'Ischemic tolerance' phenomenon found in the brain

Kazuo Kitagawa, Masayasu Matsumoto, Masafumi Tagaya, Ryuji Hata, Hirokazu Ueda, Michio Niinobe, Nobuo Handa, Ryuzo Fukunaga, Kazufumi Kimura, Katsuhiko Mikoshiba, Takenobu Kamada

Research output: Contribution to journalArticle

1000 Citations (Scopus)

Abstract

We investigated the possibility that neuronal cells given a mild ischemic treatment sufficient to perturb the cellular metabolism acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo. Cerebral ischemia was produced in the gerbils by occlusion of both common carotids for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. Minor 2-min ischemia in this model depletes high-energy phosphate compounds and perturbs the protein synthesis, but nerver causes neuronal necrosis, and therefore was chosen as mild ischemic treatment. Single 2-min ischemia 1 day or 2 days before 5 min ischemia exhibited only partial protective effects against delayed neuronal death. However, two 2-min ischemic treatments at 1 day intervals 2 days before 5 min ischemia exhibited drastically complete protection against neuronal death. The duration and intervals of ischemic treatment, enough to perturb cellular metabolism and cause protein syhthesis, were needed respectively, because neither 1-min ischemia nor 2-min ischemia received twice at short intervals exhibited protective effects. This 'ischemic tolerance' phenomenon induced by ischemic stress - which is unquestionably important - and frequent stress in clinical medicine, is intriguing and may open a new approach to investigate the pathophysiology of ischemic neuronal damage.

Original languageEnglish
Pages (from-to)21-24
Number of pages4
JournalBrain Research
Volume528
Issue number1
DOIs
Publication statusPublished - 24-09-1990

Fingerprint

Ischemia
Brain
Gerbillinae
Clinical Medicine
Brain Ischemia
Hippocampus
Proteins
Necrosis
Phosphates

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Kitagawa, K., Matsumoto, M., Tagaya, M., Hata, R., Ueda, H., Niinobe, M., ... Kamada, T. (1990). 'Ischemic tolerance' phenomenon found in the brain. Brain Research, 528(1), 21-24. https://doi.org/10.1016/0006-8993(90)90189-I
Kitagawa, Kazuo ; Matsumoto, Masayasu ; Tagaya, Masafumi ; Hata, Ryuji ; Ueda, Hirokazu ; Niinobe, Michio ; Handa, Nobuo ; Fukunaga, Ryuzo ; Kimura, Kazufumi ; Mikoshiba, Katsuhiko ; Kamada, Takenobu. / 'Ischemic tolerance' phenomenon found in the brain. In: Brain Research. 1990 ; Vol. 528, No. 1. pp. 21-24.
@article{8217cba0323f4612adebce22dfe007eb,
title = "'Ischemic tolerance' phenomenon found in the brain",
abstract = "We investigated the possibility that neuronal cells given a mild ischemic treatment sufficient to perturb the cellular metabolism acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo. Cerebral ischemia was produced in the gerbils by occlusion of both common carotids for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. Minor 2-min ischemia in this model depletes high-energy phosphate compounds and perturbs the protein synthesis, but nerver causes neuronal necrosis, and therefore was chosen as mild ischemic treatment. Single 2-min ischemia 1 day or 2 days before 5 min ischemia exhibited only partial protective effects against delayed neuronal death. However, two 2-min ischemic treatments at 1 day intervals 2 days before 5 min ischemia exhibited drastically complete protection against neuronal death. The duration and intervals of ischemic treatment, enough to perturb cellular metabolism and cause protein syhthesis, were needed respectively, because neither 1-min ischemia nor 2-min ischemia received twice at short intervals exhibited protective effects. This 'ischemic tolerance' phenomenon induced by ischemic stress - which is unquestionably important - and frequent stress in clinical medicine, is intriguing and may open a new approach to investigate the pathophysiology of ischemic neuronal damage.",
author = "Kazuo Kitagawa and Masayasu Matsumoto and Masafumi Tagaya and Ryuji Hata and Hirokazu Ueda and Michio Niinobe and Nobuo Handa and Ryuzo Fukunaga and Kazufumi Kimura and Katsuhiko Mikoshiba and Takenobu Kamada",
year = "1990",
month = "9",
day = "24",
doi = "10.1016/0006-8993(90)90189-I",
language = "English",
volume = "528",
pages = "21--24",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

Kitagawa, K, Matsumoto, M, Tagaya, M, Hata, R, Ueda, H, Niinobe, M, Handa, N, Fukunaga, R, Kimura, K, Mikoshiba, K & Kamada, T 1990, ''Ischemic tolerance' phenomenon found in the brain', Brain Research, vol. 528, no. 1, pp. 21-24. https://doi.org/10.1016/0006-8993(90)90189-I

'Ischemic tolerance' phenomenon found in the brain. / Kitagawa, Kazuo; Matsumoto, Masayasu; Tagaya, Masafumi; Hata, Ryuji; Ueda, Hirokazu; Niinobe, Michio; Handa, Nobuo; Fukunaga, Ryuzo; Kimura, Kazufumi; Mikoshiba, Katsuhiko; Kamada, Takenobu.

In: Brain Research, Vol. 528, No. 1, 24.09.1990, p. 21-24.

Research output: Contribution to journalArticle

TY - JOUR

T1 - 'Ischemic tolerance' phenomenon found in the brain

AU - Kitagawa, Kazuo

AU - Matsumoto, Masayasu

AU - Tagaya, Masafumi

AU - Hata, Ryuji

AU - Ueda, Hirokazu

AU - Niinobe, Michio

AU - Handa, Nobuo

AU - Fukunaga, Ryuzo

AU - Kimura, Kazufumi

AU - Mikoshiba, Katsuhiko

AU - Kamada, Takenobu

PY - 1990/9/24

Y1 - 1990/9/24

N2 - We investigated the possibility that neuronal cells given a mild ischemic treatment sufficient to perturb the cellular metabolism acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo. Cerebral ischemia was produced in the gerbils by occlusion of both common carotids for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. Minor 2-min ischemia in this model depletes high-energy phosphate compounds and perturbs the protein synthesis, but nerver causes neuronal necrosis, and therefore was chosen as mild ischemic treatment. Single 2-min ischemia 1 day or 2 days before 5 min ischemia exhibited only partial protective effects against delayed neuronal death. However, two 2-min ischemic treatments at 1 day intervals 2 days before 5 min ischemia exhibited drastically complete protection against neuronal death. The duration and intervals of ischemic treatment, enough to perturb cellular metabolism and cause protein syhthesis, were needed respectively, because neither 1-min ischemia nor 2-min ischemia received twice at short intervals exhibited protective effects. This 'ischemic tolerance' phenomenon induced by ischemic stress - which is unquestionably important - and frequent stress in clinical medicine, is intriguing and may open a new approach to investigate the pathophysiology of ischemic neuronal damage.

AB - We investigated the possibility that neuronal cells given a mild ischemic treatment sufficient to perturb the cellular metabolism acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo. Cerebral ischemia was produced in the gerbils by occlusion of both common carotids for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. Minor 2-min ischemia in this model depletes high-energy phosphate compounds and perturbs the protein synthesis, but nerver causes neuronal necrosis, and therefore was chosen as mild ischemic treatment. Single 2-min ischemia 1 day or 2 days before 5 min ischemia exhibited only partial protective effects against delayed neuronal death. However, two 2-min ischemic treatments at 1 day intervals 2 days before 5 min ischemia exhibited drastically complete protection against neuronal death. The duration and intervals of ischemic treatment, enough to perturb cellular metabolism and cause protein syhthesis, were needed respectively, because neither 1-min ischemia nor 2-min ischemia received twice at short intervals exhibited protective effects. This 'ischemic tolerance' phenomenon induced by ischemic stress - which is unquestionably important - and frequent stress in clinical medicine, is intriguing and may open a new approach to investigate the pathophysiology of ischemic neuronal damage.

UR - http://www.scopus.com/inward/record.url?scp=0025172696&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025172696&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(90)90189-I

DO - 10.1016/0006-8993(90)90189-I

M3 - Article

C2 - 2245337

AN - SCOPUS:0025172696

VL - 528

SP - 21

EP - 24

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -

Kitagawa K, Matsumoto M, Tagaya M, Hata R, Ueda H, Niinobe M et al. 'Ischemic tolerance' phenomenon found in the brain. Brain Research. 1990 Sep 24;528(1):21-24. https://doi.org/10.1016/0006-8993(90)90189-I