| Project/Area Number |
61480191
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Iwate Medical University |
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Principal Investigator |
SATO Shunichi Iwate Medical University School of Medicine, Professor, 医学部, 教授 (10048275)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Akinobu Iwate Medical University School of Medicine, Instructor, 医学部, 助手 (50177424)
SUZUKI Kazuyuki Iwate Medical University School of Medicine, Assistant, 医学部, 講師 (00137499)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 1987: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1986: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | Hepatic encephalopathy / EcK fistula dogs / DMN acute hepatic failure / 脳CCK-SIR / 脳遊離アミノ酸 / 血液・髄液アンモニア / 脳CCK-8IR |
|---|
| Research Abstract |
Cholecystokinin-like immunoreactivity(CCK-LI) was measured in the brain of EcK fistula dogs and dogs with dimethylnitrosamine-induced (DMN) acute hepatic failure which were prepared as experimental models of hepatic encephalopathy (HE). The results showed a significant reduction of CCK-LI in all cortical regions of Eck fistula dogs, especially in parietal and occipital cortex in which the levels were approximatily 40% of control values. In dogs with acute hepatic failure, CCK-Li reduction was observed in the temporal and parietal cortex (65% and 47% of control values, respectively). These data were compared with the concentrations of typrosine and phenylalanine, precursors of false neurotransmitters suggested as causing HE. Phenylalanine was significantly increased in all areas of cortex of EcK fistula dogs and in occipital cortex of dogs with acute hepatic failure. Tyrosine was also significantly increased in frontal, parietal and occipital cortex of the EcK fistula dogs, and in temporal and occipital cortex of dogs with acute hepatic failure. However, amounts of reduction of CCK-LI level did not cbrrelate with those of increment of the aromatic amino acids in cortex of these HE models. Hte results imply that reduced levels of the excitatory neuropeptide CCK may be elicited by the mechanism distinct from that inducing increase of false neurotransmitters.
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