Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia

Wise Young, Z. Harry Rappaport, David J. Chalif, Eugene S. Flamm

Research output: Contribution to journalArticle

127 Citations (Scopus)

Abstract

Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and fron toparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H<inf>2</inf>O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2,4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H<inf>2</inf>O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p <0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 μxmoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia. To explain the dominance of Na gain over K loss, we reject the hypothesis of a selective increase of blood—brain barrier Na permeability and propose instead that glial buffering of K ions released by Ischemic neurons reduced the driving force for K clearance during the first 2-4 hours after MCAo.

Original languageEnglish (US)
Pages (from-to)751-759
Number of pages9
JournalStroke
Volume18
Issue number4
StatePublished - 1987
Externally publishedYes

Fingerprint

Middle Cerebral Artery Infarction
Potassium
Ischemia
Sodium
Ions
Water
Brain
Basal Ganglia
Brain Ischemia
Neuroglia
Permeability
Edema
Spectrum Analysis
Reference Values
Neurons
Weights and Measures

Keywords

  • Atomic absorption spectroscopy
  • Edema infarct
  • Ionic diffusion
  • Middle cerebral artery
  • Potassium
  • Sodium

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialized Nursing
  • Neuroscience(all)

Cite this

Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia. / Young, Wise; Rappaport, Z. Harry; Chalif, David J.; Flamm, Eugene S.

In: Stroke, Vol. 18, No. 4, 1987, p. 751-759.

Research output: Contribution to journalArticle

Young, Wise ; Rappaport, Z. Harry ; Chalif, David J. ; Flamm, Eugene S. / Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia. In: Stroke. 1987 ; Vol. 18, No. 4. pp. 751-759.
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abstract = "Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and fron toparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H2O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2,4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H2O concentrations increased to 34 and 7{\%} greater than normal by 2 hours, and 89 and 94{\%} by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37{\%} greater than normal by 2 hours, and 281 and 330{\%} by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34{\%} of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p <0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 μxmoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia. To explain the dominance of Na gain over K loss, we reject the hypothesis of a selective increase of blood—brain barrier Na permeability and propose instead that glial buffering of K ions released by Ischemic neurons reduced the driving force for K clearance during the first 2-4 hours after MCAo.",
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N2 - Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and fron toparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H2O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2,4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H2O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p <0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 μxmoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia. To explain the dominance of Na gain over K loss, we reject the hypothesis of a selective increase of blood—brain barrier Na permeability and propose instead that glial buffering of K ions released by Ischemic neurons reduced the driving force for K clearance during the first 2-4 hours after MCAo.

AB - Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and fron toparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H2O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2,4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H2O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p <0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 μxmoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia. To explain the dominance of Na gain over K loss, we reject the hypothesis of a selective increase of blood—brain barrier Na permeability and propose instead that glial buffering of K ions released by Ischemic neurons reduced the driving force for K clearance during the first 2-4 hours after MCAo.

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KW - Edema infarct

KW - Ionic diffusion

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KW - Potassium

KW - Sodium

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