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  • 1
    ISSN: 1432-0533
    Keywords: prostaglandin F2α ; Immunohistochemistry ; Ischemia ; Recirculation ; Carbodiimide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Immunohistochemical localization of prostaglandin F2α (PG F2α) was studied in 24 rats. In 21 rats, global brain ischemia was produced for 5 min by Pulsinelli's method. Prior to decapitation, 13 were recirculated for 5 min, while the remaining eight were not. Three recirculated rats were pretreated with indomethacin before the occlusion. Hypotension was induced during the occlusion to 40–50 mm Hg of mean arterial blood pressure in 11 rats including those unrecirculated, recirculated and pretreated with indomethacin. Three normal rats without occlusion of arteries served as control. The brains were snap frozen and 10-μm cryostat sections were incubated in rabbit anti-PG F2α serum and stained by the indirect immunofluorescence method after fixation in carbodiimide and in Zamboni's solution. Positive staining for PG F2α was noted mainly in pial vessels in normal and ischemic rats both with and without hypotension. The rats recirculated without hypotensive ischemia revealed a positive reaction in the walls of pial and parenchymal vessels. All rats recirculated after the hypotensive occlusion showed positive staining in blood vessels, in the cytoplasm of neurons (especially in hippocampi) and in the interfascicular oligodendrocytes. The above results indicate that recirculation after ischemia results in an increase in PG F2α in parenchymal vessels, neurons and oligodendrocytes.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Subarachnoid hemorrhage ; Prostaglandin F2-alpha ; Hippocampus ; Purkinje cell ; Intracranial hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of subarachnoid hemorrhage (SAH) with various degrees of increase in intracranial pressure (ICP) on the staining of prostaglandin F2-alpha (PG F2α) were studied in rat brains. SAH was produced in 18 rats by injection of 0.18–0.20 ml of autologous arterial blood/100 g body weight into the cisterna magna. By changing the speed of injection, the ICP was transiently increased by 346±68 (mean±S.D.) mm Hg in eight rats (including three pretreated with indomethacin), by 200±42 mm Hg in five rats, and by 6±4 mm Hg in the other five. Three rats injected with the same volume of mock cerebrospinal fluid (CSF) with ICP increased by 217±67 mm Hg and five normal rats without injection served as controls. All animals were decapitated 15 min after injection. The cryosections were stained for PG F2α using an indirect immunofluorescence method. Positive staining for PG F2α was noted only in pial vessels in all normal and mock-CSF-injected rats. In SAH rats with ICP increased by 6±4 mm Hg, there was a positive reaction in hippocampal neurons and Purkinje cells as well as blood vessels. SAH rats with higher ICP showed stronger PG F2α staining in the above areas, as well as in cerebellar granule cells. All rats pretreated with indomethacin showed a smaller increase in staining. The above results indicate that subarachnoid blood clots per se produce a rapid increase of PG F2α in neurons and blood vessels of both cerebrum and cerebellum, and that this increase is augmented by intracranial hypertension.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Endothelium-dependent relaxation ; hypoxia ; subarachnoid haemorrhage ; vasospasm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; subarachnoid haemorrhage ; vascular permeability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The time course of the blood-arterial wall barrier disruption following experimental subarachnoid haemorrhage (SAH) was studied in 24 rabbits. Animals with SAH received two successive blood injections through the cisterna magna. Horseradish peroxidase (HRP) was given intravenously 30 minutes before sacrifice to assess the integrity of the barrier. In the basilar arteries taken from animals that were sacrificed 4 days after the first SAH, HRP-reaction products were diffusely observed in the subendothelial space. Three weeks following the first SAH, permeation of HRP was still observed in half of the animals. However, in animals sacrificed 7 weeks after the first SAH, no permeation of HRP into the subendothelial space was noted. Opening of the interendothelial space seemed to be the major mechanism for HRP permeation into the subendothelial space rather than transendothelial vesicular transport. Disruption of the bloodarterial wall barrier in the major cerebral arteries following SAH may play a role in the pathogenesis of vasospasm.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0942-0940
    Keywords: Subarachnoid haemorrhage ; cerebral vasospasm ; vascular permeability ; FITC-dextran
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Disruption of the blood-arterial wall barrier in the major cerebral arteries occurs following subarachnoid haemorrhage (SAH) and may be related to the pathogenesis of cerebral vasospasm. Using FITC dextrans of various sizes, the present study was undertaken to determine if the barrier disruption shortly after SAH occurs equally to various sized tracers. Forty-two Sprague-Dawley rats were divided into 5 groups. Four groups were injected with FITC-dextrans of differing molecular weights (MW): FD4 (MW=4,080), FD40 (MW=40,500), FD 70 (MW=71,400), and FD 150 (MW=156,900). One group was injected with horseradish peroxidase (HRP: MW=40,000). Each group was further divided into two subgroups: with or without SAH. SAH was induced by injecting arterial blood into the cisterna magna. To assess the integrity of the blood-arterial wall barrier by transmission electron microscope, the tracers were intravenously injected prior to sacrificing the animals. The groups without SAH showed no permeability of tracers into the subendothelial spaces of the basilar arteries. In contrast, with the exception of FD 150, FITC-dextrans (FD 4, FD 40, FD 70) were noticed in the subendothelial spaces. The distribution of FITC-dextrans in the elastic lamina was similar to that of HRP. These results suggest that barrier disruption occurs with a wide range of molecular sizes of FITC-dextrans, although there seems to be some limitation to the permeation of the larger molecules. The present study suggests that the mechanism of barrier disruption of the major cerebral arteries in the acute stage following SAH may be vesicular rather than by separation of tight junctions.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Molecular and Cellular Probes 3 (1989), S. 263-271 
    ISSN: 0890-8508
    Keywords: Northern blot hybridization ; gene homology ; rotavirus ; transcription probe
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Molecular and Cellular Probes 3 (1989), S. 251-261 
    ISSN: 0890-8508
    Keywords: gene homology ; genogroup ; nucleic acid hybridization ; rotavirus ; transcription probe
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Molecular and Cellular Probes 5 (1991), S. 285-289 
    ISSN: 0890-8508
    Keywords: ELISA ; clinical specimens ; electropherotype ; human rotavirus ; polymerase chain reaction (PCR) ; serotype (G type)
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Molecular and Cellular Probes 7 (1993), S. 277-284 
    ISSN: 0890-8508
    Keywords: Rotavirus, PCR, diagnostics, G serotype, P serotype
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Fermentation and Bioengineering 72 (1991), S. 36-40 
    ISSN: 0922-338X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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