| Project/Area Number |
61570342
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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 |
Gastroenterology
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| Research Institution | Okayama University |
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Principal Investigator |
UKIDA Minoru Okayama University Medical School, Lecturer, 医学部附属病院, 助手 (70151842)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1987: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1986: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | glutamine / ammonia / hepatic encephalopathy / heavy nitrogen / 重窒素 / 肝不全 / グルタミン / 分枝鎖アミノ酸 / 高アンモニア血症 / カルシウムイオン / 脳性脳症 / アンモニア代謝 / グルタミン酸 / GC / MS / 臓器相関 / グルタミン代謝 / グルタミン酸代謝 / ガスクロマトグラフィー質量分析 |
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| Research Abstract |
In hyperammonemic state, glutamine accumulates in the brain to high level without increase of glutamate. Using beagle dogs treated with portacaval anastomosis (PCA), we observed that infused ammonia decreased the concentration of glutamate in cerebrospinal fluid before PCA but significantly increased 4 weeks after PCA. These observation suggests that glutamine synthesis in PCA-dog brain after the load of ammonia is limited due to long standing hyperammonemia. To test this hypothesis, we measured ^<15>N enrichment of CSF glutamate and -amino N of glutamine after continuous intravenous infusion of ^<15>N-ammonium chloride (0.6 mmol/min of ^<15>N-ammonium chloride). Infusion was stopped when the animal fell into coma.
The results were; during the coma state, ^<15>N was incorporated into glutamine- -amino N at the ratio of 5.2 atom% excess compared with only 0.9 atom% excess into glutamate in normal dogs, in contrast, in PCA-dogs, those were 3.7 atom% into glutamine- -amino N and 2.0 atom% into glutamate. These data strongly suggest that some disturbance in the process of glutamine synthesis in astroglia.
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