| Project/Area Number |
23791683
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | University of Tsukuba |
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Principal Investigator |
NAKAYAMA Shin 筑波大学, 医学医療系, 講師 (60596443)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 心肺蘇生 / 硫化水素 / 低体温 |
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| Research Abstract |
Hydrogen sulfide donor, sodium hydrogen sulfide (NaHS), can induce hypothermia and hypometabolic state, which might attenuate ischemia reperfusion injury. The protective mechanism of sulfide remains unclear. In order to exclude the hypothermic effect of sulfide, this study was designed to test whether NaHS treatment in mice after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR), followed by maintaining forced normothermia improved outcomes. Adult male mice were subjected to 8 min of CA. Mice were treated with either NaHS (3mg/kg) IP or vehicle at 30 min after CPR, then kept their head temperature above 35.0 degree Celsius using a heating pad for 6 hr. One, 4 and 12 days after CA/CPR, brains were removed for histological evaluation of neurons in the CA1 hippocampal region and the striatum. CA induced spontaneous hypothermic response, which was enhanced by NaHS. Even when the head temperature was kept constant, NaHS exerted neuroprotective effect in the striatum after CPR.
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