Postischemic hyperthermia increases expression of hsp72 mRNA after brief ischemia in the gerbil.
Brain temperature during ischemia critically determines insult severity, and temperature changes during recirculation may also affect subsequent injury. We have examined the impact of postischemic temperature on induction of the 70 kDa stress protein, hsp72, after brief ischemia in the gerbil. Animals were subjected to 2 min ischemia after which they were maintained under continuous halothane anesthesia during 3 h recirculation, and were either kept normothermic or subjected to hyperthermia comparable to that which occurs spontaneously in gerbils released from anesthesia immediately after the occlusion. Quantitative in situ hybridization showed striking dependence of hsp72 induction on postischemic hyperthermia. This result establishes that delayed temperature-sensitive signals mediate this injury-associated transcriptional response, and demonstrates that postischemic temperature must be carefully monitored in studies of gene expression and induced tolerance employing brief ischemic insults.
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Stroke Branch, National Institute of Neurological Disorders and Stroke National Institute of Health, Bethesda, MD, USA.
Nowak
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D000818:Animals; D001923:Brain Chemistry / Q000502:physiology; D005260:Female; D005334:Fever / Q000503:physiopathology*; D015870:Gene Expression / Q000502:physiology; D005849:Gerbillinae; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000235:genetics*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D012333:RNA, Messenger / Q000032:analysis; D013997:Time Factors
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D012333:RNA, Messenger