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  • 1
    Electronic Resource
    Electronic Resource
    Role of extracellular proteins in the dynamics of vasogenic brain edema (1985)
    Springer
    Acta neuropathologica 66 (1985), S. 3-11 
    Details
    ISSN: 1432-0533
    Keywords: Blood-brain barrier ; Serum proteins ; Water content ; Vasogenic brain edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship between extravasation of protein into extracellular spaces of brain parenchyma and the water content of such regions were evaluated in an experimental model. In this model, a temporary opening of the blood-brain barrier (BBB) to proteins was produced without significant injury to the cellular elements of brain tissue. Rabbits were subjected to bolus injection of their own blood under 360–400 mm Hg pressure via the internal carotid artery. The opening of the barrier and its duration were evaluated with Evans blue (EB), horseradish peroxidase (HRP), and sodium fluorescein (NaFl) tracers. The water content of brain tissue was assessed by specific gravity (SG) measurements in 1-mm-diameter tissue samples. Quantitative evaluation of protein penetration into brain tissue was carried out using125I bovine serum albumin (BSA). The opening of the BBB to proteins persisted up to 9 h, whereas the barrier remained permeable to small molecular NaFl for 24 h. The SG measurements indicated in the areas of EB extravasation a progressive increment in water content up to 9 h, i.e., the duration of BBB opening to proteins. Following this, there was a progressive clearance of edema in spite of the BBB remaining open for NaFl for 24 h. Quantitative evaluations of125I-BSA and SG in the same tissue samples, supported by statistical analysis, indicated approximately linear relationship between albumin and water, implying a strong correlation between the development of vasogenic edema and extravasation of proteins into extracellular spaces.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00698288
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  • 2
    Electronic Resource
    Electronic Resource
    Cerebral blood flow autoregulation in experimental subarachnoid haemorrhage in rat (1992)
    Springer
    Acta neurochirurgica 119 (1992), S. 128-133 
    Details
    ISSN: 0942-0940
    Keywords: Experimental subarachnoid haemorrhage ; cerebral autoregulation ; cerebral blood flow ; cerebral vasospasm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Haemodynamic instability is of great importance in clinical management of patients with subarachnoid haemorrhage (SAH). The significance of angiographically demonstrable vasospasm for disturbances of cerebral blood flow (CBF) and cerebral autoregulation has not yet been clarified. The present study was designed to describe disturbances of cerebral autoregulation during the timecourse of experimental SAH (eSAH) in rats. A second aim of the study was to relate the results to a reported timecourse of angiographic vasospasm in the same animal model. Previous studies have shown that the timecourse of angiographically visible vasospasm in eSAH is biphasic with maximal spasm at 10 min and 2 days after induction of eSAH. At 5 days, the vasospasms have resolved. CBF was measured using a133-Xenon intracarotid injection method which allowed serial measurements of mean hemispheric CBF during controlled manipulations of arterial blood pressure. In this way, an autoregulation curve could be constructed. The present study shows that autoregulation is severely disturbed or even totally absent at 2 and 5 days after eSAH. Thus there seems to be no direct correlation between presence of angiographic vasospasm and impairment of autoregulation, or that the impairment of autoregulation is more protracted than the presence of cerebral vasospasm, presuming a correlation exist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01541796
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  • 3
    Electronic Resource
    Electronic Resource
    Shunting Effects in Patients with Idiopathic Normal Pressure Hydrocephalus; Correlation with Cerebral and Leptomeningeal Biopsy Findings (1999)
    Springer
    Acta neurochirurgica 141 (1999), S. 633-639 
    Details
    ISSN: 0942-0940
    Keywords: Keywords: Brain biopsy; cerebrospinal fluid pressure; normal pressure hydrocephalus; meninges; resistance to CSF outflow.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary  Normal Pressure Hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space have been suggested as one of the patho-anatomical substrates. However, other types of adult onset dementia, predominantly Alzheimer's disease and Vascular Dementia, may mimic the clinical NPH characteristics.  The purpose of the present study was to correlate cerebral parenchymal and leptomeningeal biopsy findings to the clinical outcome after CSF shunting in a prospective group of idiopathic NPH (INPH) patients. The study comprises 27 patients with INPH, diagnosed and shunted according to generally accepted clinical, imaging and hydrodynamic criteria. In all patients a frontal leptomeningeal and brain biopsy was obtained prior to the shunt insertion.  Degenerative cerebral changes, most often Alzheimer (6 cases) or vascular changes (7 cases) were described in 14 out of 27 biopsies. Arachnoid fibrosis was found in 9 of the 18 biopsies containing arachnoid tissue. Overall, nine patients (33%) improved, of whom 6 presented Alzheimer or vascular changes in their biopsies. No correlation was found between clinical outcome and the presence or absence of degenerative cerebral changes and/or arachnoid fibrosis. However, a tendency towards higher improvement rates was noted in the subgroups presenting degenerative cerebral changes or arachnoid fibrosis. The results suggest that no constant morphological element exists in the syndrome of INPH. Various aetiologies may be involved in the pathogenesis and possibly in some cases co-existing: Patients may also improve by shunting despite the presence of degenerative cerebral parenchymal changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007010050353
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  • 4
    Electronic Resource
    Electronic Resource
    The effect of nimodipine on autoregulation of cerebral blood flow after subarachnoid haemorrhage in rat (1995)
    Springer
    Acta neurochirurgica 132 (1995), S. 98-103 
    Details
    ISSN: 0942-0940
    Keywords: Autoregulation ; cerebral blood flow ; nimodipine ; subarachnoid haemorrhage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Disturbance of the autoregulation of the cerebral blood flow (CBF) is frequently seen following subarachnoid haemorrhage (SAH) and is possibly partly caused by cerebral ischaemia. It is well-known, that the calcium channel blocker nimodipine reduces the incidence of cerebral infarction and ischaemic dysfunction after SAH. The aim of the present study was to investigate the effect of nimodipine on autoregulation of CBF in an experimental model of SAH. The autoregulation was investigated in 10 control rats with SAH and in 10 nimodipine treated rats with SAH by serial measurements of CBF using a133Xenon intracarotid injection method during controlled blood pressure manipulations. In the control rats the autoregulation was severely disturbed, no plateau was found where CBF was independent of changes in the arterial blood pressure (MABP). In rats treated with intravenous nimodipine (0.03 mg/kg bodyweight/h), CBF was 33.0% higher and MABP 5.3% higher compared with the controls. CBF was found constant in the MABP interval between 60 and 100 mmHg which indicates, that nimodipine improves the autoregulation of CBF after SAH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01404855
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  • 5
    Electronic Resource
    Electronic Resource
    Cation permeability of the blood-brain barrier in streptozotocin-diabetic rats (1987)
    Springer
    Diabetologia 30 (1987), S. 409-413 
    Details
    ISSN: 1432-0428
    Keywords: Experimental streptozotocin-diabetes ; blood-brain barrier permeability ; cations ; arterial integral uptake technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Decreased sodium permeability across the blood-brain barrier occurs in streptozotocin-treated rats after 2 weeks of diabetes. To establish whether this is a phenomenon specific for cations, the blood-brain barrier permeability for sodium, potassium and calcium was studied with an arterial integral uptake technique. Experiments were performed in control rats and, after two weeks after diabetes induction, in untreated streptozotocin-diabetic rats and in insulin-treated streptozotocin rats. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 35% (5.2±1.7 vs 3.4±1.1 10−5cm3·s−1·g−1) and potassium permeability by 39% (19.8±5.7 vs 12.1±3.9 10−5·cm3·s−1· g−1), whereas no differences in calcium permeability occurred. Insulin treatment was associated with an increase in the blood-brain barrier permeability to sodium (4.8±1.0 10−5·cm3·s−1·g−1) as compared to untreated diabetes (3.4±1.1 10−5·cm3·s−1·g−1). It is concluded that the observed changes in sodium and potassium permeability cannot be caused by electrostatic membrane changes. More specific abnormalities of the transport of sodium and potassium across the blood-brain barrier are likely to occur; disturbances in the sodium-potassium-pump activity could account for such alterations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00292543
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