title: Effect of mild hypothermia on energy state recovery following transient forebrain ischemia in the gerbil.
abstract: A transient (lasting for 15 min) bilateral carotid artery occlusion model was created by using male Mongolian gerbils ( n=20, weight 50-60 g). The animals were divided into a group with mild hypothermia (34 degrees C, n=10) and a normothermic group (37 degrees C, n=10). High-energy phosphate metabolism (ATP, PCr, Pi) and intracellular pH were sequentially measured using (31)P-MRS during ischemia and after reperfusion for 1 week. The same animals were also subjected to a histopathological evaluation. During ischemia, there were no statistically significant differences between the two groups in the quantities of the metabolites. However, after reperfusion the rate of metabolic recovery by the mildly hypothermic (MH) group was significantly higher (by 10-20%) than the normothermic (NT) group. The intracellular pH decreased about 0.4 in both groups after ischemia; and after reperfusion the intracellular pH of the MH group returned to baseline levels faster than in the NT group. One week after ischemia, energy metabolism gradually decreased about 10-20% in both groups. In the histopathological evaluation, pyramidal cell damage in the hippocampus was 33% on average in the MH group and 79% in the NT group. The neuronal damage to the cerebral cortex was 26% in the MH group and 61% in the NT group. Astrocyte reactivity in the hippocampus and cerebral cortex was 2.9% and 1.1% in the MH group and 9.7% and 5.2% in the NT group. The results of this experiment indicate that the protective effect of mild hypothermia is due to the high recovery rate of ATP and PCr and the prevention of a secondary decline in high phosphate energy.
authors.affiliation: Department of Neurosurgery, Ashikawa Medical College, Ashikawa, Japan. tekimura-nsu@umin.ac.jp
authors.forename: Teruo
authors.initials: T
authors.lastname: Kimura
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Sako
authors.forename: Kunio
authors.initials: K
authors.lastname: Tanaka
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Kusakabe
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Tanaka
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nakada
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives*; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001831:Body Temperature / Q000502:physiology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000378:metabolism* / Q000503:physiopathology; D004734:Energy Metabolism / Q000502:physiology*; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D016548:Prosencephalon / Q000378:metabolism* / Q000503:physiopathology; D020127:Recovery of Function / Q000502:physiology*; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate; D000983:Antipyrine; C008135:iodoantipyrine