title: Blood-brain barrier water permeability and brain osmolyte content during edema development.
abstract: OBJECTIVE
  To determine mechanisms that limit changes in brain water content during acute edema development.
  
  
  METHODS
  A controlled, laboratory investigation of the physiologic and biochemical correlates of osmotic edema was performed in rats. Hypoosmotic hyponatremia was induced by intraperitoneal injection of distilled water. Serum osmolality and electrolytes and regional blood-brain barrier water permeability. Surface area (P.S) product, osmolyte contents, and capillary size were determined during 120 minutes of hypoosmotic brain edema development. Cerebral water content predicted from these data using a mathematical model of brain water movements was compared with measured changes in brain water content.
  
  
  RESULTS
  Fifteen minutes after distilled water injection, mean +/- SEM blood serum osmolality and sodium concentration decreased from 291 +/- 3 mOsm and 131 +/- 13 mmol/L to 267 +/- 3 mOsm and 102 +/- 9 mmol/L, respectively. Specific gravity of cerebral gray matter, cerebral white matter, and basal ganglia decreased throughout the hypoosmotic exposure period and, for gray and white matter, correlated with blood serum osmolality and sodium plus potassium content. Glutamate, but not glutamine, glycine, or taurine, decreased 120 minutes after water injection. The regional water P.S product decreased by 40% to 60% within 60 minutes of the water injection, while capillary diameters in gray and white matter were unchanged. Brain water movements calculated from the mathematical model correctly predicted actual brain water content only if the hydraulic conductivity of the blood-brain barrier was allowed to vary in proportion to the measured P.S product and the measured loss of brain osmolytes was incorporated into the formulation.
  
  
  CONCLUSIONS
  During the first hours of hypoosmotic hyponatremia, changes in brain volume are limited by increased resistance to osmotic flux of water into the brain and reduction in the brain content of inorganic and, to a smaller degree, organic osmolytes.
authors.affiliation: Wright State University, School of Medicine, Department of Emergency Medicine, Cox Institute, Kettering, OH 45429, USA. jolson@nova.wright.edu
authors.forename: J E
authors.initials: JE
authors.lastname: Olson
authors.forename: M
authors.initials: M
authors.lastname: Banks
authors.forename: R V
authors.initials: RV
authors.lastname: Dimlich
authors.forename: J
authors.initials: J
authors.lastname: Evers
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000502:physiology*; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000737:chemistry / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D007010:Hyponatremia / Q000139:chemically induced / Q000150:complications* / Q000503:physiopathology; D008297:Male; D009994:Osmolar Concentration; D011188:Potassium / Q000032:analysis; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000032:analysis; D013997:Time Factors; D014867:Water / Q000378:metabolism*
chemical_list: D014867:Water; D012964:Sodium; D011188:Potassium