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Effects of leukocytes on brain metabolism in granulocytic brain edema
Author(s) -
Fishman Robert A.,
Sligar Kurt,
Hake Randall B.
Publication year - 1977
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410020202
Subject(s) - edema , metabolism , phosphocreatine , intracellular , endocrinology , pathology , medicine , biochemistry , pharmacology , chemistry , energy metabolism
An in vitro model has been used to study the effects of granulocytic leukocytes (WBC) on brain metabolism to elucidate the mechanism of the encephalopathy and cerebral edema of purulent meningitis and brain abscess. Single first rat cortical brain slices were incubated in normal medium or medium containing a membrane fraction of WBC prepared from rat peritoneal exudate cells induced by intraperitoneal glycogen. Membrane fraction caused “cytotoxic” brain edema with increased brain water, cellular swelling (decreased inulin space), increased intracellular sodium, and loss of intracellular potassium. The brain also showed increased glucose oxidation and lactate production associated with energy depletion demonstrated by decreases in phosphocreatine, adenosine triphosphate, and energy charge potential. The low glucose and high lactate of purulent cerebrospinal fluid reflect these changes in brain metabolism. The model of granulocytic brain edema was not affected by dexamethasone. The factors in WBC responsible for these changes were membrane bound, absent from the cytosol, and heat labile. The concentrations used are compatible with concentrations in pathological exudates. Toxic factors in pus alter the integrity of brain cell membranes and thus contribute to the encephalopathy and brain edema associated with purulent meningitis and brain abscess.