| Project/Area Number |
07670554
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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 |
Gastroenterology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
YONEDA Masashi Asahikawa Medical College Second Department of Medicine Assistant Professor, 医学部, 助手 (30261407)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Neuropeptide / Hepatic function / Hepatic prliferation / Hepatic blood flow / Neurotrnsmitter |
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| Research Abstract |
1. The central nervous system (CNS) effect of thyrotropin releasing hormone (TRH) on hepatic microcirculation was studied in rats. Hepatic microcirculation was measured by hydrogen-gas clearance method in urethane-anesthetized rats. Intracisternal injection of TRH analog dose-dependently enhanced hepatic blood flow with peak response at 30 min. The stimulation of hepatic blood flow by central TRH was abolished by atropine, indomethacin, L-NAME and vagotomy.
2. The CNS effect of TRH on hepatic proliferation was studied in awaked rats. Hepatic proliferation was assessed by thymidine incorporation into hepatic DNA.Hepatic proliferation was dose-dependently stimulated by intracisternal TRH analog with peak response at 48 h after the peptide injection and returned to basal at 72 h. Stimulation of hepatic proliferation by central TRH was abolished by hepatic branch vagotomy, atropine and indomethacin but not by L-NAME.
3. The CNS effect of TRH and corticotropin releasing factor (CRF) on CC14-induced acute liver damage in awaked rats. Intracisternal TRH analog dose-dependently inhibited the elevation of serum ALT level 24 h after CC14 injection and this inhibitory effect was abolished by atropine, indomethacin and vagotomy, but not by L-NAME or 6-OHDA.Intracisternal CRF dose dependently enhanced hepatic damage induced by CC14.
4. The CNS effect of TRH on hepatic cAMP synthesis was studied in awaked rats. Intracisternal TRH analog stimulate hepatic cAMP synthesis with peak response at 12 h.
It is of interest to investigate specific brain sites for TRH and CRF and to evaluate a role of endogenous TRH and CRF in hepatic function using specific antibody and antagonist.
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