Rewarming eliminates the protective effect of cooling against delayed neuronal death.
Mild intra-ischemic hypothermia provides neuroprotection against delayed neuronal death in the hippocampal CA1. It has recently been reported that reduction in the metabolic rate of arachidonic acid (AA) liberated during ischemia might contribute to this neuroprotection. To examine whether rewarming during the early period of recirculation accelerates AA consumption and eliminates the neuroprotection, we measured the levels of AA in the hippocampus after various recirculation times under normothermia and hypothermia with or without rewarming. The tendency for AA to disappear was significantly different between each pair of groups. Histological examination 7 days after ischemia revealed no protection in the rewarmed group. These results suggest that neuronal injury during rewarming after hypothermia may be attributed to the rate of AA metabolism.
Nakane
M
M
Department of Neurosurgery, Teikyo University School of Medicine, 11-1 Kaga 2-chome, Itabashi-ku, Tokyo 173-8605, Japan.
Kubota
M
M
Nakagomi
T
T
Tamura
A
A
Hisaki
H
H
Ueta
N
N
D000818:Animals; D001831:Body Temperature; D016923:Cell Death; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005849:Gerbillinae; D006358:Hot Temperature; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology*
D005230:Fatty Acids, Nonesterified