Project/Area Number |
15591642
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | Oita University (2004) 大分医科大学 (2003) |
Principal Investigator |
KITANO Takaaki Oita Univ., Univ.Hospital, Operating Unit(Anesthesiology), Associate Professor, 医学部, 助教授 (20211196)
|
Co-Investigator(Kenkyū-buntansha) |
NISIMARU Naoko Oita Univ., Faculty of Medicine Physiology, Associate Professor, 医学部, 助教授 (60101086)
|
Project Period (FY) |
2003 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
Keywords | ^<31>P-NMR / CO_2 acidosis / Brain Slice / intracellular pH / 呼吸性アシドーシス / 燐核磁気共鳴法 / 乳酸 |
Research Abstract |
We examined the effect of acidosis induced by increase of CO_2 tension in artificial cerebrospinal fluid(ACSF) on energy metabolism in both of intact and acidic pre-conditioned rat brain ex vivo. The levels of high-energy phosphates and pHi in the intact and acidic preconditioned brain slices were measured using ^<31>P NMR at 25℃. When CO_2 content in bubbling gas of ACSF was increased from 5% to 40%, pH_i decreased from 7.25±0.02(mean±SD,n=14) to 6.55±0.02(n=6) in intact brain slices. The level of phosphocreatine(PCr) was maintained at pH_i between 7.4 and 6.9, but decreased rapidly at pH_i less than 6.8. Following decrease in pH_i from 7.25 to 6.55, PCr levels decreased 51±0.04%(n=23). In acidic preconditioned brain slices, the decrease of PCr level followed by decrease in pH_i was similar as that in intact slices, but at pH_i between 6.6 and 6.4 decrease of PCr level in acidic preconditioned slices was distinctly smaller than that in intact slices(71±0.04 %,n=11). These results indicate that the pretreatment of the brain with acidosis induces a tolerance in energy metabolism of the brain to subsequent periods of acidosis.
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