Regional differences in the rate of energy impairment after threshold level ischemia for induction of cerebral infarction in gerbils |
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Authors: | T Kuroiwa Guenter Mies Dirk Hermann Yoji Hakamata Shuji Hanyu Umeo Ito |
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Institution: | (1) Department of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8510, Japan e-mail: kuroiwa@e-mail.ne.jp, Tel./Fax: +81-3-58035848, JP;(2) Max-Planck-Institute for Neurological Research, Cologne, Germany, DE;(3) Laboratory of Experimental Medicine, Jichi Medical School, Tochigi, Japan, JP;(4) Department of Neurology, Jichi Medical School, Tochigi, Japan, JP;(5) Department of Neurosurgery, Musashino Red Cross Hospital, Tokyo, Japan, JP |
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Abstract: | The development of infarction and/or selective neuronal death in the brain after transient cerebral ischemia depends on the
severity of the ischemic episode. After transient cerebral ischemia of the threshold level for the induction of infarction,
both changes evolve slowly in various postischemic regions. We examined the relationship of disturbances of energy metabolism
to infarction and selective neuronal death in various regions of the postischemic brain subjected to two 10-min occlusions
of the unilateral common carotid artery. Our results indicated that in various cerebral regions that developed infarction,
the tissue ATP content, in parallel with the succinic dehydrogenase activity, fell to their lowest levels at different times
over a 4-day period after circulation had been restored (earliest to latest: dorsolateral thalamus > dorsolateral caudate
> chiasmal level cortex > hippocampal CA3 sector > hippocampal CA1 sector). In the cortex at the infundibular level, disseminated
selective neuronal death developed over a 7-day period following restoration of circulation; it was accompanied by only a
slight alteration in energy metabolism. The present results indicate that regional differences existed in the rate of energy
impairment and evolving infarction in the postischemic gerbil brain. Energy impairment, in association with mitochondrial
enzymatic dysfunction, seems to be indispensable for the delayed manifestation of cerebral infarction but not for disseminated
selective neuronal death.
Received: 1 December 1999 / Revised, accepted: 6 March 2000 |
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Keywords: | Cerebral ischemia Energy failure Cerebral infarction Selective neuronal death ATP |
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