Browsing by Subject "Blood brain barrier"

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    Assessment of blood-retina1 barrier integrity
    (Murcia : F. Hernández, 1995) Vinores, S.A.
    The blood-retina1 barrier consists of two components which are comprised of the retinal vascular endothelium and the retinal pigment epithelium, respectively. Its functional integrity can be recognized by tight junctions between these cells with a paucity of endocytic vesicles within them and the presence of the molecules that regulate the ionic and metabolic gradients that constitute the barrier. The banier is compromised in severa1 disease processes and by a variety of agents, but in most cases the location and mechanism for barrier failure is not understood. Perfusion with a variety of radiolabeled tracer molecules, vitreous fluorophotometry, or magnetic resonance imaging can be used to quantitate blood-retina1 barrier leakage. Fluorescein angiography or magnetic resonance imaging can localize sites of leakage in vivo with limited resolution. Evans blue dye can be used to visualize blood-retina1 barrier failure in gross pathological specimens and immunohistochemical labeling of serum proteins such as albumin or fibrinogen can be used to localize sites of blood-retina1 barrier breakdown by light microscopy. Tracers such as horseradish peroxidase, microperoxidase, or lanthanum, or the immunocytochemical demonstration of albumin can be used to reveal bloodretinal barrier breakdown at the ultrastructural leve1 and provide insights into the mechanisms involved. This review discusses the advantages and lirnitations of each of these methods to aid in selection of the appropriate techniques to derive the desired information.
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    Cellular mechanisms of the blood-brain barrier (BBB) opening to albumin-gold complex
    (Murcia : F. Hernández, 1993) Vorbrodt, A.W.; Lossinsky, A.S.; Dobrogowska, D.H.; Wisniewski, H.M.
    Cold lesion injury applied to mouse brain and infusion of hyperosmolar L(+) arabinose solution into rat carotid artery were used as extravascular and intravascular insults, respectively, leading to blood-brain barrier (BBB) disruption. To study the cellular mechanisms of the BBB opening, heterologous (bovine) and homologous (mouse and rat) albumin-gold complexes were used as a macromolecular tracer. Both insults rapidly induce the leakage of the blood-borne tracer, although the mechanisms of their action appear to be different. Cold lesion injury (cryoinjury) leads to the opening of interendothelial junctions and concomitantly to an endothelial-platelet reaction. This insult is followed by irreversible changes such as desquamation, degeneration and necrosis of the endothelial lining, formation of thromboses, and disruption of the basement membrane. Osmotic opening occurs through at least the four mechanisms (presumably temporal and reversible) that follow: 1) opening of a part of the junctional complexes; 2) the formation of transendothelial openings (interendothelial gaps or penetrating, crater-like excavations); 3) the uncontrolled passage of tracer particles through the cytoplasm of the injured endothelial cells; and 4) segmental denudation of the endothelial lining. The basement membrane appears to represent one of the main obstacles in the passage of blood-borne albumin-gold complexes to the extracellular space in the brain parenchyma.
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    MgSO4 treatment preserves the ischemia-induced reduction in S-100 protein without modification of the expression of endothelial tight junction molecules
    (Murcia : F. Hernández, 2009) Goñi-de-Cerio, Felipe; Alvarez, Antonia; Alvarez, Francisco J.; Rey-Santano, Maria C.; Alonso-Alconada, Daniel; Mielgo, Victoria E.; Gastiasoro, Elena; Hilario, Enrique
    The aim of this work was to evaluate the effect of magnesium sulphate (MgSO4 ) administration on blood-brain barrier (BBB) permeabilization after cerebral hypoxia-ischemia (HI) induced by partial occlusion of the umbilical cord of premature fetal lambs. We also characterized BBB dysfunction in terms of the levels of expression of a panel of BBB proteins; Occludin, Claudin, Zona Occludens-1, Zonula Occludens-2, VE-cadherin and ß-catenin. Lambs were assigned to: Control group: non-injured animals, 0 h post-partial cord occlusion (0h-PCO) group: animals subjected to 60 min HI and sacrificed just after the insult, 3h-PCO group: HI injured animals resuscitated and managed on ventilation for 3 hours and MgSO4 group: animals which received a dose of 400 mg/kg MgSO4 after the HI event and managed on ventilation for 3 hours. Brains were fixed and blocks processed for S-100 protein immunohistochemistry. Other brains were dissociated and processed for S-100 and BBB protein immunochemistry for analysis by flow cytometry. The percentage of S-100 positive cells was found to be dramatically reduced in all studied brain tissues in the 3h-PCO group with respect to the other groups. No differences were found in the percentage or mean intensity of BBB protein immunolabeled cells among the groups. In the MgSO4 group, the percentage of S-100 positive cells 3 h after the HI event was similar to the control group. These results suggest that MgSO4 treatment preserves the ischemia-induced reduction in S- 100 protein without modification in the expression of endothelial tight junction molecules. We speculate that MgSO4 treatment confers neuroprotection by restoration of blood brain permeability in hypoxia-ischemia.
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    The histopathology of Candida albicans invasion in neonatal rat tissues and in the human blood-brain barrier in culture revealed by light, scanning, transmission and immunoelectron microscopy scanning
    (Murcia : F. Hernández, 2006) Lossinsky, A.S.; Jong, A.; Fiala, M.; Mukhtar, M.; Buttle, K.F.; Ingram, M.
    The present studies examined the effects of Candida albicans yeast and hyphal morphologies on tissue pathologies and transmigration properties of the fungus in two experimental models: 1) an in vivo, neonatal rat model, and 2) a cell culture model of human brain microvascular endothelial cells (ECs) (BMVEC). We inoculated a hyphae-producing strain (CAI4-URA3) and a non-hyphae-producing strain (CAI4) of C. albicans into 4-10 day old rats and BMVEC cultures. Animals were inoculated by intraperitonal (i.p.), intranasal (i.n.), oral (p.o.) and intracerebral (i.c.) routes and several tissues were examined after 24-48 hrs. Rats inoculated i.p. with the hyphae-producing strain showed pathology in the kidneys, liver, spleen, and other tissues associated with inoculation tracks of the nose, and muscle and connective tissues of the abdominal wall. Few animals inoculated i.p., however, presented evidence of meningitis. The non-hyphae phase yeast produced neither tissue pathology nor meningitis. Animals inoculated i.c. with the hyphae strain after 1 and 3 hrs expressed minimal meningitis, with an increasing neutrophillic meningitis between 4 and 18 hrs after inoculation. At 18 hrs after i.c. inoculation, however, the inflammatory foci and brain pathology were extensive and demonstrated mycelia within the lateral ventricles associated with necrosis of adjacent brain tissue. Neutrophillic meningitis at this time period was pronounced. BMVEC co-cultured 1-2 hrs with both C. albicans strains showed EC phagocytosis of hyphae and blastospores into intercellular adhesion molecule-1 (ICAM-1)-labeled caveolae suggesting a transcellular role for ICAM-1 in the internalization process of C. albicans.