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  • 1
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 11 (1981), S. 129-134 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A high amount of histamine was found in capillaries isolated by subcellular fractionation from the brain. In view of the important effects of histamine on vascular permeability in peripheral vessels, it was thought that histamine had a similar function in the cerebral vasculature. Intracarotic histamine infusion resulted in an enhanced pinocytosis of endothelial cells and the oedematous swelling of the astrocytic end-feet system. [3H]-Histamine, injected in the cerebral ventricles, accumulated in the capillary wall. Histamine and cimetidine activated hydroxyfatty acid and prostaglandin D2 synthesis in isolated brain capillaries. The possible function of the capillary histamine in the regulation of permeability of microvessels is discussed.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Histamine ; Cerebral ventricle ; Pinocytosis ; Brain-blood barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Histamine dihydrochloride (10 μg of 500 μg/ml) was infused during 1 min into the lateral cerebral ventricle of rats, which resulted in a significant stimulation of pinocytosis in the endothelial cells. Systemic injections of mepyramine or metiamide could not prevent this activation. In contrast, ranitidine, injected with histamine was able to inhibit the stimulation of pinocytosis. Albumin exudation from the blood was not found. There was also no change in water and electrolyte contents of the brain tissue. The results suggest that histamine reaching the abluminal membrane can activate the pinocytosis in the cerebral endothelial cells in the reverse direction, i.e., from brain to blood, without opening the blood-brain barrier.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 47 (1982), S. 252-258 
    ISSN: 1432-1106
    Keywords: Blood-brain barrier ; Histamine ; Antihistamines ; Pinocytosis ; Albumin immunohisto chemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of histamine administered via the common carotid artery on the transport processes of brain capillaries was investigated in rats. The fine structure of endothelial cells and the glial end-feet system was studied by electron microscopy and the serum albumin was visualized for light microscopy by the peroxidase-antiperoxidase (PAP) immunohistochemical reaction. Sixty microgram per milliliter histamine enhanced the penetration of serum albumin into the capillaries while the number of pinocytotic and coated vesicles significantly increased in the capillary endothelium. Oedematous swelling of the glial end-feet system was also observed. The stimulatory effect of histamine on the transcapillary transport could not be inhibited by a histamine H1− receptor antagonist, mepyramine. By contrast, metiamide, a histamine H2−-receptor antagonist prevented both ultrastructural changes and albumin penetration in the brain capillaries to occur.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Neurons from cerebral cortex and hippocampal CA1 sector exhibit a striking difference in vulnerability to transient ischemia. To establish whether this difference is due to the inherent (pathoclitic) properties of these neurons, the ischemic susceptibility was studied in primary cortical and hippocampal cultures by using a new model of argon-induced in vitro ischemia. Neuronal cultures were exposed at 37°C for 10–30 min to argon-equilibrated glucose-free medium. During argon equilibration, Po2 declined to 〈2.5 torr within 1 min and stabilized shortly later at ∼1.3 torr. After 30 min of in vitro ischemia, total adenylate was 〈45% and ATP content 〈15% of control in both types of culture. Cytosolic calcium activity increased from 15 to 50 nM. Reoxygenation of cultures after in vitro ischemia led to delayed neuronal death, the severity of which depended on the duration of in vitro ischemia but not on the type of neuronal cultures. Energy charge of adenylate transiently returned to ∼90% of control after 3 h, but ATP content recovered only to 40% and protein synthesis to 〈35%. Cytosolic calcium activity continued to rise after ischemia and reached values of ∼500 nM after 3 h. The new argon-induced in vitro ischemia model offers major advantages over previous methods, but despite this improvement it was not possible to replicate the differences in cortical and hippocampal vulnerability observed in vivo. Our study does not support the hypothesis that selective vulnerability is due to an inherent pathoclitic hypersensitivity.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Prostaglandins 23 (1982), S. 287-297 
    ISSN: 0090-6980
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 64 (1995), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of three metabolic inhibitors—iodoacetate, potassium cyanide, and potassium arsenate—on neuronal viability was studied in primary rat cortical and hippocampal CA1 neuronal cultures. Iodoacetate (0.1 mM) applied for 5 min to 8-day-old cultures resulted in delayed neuronal death within 3–24 h in cortical and hippocampal CA1 neurons. Neuronal degeneration was preceded by transient inhibition of energy metabolism to ∼40% and a permanent inhibition of protein synthesis to ∼50%. The inhibition of protein synthesis and the neuronal death were prevented by the free radical scavenger vitamin E but not by the glutamate antagonist MK-801. Removal of calcium during iodoacetate exposure could not protect against toxicity, and there was no increase of intracellular calcium concentration during and shortly after iodoacetate treatment. Cyanide and arsenate produced only partial neuronal degeneration, even at a dose of 10 mM. These observations demonstrate that brief exposure of neurons to low concentrations of iodoacetate produces a delayed type of neuronal death that is not mediated by either calcium or glutamate. The therapeutic effect of vitamin E points to a free-radical mediated injury and suggests that this type of pathology may also be involved in delayed neuronal death after transient energy depletion in vivo.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The role of second messengers in the regulation of protein phosphorylation was studied in microvessels isolated from rat cerebral cortex. The phosphoproteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the kinetics of 32P incorporation into specific protein substrates were evaluated by computer-aided x-ray film densitometry. With the use of this method, Ca2+-calmodulin (CAM)-, Ca2+/phospholipid (PK C)-, cyclic GMP (cGMP)-, and cyclic AMP (cAMP)-dependent protein kinases were detected. CAM-dependent protein ki-nase proved to be the major phosphorylating enzyme in the microvascular fraction of the rat cerebral cortex; the activity of cGMP-dependent protein kinase was much higher than that of the cAMP-dependent one. Autophosphoryla-tion of both the α- and β-subunits of CAM-dependent protein kinase and the proteolytic fragment of the PK C enzyme was also detected. The kinetics of phosphorylation of the individual polypeptides indicate the presence in the cerebral endothelium of phosphoprotein phosphatases. The phosphorylation of proteins in the cerebral capillaries was more or less reversible; the addition of second messengers initiated a very rapid increase in 32P incorporation, followed by a slow decrease. Because the intracellular signal transducers like Ca2+ and cyclic nucleotides are frequently regulated by different vasoactive substances in the endothe-lial cells, the modified phosphorylation evoked by these second messengers may be related in vivo to certain changes in the transport processes of the blood-brain barrier.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A fraction enriched in capillaries has been prepared from the guinea pig cerebral cortex. The purity of this fraction was checked by light- and electron-microscopic examination and by its high enrichment in alkaline phosphatase and γ-glutamyl transpeptidase. In the capillary-rich fraction, the endogenous level of histamine was 1.9%’of that measured in the initial hornogenate. The histamine-synthesizing enzyme, I-histidine decarboxylase, and the metabolizing enzyme, histamine-N-methyltransferase, were barely detectable. In addition, histamine elicits a twofold stimulation in the accumulation of cyclic AMP in this capillary fraction with an EC50 of 5 γM. Agonists and antagonists of the two types of histamine receptors (H1 and H2) were used for the characterization of the receptors mediating this action: H2-receptor agonists were able to activate the adenylate cyclase with “relative potencies” similar to that found on typical H2-receptors, and cimetidine, a specific H2-receptor antagonist, competitively inhibited the response to histamine with a K1 value reflecting its interaction with a single population of H2-receptors. On the contrary, data obtained with H1-receptor agonists and antagonists reflect their interaction with H2-receptors rather than H1-receptors. Thus H2-receptors are involved in the activation of adenylate cyclase of the capillary fraction.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Comparative Biochemistry and Physiology -- Part A: Physiology 64 (1979), S. 177-183 
    ISSN: 0300-9629
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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