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Cited by 32Traumatic Brain Injury and Neurovascular DisturbancesMigraine and Headache StudiesTraumatic Brain Injury Research

Study of regional cerebral blood flow in experimental head injury: changes following cerebral contusion and during spreading depression

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OZAWA, Yoshinori, NAKAMURA, Takao, SUNAMI, Kenro, KUBOTA, Motoo, ITO, Chiaki, MURAI, Hisayuki, YAMAURA, Akira, MAKINO, Hiroyasu·1991·Neurologia medico-chirurgica
DOI 10.2176/nmc.31.685
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Abstract

Changes in regional cerebral blood flow (rCBF) following fluid-percussion brain injury (cerebral contusion) were studied in rats using the autoradiographic method. The direct current potential was monitored to identify spreading depression (SD). The rCBF was measured during SD and 2, 4, and 24 hours after injury. rCBF was almost nil in the contused area and decreased considerably in the cortices of the injured side for 4 hours after insult, then recovered by 24 hours. Focal relative rCBF increase occurred in the parietal cortex during SD, and was probably hyperperfusion due to SD. However, the rCBF did not increase over the sham-operated control. The injury probably caused hypoperfusion within 4 hours of insult and abolished the vascular response to SD.

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  • In rodent models the primary insult usually results in spreading depolarization, but spontaneous spreading depolarizations are fewer with a shorter duration or do not occur.

    “In rodent models the primary insult usually results in spreading depolarization, but spontaneous spreading depolarizations are fewer with a shorter duration or do not occur (Sunami et al., 1989;Ozawa et al., 1991;Nilsson et al., 1993;Williams et al., 2005;von Baumgarten et al., 2008).”

    From Evolution of neuronal and astroglial disruption in the peri-contusional cortex of mice revealed by in vivo two-photon imaging (2013) · cites this paper as Ozawa et al., 1991

    Materials and Methods reports spreading-depression-associated DC-potential shifts in 13 of 27 injured rats within two hours of percussion; Results says the frequency of subsequent shifts varied, with some rats having only a few. This supports occurrence after injury and variable recurrence, but not that the primary insult usually causes spreading depolarization or that spontaneous episodes have a shorter duration. Page numbers are not available in our copy. (LLM, conf=0.84)

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Authors
OZAWA, Y., NAKAMURA, T., SUNAMI, K., KUBOTA, M., ITO, C., MURAI, H., YAMAURA, A., & MAKINO, H.
Affiliations
Chiba University (JP)
ORCID
MAKINO, Hiroyasu
Venue
Neurologia medico-chirurgica
Publisher
Japan Neurosurgical Society
Published
1991
Volume
31
Issue
11
Pages
685-690
ISSN
  • 0470-8105 (ISSN-L)
  • 1349-8029
DOI
10.2176/nmc.31.685
OpenAlex
W2018806448
Semantic Scholar
6a6e484a6def3924bbec840878ee195ef5513075
Cited by
32
References
27
Citations by year
2026: 1 · 2023: 1 · 2022: 2 · 2018: 1 · 2016: 2 · 2014: 1 · 2013: 2 · 2012: 1
FWCI
1.15
Type
journal article
Language
en
Open access
Locations
  • Neurologia medico-chirurgica (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Psychiatry and Mental health › Migraine and Headache Studies
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
Keywords
regional cerebral blood flow, fluid percussion injury, cerebral contusion, cortical spreading depression, traumatic brain injury, cortical hypoperfusion, hyperperfusion, parietal cortex, vascular response, autoradiography
MeSH terms
Animals, Blood Flow Velocity, Brain Concussion, Cerebrovascular Circulation, Craniocerebral Trauma, Male, Parietal Lobe, Rats, Inbred Strains, Cortical Spreading Depression, Time Factors, Rats

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