mountain sickness. 

Of 143 patients (62) studied retrospectively, eight stopped taking treatment because of significant peripheral edema, one had an exacerbation of cardiac failure, and one reported myalgia. HbAlc, lipid profiles, and blood pressure improved. In 38 patients taking pioglitazone brain natriuretic peptide, which may play a role in fluid retention, did not rise (63). 

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