octanoic acid/edema

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Octanoic acid inhibits astrocyte volume control: implications for cerebral edema in Reye's syndrome.

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Octanoic acid has been implicated in the pathogenesis of cytotoxic cerebral edema in Reye's syndrome. Using astrocytes from primary culture, we studied the dose-dependent effects of octanoate on cellular volume regulation and metabolism. Astrocyte volume recovery following hypoosmotic swelling was

Brain edema in acute liver failure. Insight from experimental studies.

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Brain edema is a leading cause of death in fulminant hepatic failure (FHP). Animal studies are needed to gain further insight into its pathogenesis. The authors describe and analyze the results of brain studies in two animal models of FHF, the rabbit with galactosamine induced hepatitis and the

Ammonia-induced swelling of rat cerebral cortical slices: implications for the pathogenesis of brain edema in acute hepatic failure.

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The pathogenesis of brain edema in fulminant hepatic failure is incompletely understood. Our previous studies in models of this disease suggest the presence of a cytotoxic mechanism; as cortical astrocytes appeared predominantly swollen, we hypothesized that ammonia, metabolized to glutamine solely

Preparation and evaluation of pranoprofen gel for percutaneous administration.

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The percutaneous delivery of nonsteroidal anti-inflammatory drug (NSAID) has the advantages of avoiding the hepatic first pass effect and delivering the drug to the inflammation site at a sustained, concentrated level over an extended period of time. Hydroxypropyl methylcellulose (HPMC) and

Topical effects of absorption enhancing agents on the rectal mucosa of rats in vivo.

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In the present study, attempts have been made to assess the effects of cefoxitin formulations with various absorption promoters on mucosal integrity after rectal delivery in rats. Observations were made at 2 and 24 h following drug administration. On macroscopic and histologic evaluation, all drug

Dibenz[b,e]oxepinalkanoic acids as nonsteroidal antiinflammatory agents. 3. omega-(6,11-Dihydro-11-oxodibenz[b,e]oxepin-2-yl)alkanoic acids.

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Omega-(6,11-Dihydro-11-oxodibenz[b,e]oxepin-2-yl)butyric, -hexanoic, and -octanoic acids were evaluated in the carrageenan paw edema assay. The most active compound, the butyric acid analogue, was 1.80 times more potent than the hexanoic compound, 1.15 times more potent than the octanoic analogue,

Pathophysiology of hepatic encephalopathy: The concept of synergism.

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Hepatic encephalopathy (HE) remains a severe neuropsychiatric complication of liver failure. Neuropathological evaluation of material from patients who died in hepatic coma reveals morphologic changes primarily to astrocytes (cytotoxic edema, Alzheimer Type II astrocytosis) accompanied by discreet

Early changes in the permeability of the blood-brain barrier produced by toxins associated with liver failure.

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Our study was designed to determine whether substances that appear in the serum during the course of liver failure have a detrimental effect on the passive permeability of the blood-brain [blood-cerebrospinal fluid (CSF)] barrier. Lactic acid, octanoic acid, and ammonia were infused into rabbits for

Occludin oligomeric assemblies at tight junctions of the blood-brain barrier are altered by hypoxia and reoxygenation stress.

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Hypoxic (low oxygen) and reperfusion (post-hypoxic reoxygenation) phases of stroke promote an increase in microvascular permeability at tight junctions (TJs) of the blood-brain barrier (BBB) that may lead to cerebral edema. To investigate the effect of hypoxia (Hx) and reoxygenation on oligomeric

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