The blood-brain barrier to horseradish peroxidase under normal and experimental conditions

1977 ◽  
Vol 39 (3) ◽  
pp. 181-187 ◽  
Author(s):  
Erik Westergaard
Keyword(s):  
Horseradish Peroxidase ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Experimental Conditions ◽  
Blood Brain

Effect of atrial natriuretic factor on blood–brain barrier permeability

1989 ◽  
Vol 67 (6) ◽  
pp. 637-640 ◽  
Author(s):  
Sukriti Nag ◽  
Stephen C. Pang
Keyword(s):  
Horseradish Peroxidase ◽  
Blood Brain Barrier ◽  
Atrial Natriuretic Factor ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Natriuretic Factor ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Atrial Natriuretic

Recent studies have demonstrated receptors for atrial natriuretic factor on endothelium of intracerebral vessels. The physiological role of these receptors is not known. The present study was undertaken to determine whether atrial natriuretic factor has an effect on blood–brain barrier permeability to protein and ions using horseradish peroxidase and lanthanum as markers of permeability alterations. This study does not demonstrate a significant effect of atrial natriuretic factor on blood–brain barrier permeability mechanisms in steady states.Key words: blood–brain barrier, atrial natriuretic factor, horseradish peroxidase, lanthanum, ultrastructure.

O2 radicals in arachidonate-induced increased blood-brain barrier permeability to proteins

1986 ◽  
Vol 251 (4) ◽  
pp. H693-H699 ◽  
Author(s):  
E. P. Wei ◽  
M. D. Ellison ◽  
H. A. Kontos ◽  
J. T. Povlishock
Keyword(s):  
Horseradish Peroxidase ◽  
Blood Brain Barrier ◽  
Topical Application ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Cranial Window ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Pial Arterioles

We studied the effect of topical application of arachidonate on the brain surface on blood-brain barrier permeability to either 125I-labeled human albumin or to horseradish peroxidase administered intravenously. Arachidonate was applied under a cranial window, and the concentration of albumin was measured in brain after elimination of the blood by perfusion-fixation. Permeability to 125I-labeled albumin was increased in the superficial 4 mm of the cortex but not in the deeper cortical layer 4-6 mm from the surface. This increased permeability to albumin was prevented by simultaneous topical application of superoxide dismutase (60 U/ml) and catalase (40 U/ml). Alterations in vascular permeability to horseradish peroxidase were evaluated in semiquantitative fashion, and they behaved similarly. Extravasated horseradish peroxidase was found in the wall of penetrating arterioles, and to a lesser extent in the wall of intraparenchymal vessels and capillaries, but not in the wall of pial arterioles or veins, although these latter vessels displayed focal endothelial lesions. We conclude that arachidonate increases the blood-brain barrier permeability to proteins. This increase in permeability is mediated by O2 radicals. The increased permeability occurs primarily in penetrating arterioles and not in pial arterioles or veins.

scholarly journals Pharmacological Modification of Blood-Brain Barrier Permeability Following a Cold Lesion

1984 ◽  
Vol 11 (4) ◽  
pp. 447-451 ◽  
Author(s):  
Jennifer J. Raymond ◽  
David M. Robertson ◽  
Henry B. Dinsdale ◽  
Sukriti Nag
Keyword(s):  
Horseradish Peroxidase ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Cold Lesion ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Contralateral Cortex ◽  
Bbb Permeability ◽  
Pharmacological Modification

ABSTRACTThe effect of desipramine, imidazole, thioridazine and trifluoperazine on blood-brain barrier(BBB) permeability after a 24 hour cold lesion was studied in rats. Changes in BBB permeability were determined using a quantitative horseradish peroxidase (HRP) assay. The four drugs tested did not alter the quantity of HRP in the cortex of control animals, or in the contralateral cortex of test animals. However, imidazole, desipramine and trifluoperazine significantly reduced the HRP extravasation in and around the cold lesion. Several mechanisms for this effect are suggested; one possible mechanism common to all these drugs is the reduction of increased vesicular transport in cortical vessels adjacent to the cold lesions.

scholarly journals Blood–Brain Barrier Disruption in White Matter Lesions in a Rat Model of Chronic Cerebral Hypoperfusion

2002 ◽  
Vol 22 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Masaki Ueno ◽  
Hidekazu Tomimoto ◽  
Ichiro Akiguchi ◽  
Hideaki Wakita ◽  
Haruhiko Sakamoto
Keyword(s):  
Endothelial Cells ◽  
White Matter ◽  
Horseradish Peroxidase ◽  
Corpus Callosum ◽  
Blood Brain Barrier ◽  
White Matter Lesions ◽  
Brain Barrier ◽  
Cerebral Hypoperfusion ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Blood–brain barrier damage has been implicated in the pathogenesis of cerebrovascular white matter lesions. This type of lesion is responsible for cognitive impairment in the elderly and can be induced by permanent ligation of the bilateral common carotid arteries in the rat. Because it is unclear whether the blood–brain barrier is impaired, we examined whether vascular permeability to horseradish peroxidase is altered using this model. According to light microscopic results, the reaction product of horseradish peroxidase was most intensely localized to the paramedian part of the corpus callosum in the brain, occurring to a small degree at 3 hours, day 1, markedly on day 3, but reduced on days 7 and 14. By electron microscopic study of the same area, the reaction product of horseradish peroxidase was localized to the plasmalemmal vesicles in the endothelial cells 3 hours after ligation, but appeared in the cytoplasm on days 1 and 3, suggesting a diffuse leakage of horseradish peroxidase. In addition, the reaction product was dispersed into the cytoplasm of glial cells in the perivascular regions on day 3. The luminal surface of the endothelial cell cytoplasm appeared irregular on day 7, suggesting a conformational change of the endothelial cells. Collagen fibrils proliferated in the thickened basal lamina and mitochondria degenerated in the pericyte on days 7 and 14. Perivascular glial endfeet were swollen throughout the survival period. In sham-operated rats, the reaction product of horseradish peroxidase was not observed at any time interval, except in vesicular structures. These findings indicate that chronic cerebral hypoperfusion induces blood–brain barrier damage with subsequent morphologic changes of the vascular structures in the corpus callosum. An extravasation of macromolecules, such as proteases and immunoglobulins, may contribute to the pathogenesis of white matter lesions.

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