| Project/Area Number |
03670721
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Toyama Medical and Pharmaceutical University |
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Principal Investigator |
ITO Yusuke Medicine,Anaesthesiology, Professor, 医学部, 教授 (70018307)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Toru Medicine,Anaesthesiology, research associate, 医学部, 助手 (20173750)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1992: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1991: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | HYPOXIA / HEAT SHOCK PROTEIN / 熱ショック蛋白質 |
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| Research Abstract |
It is known that heat shock protein (HSP) is induced responding to various stresses not only a heat shock which is the origin of a name of this protein. One of inducible stresses is the ischemic condition. In this study we investigate the locality of HSP induction under the low oxygen condition using a hypoxic model of 5 % oxygen inhalation that we have used since before in this research and 2 min anoxia model suspending the ventilator. Additionally, we persuaded the fluctuation of HSP induction quantitatively by the method of immunoblotting technique. In the ischemic model of gerbil the HSP was induced strongly in our experiment as well as previously reported. On the other hand, the induction of HSP was slight in the rat hypoxic model and even in the rat ischemic model. Two reasons are conceivable to this result. There are some reports since before that rat is a comparatively strong animal species in the low oxygen condition. Therefore,HSP induction was small in hypoxic rat's brain. A
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nother reason is that our experiment model of low oxygen condition accompanies a decrease of the heart rate unlike a brain ischemic model. Therefore an influence is exerted on a whole body. The incomplete ischemic condition like this becomes a fatal blow for a digestive organ system particularly the small intestine. Acker et al reported that in the case of a decreased blood flow a blood flow circulates to a brain and a heart preferentially. Therefore,these organs were protected in the incomplete ischemia. When an extent of a hypoxic load is strong,the induction of HSP increased. It peaked in a day or two. The phenomenon of ischemic tolerance well known if it gets weak ischemia done before severe ischemia is suffered. We tried to apply the 2nd load in a day after a mild hypoxic event. Surely the HSP was induced, but the injury was accumulative rather than the acquisition of tolerance. Although congestion and bleeding were seen at the small intestine and the cecum,there was not a change especially in a nerve cell of the nerve terminals which distributes to intestines even in such a case. The acquisition of ischemic tolerance by the HSP may limit to a nerve cell only. Less
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