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  • 1
    ISSN: 1432-0533
    Schlagwort(e): Prostaglandin F2-alpha ; Immunohistochemistry ; Transient increase ; Hippocampus ; Purkinje cell
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The changes in prostaglandin F2-alpha (PG F2α) staining over 3 days of recirculation in both fore-and hindbrains were studied. Five minutes of global ischemia was produced in 24 rats by Pulsinelli's method with hypotension around 50 mm Hg of mean arterial blood pressure. Eight rats (including three pretreated with indomethacin) were recirculated for 5 min, three for 1 h, five for 2 h and five for 3 days. Five normal rats without occlusion of vessels served as controls. The brains were snap frozen. Ten-micrometer cryosections were stained for PG F2α by the indirect immunofluorescence method after fixation in carbodiimide and in Zamboni's solution. Positive staining for PG F2α was noted in pial vessels in all normal and ischemic rats. Recirculated rats revealed the strongest reaction at 5 min after recirculation in blood vessels and in neuronal cytoplasm (especially in hippocampi and in Purkinje cells). The intensity of staining was markedly reduced after 1 h. Rats pretreated with indomethacin showed less increase in staining. The above results indicate that recirculation after ischemia produces a transient increase in PG F2α in blood vessels and neurons of both fore- and hindbrains.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0533
    Schlagwort(e): Subarachnoid hemorrhage ; Prostaglandin F2-alpha ; Hippocampus ; Purkinje cell ; Intracranial hypertension
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 0942-0940
    Schlagwort(e): Cerebral vasospasm ; subarachnoid haemorrhage ; vascular permeability
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    ISSN: 0942-0940
    Schlagwort(e): Subarachnoid haemorrhage ; cerebral vasospasm ; vascular permeability ; FITC-dextran
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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