1994 Fiscal Year Final Research Report Summary
CONTRIBUTION OF STRESS PROTEIN ON THE RECOVERY PROCESS FROM DAMAGE OF COMPLETE GLOBAL BRAIN ISCHEMIA.
| Project/Area Number |
05454413
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
IWATSUKI Naofumi Tohoku University, Dental Hospital, Professor, 歯学部・附属病院, 教授 (50004908)
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| Co-Investigator(Kenkyū-buntansha) |
ASANO Mitsuya Tohoku University, University Hospital, Assistant, 医学部・附属病院, 助手 (30250757)
TAKAHASHI Masahiko Tohoku University, University Hospital, Assistant, 医学部・附属病院, 助手 (60236320)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Ischemia / Brain / Kidney / Apoptosis / Genetic deficit mice / Fas / Fas ligand / Neutrophil |
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| Research Abstract |
1. Model of complete brain ischemia on a guinea pig : AL shape wire (a long part 10 mm, a short part =20 nun) with 2 mm diameter was inserted into mediastinum at the right wedge of sternum and it's short part was slipped in behind ascending aorta with blind manner, then the aorta was occluded by hanging up the L shape wire and pushing down the sternum to the back. This maneuver was proofed to produce 0 blood pressure, no cerebral biQod flow, flat EEG and ischemic changes in brain under the histological examination.
2. Stress protein (HSP) and apoptosis by ischemic insult : (1) Apoptosis in ischemic kidney : Temporal occlusion of the renal artery induced apoptosis (measured by TUNEL method) with the occluded time dependent manner in a mice kidney. The ischemia induced apoptosis was less on the mice with genetic deficit of Fas or Fas ligand, suggesting the important role of the Fas-Fas ligand system for this induction. (2) Apoptosis in ischemic brain : The temporal occlusion model of mid cerebra] artery in mice was used in this study. An ischemic time depending apoptosis was induced on mainly border of infarction produced by mid cerebral artery occlusion, suggesting the contribution of apoptosis to development of infarct size. The appearance of apoptosis was less on the mice with genetic deficit of Fas or Fas ligand than the normal mice, suggesting the interaction of the Fas-Fas ligand system for the apoptosis induction. Some neutrophil appeared on border of infarction showed apoptotic changes, but these changes were not differ between the normal and genetic deficit mice. The role of neutophilic apoptosis is the subject of the further investigation. (3) HSP and ischemic brain : On mid cerebral artery occlusion model measurement of HSPs have been carried out.
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