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sucrose/edema

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Microgravimetric methods are very useful for quantitative studies on brain edema. One of the techniques available is based on a gradient made up by NaCl and polyvinyl pyrrolidone-coated silica particles (Percoll). The present study was performed to find a way of minimizing fluid shifts between the

[14C]urea and [14C]sucrose as permeability indicators in histamine pulmonary edema.

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To see whether, by avoiding red blood cell transport effects, [14C]-sucrose would be a more sensitive lung vascular permeability indicator than [14C]urea, we compared the effects of 4 microgram/kg-min intravenous histamine phosphate infusions on lung vascular permeability-surface area products (PS)

Clearance of edema fluid into cerebrospinal fluid. A mechanism for resolution of vasogenic brain edema.

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The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I131 and sucrose-C14 lebeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternal perfusion. The
The effect of dexamethasone administration and withdrawal was studied with respect to blood-brain barrier function. The tracers alpha-[3H]aminoisobutyric acid (AIB) (MW 104) and [14C]sucrose (MW 342), which have a low permeability across the intact endothelium, were simultaneously injected

Diffusion tensor imaging supports the cytotoxic origin of brain edema in a rat model of acute liver failure.

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OBJECTIVE Brain edema is a severe complication of acute liver failure (ALF) that has been related to ammonia concentrations. Two mechanisms have been proposed in the pathogenesis: vasogenic edema that is secondary to the breakdown of the blood-brain barrier and cytotoxic edema caused by ammonia

Perineurial permeability and endoneurial edema during Wallerian degeneration of the frog peripheral nerve.

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Perineurial permeabilities to [3H]sucrose and [14C]dextran (MW = 70,000), and water content, conduction velocity (CV) and maximum amplitude (MAP) of the compound action potential, were determined in Wallerian degenerated nerves (sciatic or tibial) of the frog and compared with values in the

Role of blood-brain barrier permeability in focal ischemic brain edema.

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We studied how changes in BBB function are related to the development of ischemic brain edema. Focal cerebral ischemia was produced by left MCA occlusion in rats. The permeability of the BB to small or large molecules was evaluated qualitatively by the extravasation of EB or NaFl dyes and

Transport of sodium from blood to brain in ischemic brain edema.

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Brain water and sodium increase during ischemia, suggesting that the blood-brain barrier permeability to sodium is increased. To test this hypothesis we measured the permeability-surface area products of 22Na and [3H]sucrose in gerbils following 3 hours of unilateral ischemia. In animals with
White matter (WM) injury after bilateral common carotid artery occlusion (BCAO) in rat is associated with disruption of the blood-brain barrier (BBB) by matrix metalloproteinases (MMPs). We hypothesized that WM injury as seen on magnetic resonance imaging (MRI) would correlate with regions of

Compositional changes in lipid microdomains of air-blood barrier plasma membranes in pulmonary interstitial edema.

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We evaluated in anesthetized rabbits the compositional changes of plasmalemmal lipid microdomains from lung tissue samples after inducing pulmonary interstitial edema (0.5 ml/kg for 3 h, leading to approximately 5% increase in extravascular water). Lipid microdomains (lipid rafts and caveolae) were
Glycyrrhizic acid (GA) ameliorates many components of the metabolic syndrome, but its potential therapeutic use is marred by edema caused by inhibition of renal 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2). We assessed whether 100 mg/kg per day GA administered orally could promote metabolic
Nerve water content and the permeability-surface area product (PA) to [3H]-or [14C]sucrose at the blood-nerve barrier were determined in unanesthetized control rats fed a normal diet and in rats fed galactose with or without an aldose reductase inhibitor (Statil or AL 1576) or a thromboxane

Stimulation of aldosterone biosynthesis by experimental edema: role of the kidneys.

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The role of the kidneys in the stimulation of aldosterone biosynthesis by sodium sequestration was investigated in potassium-depleted rats. After 2 wk on a potassium-deficient diet, rats were treated by subcutaneous injections of polyethylene glycol or formalin and were then kept on sucrose and
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