Dynamic changes in cortical NADH fluorescence and direct current potential in rat focal ischemia: Relationship between propagation of recurrent depolarization and growth of the ischemic core

T. Higuchi, Yoshimasa Takeda, M. Hashimoto, O. Nagano, M. Hirakawa

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50% neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in 23 ± 29% neuronal injury due to the short depolarization time, whereas the sites showing recurrent depolarizations and eventually persistent depolarization resulted in infarction. The NADH fluorescence images showed that recurrent depolarizations propagated along the margin of the ischemic core. In 85.9% of the recurrent depolarizations, the fluorescence disappeared without leaving any traces and did not affect the area of the ischemic core. However, in 47.5% of the animals, 14.1% of recurrent depolarizations merged with the ischemic core and increased the area by 6 ± 4 mm 2. These findings suggest that recurrent depolarization increases the severity of neuronal injury but does not cause infarction by itself if persistent depolarization does not follow, and that the area of persistent depolarization is enlarged with 14.1% of recurrent depolarizations.

Original languageEnglish
Pages (from-to)71-79
Number of pages9
JournalJournal of Cerebral Blood Flow and Metabolism
Volume22
Issue number1
Publication statusPublished - 2002

Fingerprint

NAD
Ischemia
Fluorescence
Infarction
Wounds and Injuries
Growth
Parietal Lobe
Common Carotid Artery
Temporal Lobe
Ultraviolet Rays

Keywords

  • Brain ischemia
  • DC potential
  • Focal cerebral ischemia
  • Ischemic depolarization
  • NADH
  • Spreading depression

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Dynamic changes in cortical NADH fluorescence and direct current potential in rat focal ischemia: Relationship between propagation of recurrent depolarization and growth of the ischemic core",
abstract = "Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50{\%} neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in 23 ± 29{\%} neuronal injury due to the short depolarization time, whereas the sites showing recurrent depolarizations and eventually persistent depolarization resulted in infarction. The NADH fluorescence images showed that recurrent depolarizations propagated along the margin of the ischemic core. In 85.9{\%} of the recurrent depolarizations, the fluorescence disappeared without leaving any traces and did not affect the area of the ischemic core. However, in 47.5{\%} of the animals, 14.1{\%} of recurrent depolarizations merged with the ischemic core and increased the area by 6 ± 4 mm 2. These findings suggest that recurrent depolarization increases the severity of neuronal injury but does not cause infarction by itself if persistent depolarization does not follow, and that the area of persistent depolarization is enlarged with 14.1{\%} of recurrent depolarizations.",
keywords = "Brain ischemia, DC potential, Focal cerebral ischemia, Ischemic depolarization, NADH, Spreading depression",
author = "T. Higuchi and Yoshimasa Takeda and M. Hashimoto and O. Nagano and M. Hirakawa",
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T1 - Dynamic changes in cortical NADH fluorescence and direct current potential in rat focal ischemia

T2 - Relationship between propagation of recurrent depolarization and growth of the ischemic core

AU - Higuchi, T.

AU - Takeda, Yoshimasa

AU - Hashimoto, M.

AU - Nagano, O.

AU - Hirakawa, M.

PY - 2002

Y1 - 2002

N2 - Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50% neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in 23 ± 29% neuronal injury due to the short depolarization time, whereas the sites showing recurrent depolarizations and eventually persistent depolarization resulted in infarction. The NADH fluorescence images showed that recurrent depolarizations propagated along the margin of the ischemic core. In 85.9% of the recurrent depolarizations, the fluorescence disappeared without leaving any traces and did not affect the area of the ischemic core. However, in 47.5% of the animals, 14.1% of recurrent depolarizations merged with the ischemic core and increased the area by 6 ± 4 mm 2. These findings suggest that recurrent depolarization increases the severity of neuronal injury but does not cause infarction by itself if persistent depolarization does not follow, and that the area of persistent depolarization is enlarged with 14.1% of recurrent depolarizations.

AB - Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50% neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in 23 ± 29% neuronal injury due to the short depolarization time, whereas the sites showing recurrent depolarizations and eventually persistent depolarization resulted in infarction. The NADH fluorescence images showed that recurrent depolarizations propagated along the margin of the ischemic core. In 85.9% of the recurrent depolarizations, the fluorescence disappeared without leaving any traces and did not affect the area of the ischemic core. However, in 47.5% of the animals, 14.1% of recurrent depolarizations merged with the ischemic core and increased the area by 6 ± 4 mm 2. These findings suggest that recurrent depolarization increases the severity of neuronal injury but does not cause infarction by itself if persistent depolarization does not follow, and that the area of persistent depolarization is enlarged with 14.1% of recurrent depolarizations.

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KW - Spreading depression

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