Free radicals as triggers of brain edema formation after stroke

Jihoe Heo, Won Han Sang, Koo Lee Seung

Research output: Contribution to journalReview article

201 Citations (Scopus)

Abstract

Brain edema is a leading cause of death after stroke. Cytotoxic edema, which is most severe in astrocytes, begins within a few minutes of adenosine triphosphate depletion and reflects the ultimate infarct size. Vasogenic edema is caused by uncontrolled fluid leakage from the blood to the brain parenchyma through a weakened blood-brain barrier (BBB) and contributes to an actual net volume increase of the brain, which often leads to death. Recent research on ischemia-induced injury mechanisms of the microvasculature has led to the disclosure of the mechanisms and cellular pathways leading to BBB breakdown. In addition, the introduction of magnetic resonance imaging to clinical practice has enabled the evaluation of edema severity in stroke patients and differentiation between cytotoxic and vasogenic edema. Free radicals exert their deleterious actions during both cytotoxic and vasogenic edema. They can contribute to BBB disruption directly and can also trigger molecular pathways related to the dysfunction of ion transporters in the cell membrane and those related to increased vascular permeability. The development of effective therapeutic strategies aimed at reducing brain edema based on targeting specific molecular pathways involved may reduce death and disability from stroke.

Original languageEnglish
Pages (from-to)51-70
Number of pages20
JournalFree Radical Biology and Medicine
Volume39
Issue number1
DOIs
Publication statusPublished - 2005 Jul 1

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Brain Edema
Free Radicals
Edema
Brain
Stroke
Blood-Brain Barrier
Leakage (fluid)
Magnetic resonance
Cell membranes
Disclosure
Capillary Permeability
Microvessels
Blood
Adenosine Triphosphate
Astrocytes
Ions
Cause of Death
Imaging techniques
Ischemia
Fluids

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology (medical)

Cite this

Heo, Jihoe ; Sang, Won Han ; Seung, Koo Lee. / Free radicals as triggers of brain edema formation after stroke. In: Free Radical Biology and Medicine. 2005 ; Vol. 39, No. 1. pp. 51-70.
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Free radicals as triggers of brain edema formation after stroke. / Heo, Jihoe; Sang, Won Han; Seung, Koo Lee.

In: Free Radical Biology and Medicine, Vol. 39, No. 1, 01.07.2005, p. 51-70.

Research output: Contribution to journalReview article

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AU - Heo, Jihoe

AU - Sang, Won Han

AU - Seung, Koo Lee

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N2 - Brain edema is a leading cause of death after stroke. Cytotoxic edema, which is most severe in astrocytes, begins within a few minutes of adenosine triphosphate depletion and reflects the ultimate infarct size. Vasogenic edema is caused by uncontrolled fluid leakage from the blood to the brain parenchyma through a weakened blood-brain barrier (BBB) and contributes to an actual net volume increase of the brain, which often leads to death. Recent research on ischemia-induced injury mechanisms of the microvasculature has led to the disclosure of the mechanisms and cellular pathways leading to BBB breakdown. In addition, the introduction of magnetic resonance imaging to clinical practice has enabled the evaluation of edema severity in stroke patients and differentiation between cytotoxic and vasogenic edema. Free radicals exert their deleterious actions during both cytotoxic and vasogenic edema. They can contribute to BBB disruption directly and can also trigger molecular pathways related to the dysfunction of ion transporters in the cell membrane and those related to increased vascular permeability. The development of effective therapeutic strategies aimed at reducing brain edema based on targeting specific molecular pathways involved may reduce death and disability from stroke.

AB - Brain edema is a leading cause of death after stroke. Cytotoxic edema, which is most severe in astrocytes, begins within a few minutes of adenosine triphosphate depletion and reflects the ultimate infarct size. Vasogenic edema is caused by uncontrolled fluid leakage from the blood to the brain parenchyma through a weakened blood-brain barrier (BBB) and contributes to an actual net volume increase of the brain, which often leads to death. Recent research on ischemia-induced injury mechanisms of the microvasculature has led to the disclosure of the mechanisms and cellular pathways leading to BBB breakdown. In addition, the introduction of magnetic resonance imaging to clinical practice has enabled the evaluation of edema severity in stroke patients and differentiation between cytotoxic and vasogenic edema. Free radicals exert their deleterious actions during both cytotoxic and vasogenic edema. They can contribute to BBB disruption directly and can also trigger molecular pathways related to the dysfunction of ion transporters in the cell membrane and those related to increased vascular permeability. The development of effective therapeutic strategies aimed at reducing brain edema based on targeting specific molecular pathways involved may reduce death and disability from stroke.

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