MISC

1999年6月

Effects of nitric oxide synthase inhibition on the cerebral circulation and brain damage during kainic acid-induced seizures in newborn rabbits

BRAIN & DEVELOPMENT
  • Y Takei
  • ,
  • S Takashima
  • ,
  • J Ohyu
  • ,
  • T Takami
  • ,
  • T Miyajima
  • ,
  • A Hoshika

21
4
開始ページ
253
終了ページ
259
記述言語
英語
掲載種別
DOI
10.1016/S0387-7604(99)00019-4
出版者・発行元
ELSEVIER SCIENCE BV

The nitric oxide (NO) synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), was used to investigate the effect of endogenous NO on the cerebral circulation and brain damage during kainic acid (KA)-induced seizures in newborn rabbits. The cerebral blood flow (CBF), by laser doppler flowmetry, cerebral oxygenation (concentrations of oxy-(HbO(2)), deoxy-(HbR) and total hemoglobin (tHb) in brain tissue), by near-infrared spectroscopy (NIRS), mean arterial blood pressure (MABP), electroencephalography (EEG), and hippocampal neuronal damage were evaluated. Pretreatment with L-NAME caused significant decreases in CBF, HbO(2), and tHb, and a significant increase in HbR during KA-induced seizures, compared with pretreatment with saline (P < 0.05), without a significant difference in MABP. Our study also demonstrated that pretreatment with L-NAME reduced the seizure activity and neuronal cell death in the hippocampus elicited by the systemic administration of KA in the neonatal brain. These results suggest that NO is of major importance in the neurodestructive process in spite of its roles in maintaining both the CBF and cerebral oxygenation during KA-induced seizures in the neonatal brain. (C) 1999 Elsevier Science B.V. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/S0387-7604(99)00019-4
CiNii Articles
http://ci.nii.ac.jp/naid/10007332799
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000080858900006&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/S0387-7604(99)00019-4
  • ISSN : 0387-7604
  • CiNii Articles ID : 10007332799
  • Web of Science ID : WOS:000080858900006

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