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Brain cerebrospinal fluid

Florfenicol concentrations in the brain, cerebrospinal fluid (CSF), and aqueous humor were one-fourth to one-half the corresponding semm concentrations. Concentrations in these tissues and fluids did not decrease as rapidly, maintaining a low, but fairly constant value. Because the brain, CSF, and aqueous humour are separated from the blood by specialized barriers, florfenicol can seemingly only cross these barriers to a limited extent. [Pg.517]

Amperometric detection was achieved on two patches of C films (formed by CVD of 3,4,9,10-perylenetetracarboxylie dianhydride) on a glass chip. The microchannels were formed using a 23- im-thick photoresist as a spacer. Glucose oxidase and lactate oxidase were immobilized with HRP on the C films via a coated film of osmium PVPD polymer. Simultaneous measurements of glucose and lactate in rat brain cerebrospinal fluid (first perfused with 50 mM veratridine) were achieved. These two films were spatially separated in order to avoid interdiffusion of H202 formed from the two separate enzymatic reactions. Moreover, the two films were preceded by a third C film immobilized with ascorbate oxidase in order to remove ascorbic acid interference [759]. [Pg.217]

Figure 31.4. Time coui se of cellular and molecular acdvadon folowing stioke. Diagrammadc representadon of die dme course of cellular acdvadori (PNL, polymorphonuclear leukocytes M(j), macrophages) and inflammatory molecular expression (GM, granulocyte and monocyte coloriy-sdmuladng factor ICAM, soluble intercellular adhesion molecule-1 VCAM, soluble vascular- cell adliesiori molecule-1 TNF-a, tumor necrosis factor a IL-1(5, interleukin 1(5 IL-6, interleukin 6 IL-8, interleukin 8 IL-10, interleukin 10) in human brain, cerebrospinal fluid (CSF) and blood after sUoke. Reproduced from Nilupul Perera M, Ma HK, Arakawa S, Howells DW, Markus R, Rowe CC, Donnan GA (2006). InPammation following stroke. J Clin Neurosci, 13 1-8 (with permission from Elsevier). Figure 31.4. Time coui se of cellular and molecular acdvadon folowing stioke. Diagrammadc representadon of die dme course of cellular acdvadori (PNL, polymorphonuclear leukocytes M(j), macrophages) and inflammatory molecular expression (GM, granulocyte and monocyte coloriy-sdmuladng factor ICAM, soluble intercellular adhesion molecule-1 VCAM, soluble vascular- cell adliesiori molecule-1 TNF-a, tumor necrosis factor a IL-1(5, interleukin 1(5 IL-6, interleukin 6 IL-8, interleukin 8 IL-10, interleukin 10) in human brain, cerebrospinal fluid (CSF) and blood after sUoke. Reproduced from Nilupul Perera M, Ma HK, Arakawa S, Howells DW, Markus R, Rowe CC, Donnan GA (2006). InPammation following stroke. J Clin Neurosci, 13 1-8 (with permission from Elsevier).
In adcUdon to the biogenic amines, the amino acid neurotransmitters are also implicated in the neurochemistry of major depressive disorder. Neurotransmitter y-aminobutyric acid (GABA) levels are low in brain, cerebrospinal fluid, and blood of padents w ith major depressive disorder (Petty, 1995 Brambilla et al., 2003). [Pg.498]

N,N-dimethyltryptamine (DMT) (fig. 6) has been found to occur endogenously at very low concentrations within the human brain, cerebrospinal fluid, and blood. Its function is unknown, but some have speculated that it plays neurotransmitter-like roles in psychotic mental states and dream-sleep imagery (Barker ef al. 1981 Callaway 1988 Strassman 2001). Thus, all humans are, presumably at all times, in possession of a Schedule 1 substance /hd therefore in violation of United States and international law ... [Pg.100]

Baehr, C., Reichel, V., and Pricker, G. (2006) Choroid plexus epithelial monolayers — a cell culture model from porcine brain. Cerebrospinal Fluid Research, 3, 13. [Pg.262]

In animals with either acute or chronic renal failure, both urea concentration and osmolality are similar in brain, cerebrospinal fluid, and plasma. The solute content of brain in animals with acute renal failure is such that essentially all of the increase in brain osmolality is due to an increase of brain urea concentration. However, in animals with chronic renal failure, about half of the increase in brain osmolality is due to the... [Pg.206]

In addition to the tissues and fluids mentioned above, kininogenase activity has also been found under physiological and pathological conditions in a number of other organs and fluids brain, cerebrospinal fluid, peripheral nerve, bronchial... [Pg.360]

Specific barriers may serve to limit dmg distribution. The placental barrier is of obvious importance to dmg action in the fetus. Dmg transfers across the placenta primarily by Hpid solubiHty. Hence, this barrier is not particularly restrictive. Similarly, the Hpid solubiHty of a dmg is a primary deterrninant in access to the brain and cerebrospinal fluid. Generally, hydrophilic or charged dmgs can also penetrate to these latter areas, but the result is slow and incomplete. The blood brain barrier is composed of cells having tight junctions which are much less permeable to solutes than are the endotheHal cells of other tissues. [Pg.269]

The area postrema is a circumventricular brain region positioned on the dorsal surface of the medulla on the floor of the fourth ventricle. The blood-brain barrier and the cerebrospinal fluid-brain barrier are absent in this region and consequently many substances that do not pass across capillaries in other regions of the brain can do so in the area postrema. The chemoreceptor trigger zone (CTZ), located in the lateral area postrema is sensitive to blood-borne emetogens. Nerves from the CTZ connect with the vomiting centre. [Pg.218]

Glycosydation AChE and BChE carry 3 and 9, respectively, N-glycosylation consensus sequences attaching carbohydrate residues to the core protein via asparagines. Different molecular forms of the enzymes in various tissues, show different number and composition of carbohydrate residues. N-glycosylation at all sites was shown to be important for effective biosynthesis, secretion and clearance of ChEs from the circulation. Altered patterns of AChE glycosylation have been observed in the brain and cerebrospinal fluid of Alzheimer s disease (AD) patients, with potential diagnostic value. [Pg.359]

Ricaurte, G.A. DeLanney, L.E. Wiener, S.G. Irwin, L and Langston, J.W. 5-Hydroxyindoleacetic acid in cerebrospinal fluid reflects serotonergic damage induced by 3,4-methylenedioxymethamphetamine in CNS of nonhuman primates. Brain Res 474 359-363. 1988b. [Pg.321]

There are several ways in which possible neurotoxic effects might be studied. First, measurement of cerebrospinal fluid concentrations of dopamine or serotonin metabolites would be a straightforward way of assessing neurotoxicity. There are pitfalls in this approach (as outlined by Dr. Ricaurte (this volume), such as the facts that lumbar cerebrospinal fluid might reflect spinal cord neurochemistry more than it reflected brain neurochemistry, and drugs like /r-chloroamphetamine affect serotonin neurons in spinal cord less than they do those in brain (Sanders-Bush... [Pg.348]

The CTZ, located outside the blood-brain barrier (BBB), is exposed to cerebrospinal fluid and blood.2,3 Therefore it is easily stimulated by uremia, acidosis, and the circulation of toxins such as chemotherapeutic agents. The CTZ has many serotonin type 3 (5-HT3), neurokinin-1 (NKj), and dopamine (D2) receptors.2 Visceral vagal nerve fibers are rich in 5-HT3 receptors. They respond to gastrointestinal distention, mucosal irritation, and infection. [Pg.297]


See other pages where Brain cerebrospinal fluid is mentioned: [Pg.11]    [Pg.236]    [Pg.56]    [Pg.339]    [Pg.40]    [Pg.434]    [Pg.434]    [Pg.365]    [Pg.56]    [Pg.357]    [Pg.565]    [Pg.257]    [Pg.449]    [Pg.11]    [Pg.236]    [Pg.56]    [Pg.339]    [Pg.40]    [Pg.434]    [Pg.434]    [Pg.365]    [Pg.56]    [Pg.357]    [Pg.565]    [Pg.257]    [Pg.449]    [Pg.278]    [Pg.308]    [Pg.78]    [Pg.1274]    [Pg.159]    [Pg.12]    [Pg.15]    [Pg.26]    [Pg.124]    [Pg.142]    [Pg.154]    [Pg.233]    [Pg.235]    [Pg.10]    [Pg.83]    [Pg.230]    [Pg.231]    [Pg.223]    [Pg.321]    [Pg.1034]   
See also in sourсe #XX -- [ Pg.374 ]

See also in sourсe #XX -- [ Pg.4 ]




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