| Project/Area Number |
18591697
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Gifu University |
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Principal Investigator |
IIDA Hiroki Gifu University, Graduate School of Medicine, Associate Professor (30159561)
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| Co-Investigator(Kenkyū-buntansha) |
IIDA Mami Gifu University, Graduate School of Medicine, Part time lecture (80350859)
DOHI Shuji Gifu University, Graduate School of Medicine, Professor (40155627)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,550,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥450,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Aortic clamp and unclamp / Spinal ischemia / Remote preconditioning / Angiotensin II / Rho-kinase / Free radical / Spinal cord tissue oxygen pressure / Limb ischemia / プレコンディショニング / 脳血管 |
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| Research Abstract |
Pentobarbital anesthetized rabbits were prepared for measurement of cerebral pial vessel diameter in a cranial window preparation or spinal cord partial tissue oxygen pressure (PtO2). We investigated the experiments according to following protocols.
1) We studied the effect of aortic clamping and declamping as a remote preconditioning intervention on cerebral pial vessel diameter. Although infrarenal aortic cross-clamping did not affect pial vessel diameter, release of a 20-min aortic cross-clamp caused pial arterioles to dilate and then constrict. A significant constriction persisted for at least 60 min. To clarify the mechanism of remote preconditioning regarding humoral factor, we examined whether angiotensin II typel receptor blocker, Rho-kinase inhibitor, or free radical scavenger, would affect the respose observed after aortic cross-clamping and release on cerebral vessels. All three drugs significantly attenuated the constriction of pial arterioles. Thus angiotensin II, Rho-kinase, and free radical could be possible to be candidates for humoral factors related to remote conditioning on spinal protection.
2) We measured directly the tissue oxygen partial pressure of the spinal cord to assess the efficacy of remote preconditioning in preventing apinal cord ischemic injury in an experimental model. PtO2 were significantly lower in the preconditioning intervention group at 20 min after aortic cross-clamping and 0, 2 min after aortic unclamping. Remote preconditioning performed in fore and hind legs protected the decrease of PtO2 compared with control group. Thus, the effect on PtO2 by such intervention may relate to the mechanism of spinal protection induced by remote preconditioning by transient upper and lower limbs ischemia.
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