2011 Fiscal Year Final Research Report
The roles of sex hormone and gender difference for spinal cord protection in spinal cord ischemia
| Project/Area Number |
21591970
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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 岐阜大学, 医学系研究科, 教授 (30159561)
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| Co-Investigator(Kenkyū-buntansha) |
IIDA Mami 岐阜大学, 医学系研究科, 非常勤講師 (80350859)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 性ホルモン / エストロジェン / リモートプレコンディショニング |
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| Research Abstract |
We evaluated the tissue oxygen partial pressure of spinal cord(PsptO2) following aortic cross-clamping and-unclamping, and then clarified the mechanism of improvement in the PsptO2 following spinal ischemia observed with remote ischemic preconditioning(RIPC) or intravenous estrogen in rabbits. In isoflurane anesthetized rabbits(n=36), we prepared for measurement of PsptO2 following aortic cross-clamping using tissue PO2 monitoring. In the first set of experiment, we allocated 18 animals into 3 groups,(a) control group ; n=6,(b) RIPC group ; n=6,(c) glibenclamide pretreatment(0. 3mg/kg) group ; n=6. In the second set of experiment, we also allocated 18 animals into 3 groups,(d) control group ; n=6,(e) estrogen(17ss estradiol : 20μg) group ; n=6,(f) fulvestrant pretreatment(1mg/kg) group ; n=6. RIPC improved deterioration of the values in PsptO2 at 20 min after aortic cross-clamping and 0, 2, 5 min after aortic unclamp. The improvement was diminished by pretreatment of glibenclamide. Administration of 17s estradiol improved deterioration of the values in PsptO2 at 20 min after aortic cross-clamping and 0, 2, 5 min after aortic unclamp. The improvement was diminished by pretreatment of fulvestrant.
In conclusion, after aortic cross-clamping, the RIPC performed improves the deterioration in PsptO2 through the KATP channel activation and 17ss estradiol improves the deterioration in PsptO2 through the estrogen receptor activation.
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