Abstract
The cellular response resulting from breakdown of the blood-brain barrier was evaluated 24 h after hyperosomotic infusion of mannitol into the internal carotid artery in the rat. Heat shock protein (HSP-70), a marker of cellular stress and/or injury, was induced in scattered patches of neurons and glia in regions of barrier breakdown. These findings suggest that osmotically induced breakdown of the blood-brain barrier may result in cell injury.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies, Monoclonal
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Blood Pressure / drug effects
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Blood-Brain Barrier / physiology*
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Gene Expression / physiology
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HSP70 Heat-Shock Proteins / genetics
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HSP70 Heat-Shock Proteins / metabolism*
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Immunoenzyme Techniques
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Immunoglobulin G / immunology
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Immunoglobulin G / metabolism*
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Mannitol / pharmacology
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Neuroglia / metabolism
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Neurons / metabolism
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Osmotic Pressure
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Rats
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Rats, Sprague-Dawley
Substances
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Antibodies, Monoclonal
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HSP70 Heat-Shock Proteins
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Immunoglobulin G
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Mannitol