| Project/Area Number |
61570101
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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 |
General pharmacology
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| Research Institution | Kyoto University |
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Principal Investigator |
KURAHASHI Kazuyoshi Radioisotope Research Center, Kyoto University, Associate Professc, 放射性同位元素総合センター, 助教授 (10025653)
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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 |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Intracellularly accumulated catecholamine / C-AMP / Lactate / 乳酸産生 / カテコラミン / 心筋細胞内蓄積 / 細胞内受容体 / 心室細動 / 【Ca^(2+)】括抗薬 / 【α_1】-遮断薬 |
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| Research Abstract |
We have reported that the increase in extraneuronal accumulation of catecholamine in rat heart increases the incidence of ventricullar fibrillation. The present experiments were undertaken to investigate whether the increase in extraneuronal accumulation of isoprenaline affects cyclic AMP production and lactate production, and to examine effect of ischemia on the extraneuronal uptake mechanism. In perfused rat hearts, the increase in intracellular accumulation of isoprenaline under COMT inhibition did not enhance the cyclic AMP production in the heart. The lactate production was increased by the enhancement of accumulation of isoprenaline and was decreased by the reduction of it. The extraneuronal uptake mechanism was not inhibited by glucose-deprivation or anoxic conditions, and was inhibited by both of them.
From these results, it was concluded that the intracellularly accumulated amine may inhibit adenylate cyclase system but enhance glycolysis in rat heart, and it was suggested that ischemia may inhibit the extraneuronal uptake mechanism.
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