論文

査読有り
2017年9月

Venous or arterial blood components trigger more brain swelling, tissue death after acute subdural hematoma compared to elderly atrophic brain with subdural effusion (SDE) model rats

BRAIN RESEARCH
  • Daisuke Wajima
  • ,
  • Fumiya Sato
  • ,
  • Kenya Kawamura
  • ,
  • Keisuke Sugiura
  • ,
  • Ichiro Nakagawa
  • ,
  • Yasushi Motoyama
  • ,
  • Young-Soo Park
  • ,
  • Hiroyuki Nakase

1670
開始ページ
165
終了ページ
172
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.brainres.2017.06.017
出版者・発行元
ELSEVIER SCIENCE BV

Acute subdural hematoma (ASDH) is a frequent complication of severe head injury, whose secondary ischemic lesions are often responsible for the severity of the disease. We focused on the differences of secondary ischemic lesions caused by the components, 0.4 ml venous- or arterial-blood, or saline, infused in the subdural space, evaluating the differences in vivo model, using rats. The saline infused rats are made for elderly atrophic brain with subdural effusion (SDE) model.
Our data showed that subdural blood, both venous- and arterial-blood, aggravate brain edema and lesion development more than SDE. This study is the first study, in which different fluids in rats' subdural space, ASDH or SDE are compared with the extension of early "and delayed brain damage by measuring brain edema and histological lesion volume.
Blood constituents started to affect the degree of ischemia underneath the subdural hemorrhage, leading to more pronounced breakdown of the blood-brain barrier and brain damage. This indicates that further strategies to treat blood-dependent effects more efficiently are in view for patients with ASDH. (C) 2017 Elsevier B.V. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.brainres.2017.06.017
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28645494
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000407666000018&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.brainres.2017.06.017
  • ISSN : 0006-8993
  • eISSN : 1872-6240
  • PubMed ID : 28645494
  • Web of Science ID : WOS:000407666000018

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