2001 Fiscal Year Final Research Report Summary
Apoptosis after subarachnoid hemorrhage and its prevention
| Project/Area Number |
11470294
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
YAMADA Kazuyo Nagoya City University, Medical School, Professor, 医学部, 教授 (90150341)
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| Co-Investigator(Kenkyū-buntansha) |
IWATA Akira Nagoya City University, Medical School, Professor, 医学部, 助手 (90275131)
AIHARA Noritaka Nagoya City University, Medical School, Research Associate, 医学部, 助手 (00264739)
MASE Mitsuhito Nagoya City University, Medical School, Assistant Professor, 医学部, 講師 (60238920)
SHIMADA Shoichi Nagoya City University, Medical School, Professor, 医学部, 教授 (20216063)
加藤 泰治 名古屋市立大学, 医学部, 教授 (60094364)
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| Project Period (FY) |
1999 – 2000
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| Keywords | apoptosis / subarachnoid hemorrhage / apoptosis / immediate early gene / stress gene / neuron / transporter / intracranial pressure |
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| Research Abstract |
Subarachnoid hemorrhage (SAH) cause various type of neurologic deficits. Some of those are caused by cerebrovascular spasm, but others are caused by impact of SAH. The present project was designed to study the impact to the brain. Rat model of SAH was developed in our laboratory and used for in situ hybridization. We identified that apoptosis promoting bax and ice genes ware expressed in the CA1 of hippocampus within 24 hours after SAH. The bcl-2, apoptosis suppressing gene, was also expressed in those areas, but the ratio of bax/bcls tended to increase. Immediate early gene, c-fos and c-jun are expressed in the CA1 area of hippocampus. When monitoring intracranial pressure, SAH induced steep increase of ICP and perfusion pressure was low for 5- 15 minutes. Therefore, transient ischemia occurred in the brain and most vulnerable CA1 area was affected. TUNEL staining showed positive cells at CA1 area 2 days post ictus. Osmolyte channel transporter was also increased its mRNA expression at CA1. These data clearly demonstrate stress of SAH may induce neurological dysfunction and may relate neurological sequelae caused by SAH.
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[Publications] Yamada K, Nakatsuka M, Masago A, Taki H.: "Apoptosis-related genes are expressed in the rat model of subarachnoid hemorrhage in Ito U, Fieschi C, Orzi F, Kuroiwa T, Klatzo I (Eds)"Maturation Phenomenon in Cerebral Ischemia III, Springer, Berlin, Heidelberg. 65-68 (1999)
Description
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