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  • 1
    Electronic Resource
    Electronic Resource
    The blood-brain barrier to horseradish peroxidase at the onset of bicuculline-induced seizures in hypothalamus, pallidum, hippocampus, and other selected regions of the rabbit (1986)
    Springer
    Acta neuropathologica 69 (1986), S. 1-16 
    Details
    ISSN: 1432-0533
    Keywords: Blood-brain barrier ; Epileptic seizures ; Pinocytosis ; Hypothalamus ; Pallidum ; Hippocampus ; Septum ; Thalamus ; Periaque-ductal gray ; Cerebellar cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rabbits were subjected to bicuculline-induced generalized seizures of 15-min duration to elucidate the mechanism by which the macromolecule horseradish peroxidase (HRP) traverses the blood-brain barrier (BBB) in specific brain areas. Transendothelial pinocytosis at the level of arterioles was the main route of passage. In addition, in thalamus and hippocampus pinocytotic vesicles were observed in capillaries. In thalamus, hypothalamus and septum vesicles in the endothelium of venules were also present. Repeatedly, pinocytotic vesicles were ejecting their content into the interendothelial clefts, so that the presence of HRP reaction product between adjacent tight junctions cannot be considered a conclusive evidence for their opening. The HRP, which had reached the neuropil due to the seizure-evoked BBB opening, accumulated in the interstitial spaces and penetrated the synaptic cleft. Uptake of the tracer in vesicular form into presynaptic boutons, presumably excitatory ones as diagnosed by their ultrastructural features, was observed in all brain regions. The uptake was rare in septum, periaqueductal gray, hypothalamus, and cerebellar cortex; frequent in pallidum, hippocampus, and medulla oblongata; and very intense in thalamus. Uptake in postsynaptic dendrites was present mostly in the vicinity of boutons. Incorporation into glial processes was rare and confined to perivascular astrocytes. It is suggested, that HRP traverses the BBB by regionally selective, transmitter-controlled pinocytotic transport and that the neuronal uptake of the foreign protein is at least partially dependent on the involvement of synapses of particular brain regions in the paroxysmal activity during the generalized seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687032
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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Microvascular disturbances and edema formation after repetitive ischemia of gerbil brain (1988)
    Springer
    Acta neuropathologica 75 (1988), S. 288-294 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Brain edema ; Cerebral microcirculation ; Hypoperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three transient episodes of 5 min ischemia spaced at 1-h intervals were produced in Mongolian gerbils by bilateral carotid artery occlusion with an implanted vascular occlusion device. The interval of 1 h was chosen to allow for the development of postischemic hypoperfusion between the ischemic episodes. Three minutes and 1 h after each ischemic episode, and 6 and 24 h after the third occlusion, Evan's blue (EB) was injected intravenously to trace circulating blood, and the number of perfused capillaries was determined in various brain regions by fluorescence microscopy. Brain edema was evaluated by measuring specific gravity in tissue samples taken from adjacent areas. Repetitive ischemia caused progressively increasing brain edema and a progressive reduction of the number of perfused capillaries. Immediately after each ischemic episode, transient recruitment of capillaries occurred, thus excluding noreflow as a main pathogenetic factor of microcirculatory disturbances. The pattern of microcirculation 6 and 24 h after the last occlusion revealed a redistribution of circulating blood, characterized by a reduction in the number of EB-filled capillaries associated with a noticeable dilatation of the larger vascular channels. Our studies suggest a close interrelationship between post-ischemic microcirculatory hypoperfusion and the development of brain edema, the degree and extent of which progresses with the repetition of ischemic episodes when they are carried out during the periods of hypoperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690537
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  • 4
    Electronic Resource
    Electronic Resource
    The biphasic opening of the blood-brain barrier to proteins following temporary middle cerebral artery occlusion (1985)
    Springer
    Acta neuropathologica 68 (1985), S. 122-129 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Blood-brain-barrier ; Cerebral blood flow ; Reactive hyperemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The behavior of the blood-brain barrier (BBB) was studied in cats following release after 1-h middle cerebral artery (MCA) occlusion. The regional cerebral blood flow (rCBF) was determined by hydrogen clearance method in the caudate nucleus and the cerebral cortex. The BBB was assayed with Evans blue (EB) tracer and by immunohistochemical peroxidaseantiperoxidase (PAP) method. Following release of MCA occlusion, there were two openings of the BBB, separated by a refractory period. The first opening, occurred shortly after recirculation; this was associated with rCBF below 15 ml/100 g/min during the ischemic period and a pronounced reactive hyperemia promptly following release of MCA occlusion. A refractory period of the BBB was indicated by the absence of EB leakage in cats injected with the tracer 30 min before killing at 3 h after recirculation, although the rCBF values in these animals were even lower (6±1 ml/100 g/min) during occlusion, and all of them showed a pronounced hyperemia after recirculation. The occurrence of the previous BBB opening in these animals was confirmed by the PAP staining. The second opening of the BBB was observed at 5 and 72 h after recirculation in cats which were injected with EB 30 min before killing, and which showed rCBF below 15 ml/100 g/min during occlusion, followed by a pronounced reactive hyperemia. No EB extravasations were observed at any time in cats in which the rCBF during occlusion was above 15 ml/100 g/min and which failed to show a marked reactive hyperemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688633
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  • 5
    Electronic Resource
    Electronic Resource
    Ultrastructural observations on the transvascular route of protein removal in vasogenic brain edema (1985)
    Springer
    Acta neuropathologica 66 (1985), S. 265-273 
    Details
    ISSN: 1432-0533
    Keywords: Cold-lesion injury ; Brain edema ; Blood-brain barrier ; Alkaline phosphatase ; Anionic sites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Micro-blood vessels (MBVs), located in the area of edema, were studied in cat brain at various time intervals (1 h, 24 h, 7 days) after cold-lesion injury. Both cold-injured and adjacent gyri were examined for blood-brain barrier (BBB) permeability to i. v. injected horseradish peroxidase (HRP) with circulation times of 40 min and 24 h. Evans blue (EB) was used as a tracer for gross evaluation of the extension of brain edema. Localization of alkaline phosphatase (AP) and binding of cationized ferritin (CF), considered as a marker of anionic sites, were also studied ultrastructurally. Twenty-four hours after cold injury, the extravasated edema fluid, outlined by EB tracer, was observed to be spreading through the white matter (WM) into the adjacent gyrus. At this time, numerous, larger than capillary MBVs, presumably arterioles and venules located in the edematous WM, showed accumulations of HRP injected at the time of the operation, in the basement membrane, in abluminal pits, and in numerous pinocytotic vesicles and vacuoles of endothelial cells (ECs). The animals killed after 24 h with 40 min HRP circulation showed extravasation of HRP tracer in a zone underlying the necrotic cold injury lesion. On the other hand, there was no evidence of an abnormal HRP leakage in the further removed areas of edema in the WM, particularly in the adjacent gyrus. These observations suggest that a reverse, vesicular transport of HRP across the ECs of some MBVs represents one of several possible mechanisms responsible for the removal of extravasated proteins and of edematous fluid from brain extracellular space. This reverse transport is accompanied by a disruption of the surface anionic layer and changed polarity of ECs manifested by the relocation of AP activity from luminal to abluminal plasmalemma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690958
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