Intra-ischemic hypothermia attenuates intercellular adhesion molecule-1 (ICAM-1) and migration of neutrophil

J. Inamasu, S. Suga, S. Sato, T. Horiguchi, K. Akaji, K. Mayanagi, T. Kawase

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Adhesion of neutrophil to the endothelium and subsequent transmigration has been reported to contribute to progression of focal ischemia. Hypothermia has been known to attenuate ischemic insult through various mechanisms of action. The authors evaluated the effect of hypothermia on expression of intercellular adhesion molecule-1 (ICAM-1) protein and on transmigration of neutrophil with immunohistochemical method. Transient focal ischemia model in rats was employed, and animals received 2 h of either normothermic or hypothermic ischemia. To confirm the effectiveness of hypothermia on neuroprotection, cortical infarct area was compared between the two groups. Our results demonstrated that hypothermia reduced both the number of microvessels expressing ICAM-1 and that of neutrophils migrating into ischemic tissue. Comparison of cortical infarct area showed persistent protective effect. This study indicates that reduction of ICAM-1 expression and subsequent reduction of migrating neutrophil in hypothermia can contribute to attenuation of ischemic damage.

Original languageEnglish
Pages (from-to)105-111
Number of pages7
JournalNeurological Research
Volume23
Issue number1
DOIs
Publication statusPublished - 2001 Feb 10

Keywords

  • Focal ischemia
  • ICAM-1
  • Intra-ischemic hypothermia
  • Neutrophil

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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