| Project/Area Number |
11670056
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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 |
General physiology
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| Research Institution | National Cardiovascular Center, Research Institute |
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Principal Investigator |
YAMAZAKI Toji National Cardiovascular Center, Research Institute Department of Cardiac Physiology Senior Staff, 心臓生理部, 室長 (20116122)
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| Co-Investigator(Kenkyū-buntansha) |
AKIYAMA Tsuyoshi National Cardiovascular Center, Research Institute Department of Cardiac Physiology Staff, 心臓生理部, 室員 (70202554)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Calcium ion / norepinephrine / acetycholine / 交感神経終末 / マイクロダイアリシス / 迷走神経終末 |
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| Research Abstract |
1) To investigate the effect of hypoxia on endogenous norepinephrine (NE) release from cardiac sympathetic nerve ending, we administered sodium cyanide (NaCN) for 30 min into the myocardial interstitial space through a dialysis probe and measured dialysate NE levels. During the NaCN perfusion, a marked and concentration-dependent increase in dialysate NE was observed. This cyanide induced NE response was suppressed by pretreatment with despiramine (a membranous NE transport inhibitor). Further, the cyanide induced NE response was suppressed by pretreatment with TMB-8 (intracellular Ca^<2+> antagonist) but unaffected by ω-conotoxin GVIA (NE releasing inhibitor). Our data suggest that two independent (desipramine or TMB-8 suppressive) mechanisms contributed to the amount of NE efflux induced by cyanide in in vivo cardiac sympathetic nerve.
2) Acute myocardial ischemia induced by coronary occlusion increased myocardial interstitial acetylcholine (ACh) and NE levels in ischemic region, whereas, in non-ischemic region, coronary occlusion increased myocardial ACh level but decreased the NE level. The ACh release in the ischemic region is mainly attributed to local release mechanism, whereas the ACh release in the non-ischemic region depends on the increased vagal efferent nerve activity. The local release mechanism would depend on intracellular Ca^<2+> mobilization but not on N-type Ca^<2+> channel opening.
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