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Hypothermia attenuates delayed cortical cell death and ROS generation following CO inhalation.

Authors
  • Uemura, Koichi
  • Hoshino, Sumihisa
  • Uchida, Koji
  • Tsuruta, Ryosuke
  • Maekawa, Tsuyoshi
  • Yoshida, Ken-ichi
Type
Published Article
Journal
Toxicology Letters
Publisher
Elsevier
Publication Date
Nov 30, 2003
Volume
145
Issue
2
Pages
101–106
Identifiers
PMID: 14581162
Source
Medline
License
Unknown

Abstract

Carbon monoxide (CO) is the most popular cause of poisoning. The bilateral basal ganglia lesion characterizes the delayed neuronal cell death (DCD). We demonstrated there were both apoptosis and necrosis in the cortex, basal ganglia and hippocampus in a case of human CO accident. To elucidate the mechanism of DCD after CO inhalation, histological studies on the rat brain were conducted. Rats were ventilated with nitrous oxide (sham group), 10% O(2) (hypoxia group) or 1005 ppm CO (CO group) for 90 min, while the pericranial temperature was controlled at either 32, 37, or 39 degrees C during CO inhalation. After reoxygenation for 30 min, the rats were allowed to recover for 48 h. The ratio of eosinophilic and HNE-positive neurons in the cortex were higher in the CO group than in the hypoxia group at 37 degrees C, while the PaO(2) was much lower in the hypoxia than in the CO group. The damage was alleviated in the hypothermia (32 degrees C) as compared with normothermia, while the hyperthermia (39 degrees C) did not significantly increased it. CO inhalation injures neuron by reactive oxygen species (ROS), independent of hypoxia, as can be concluded from the histological comparison of DCD with HNE immunoreactivity.

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