2013 Fiscal Year Final Research Report
Central and peripheral effects of dexmedetomidine on autonomic cardiovascular regulation
| Project/Area Number |
23592319
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
KAWADA Toru 独立行政法人国立循環器病研究センター, 研究所, 室長 (30243752)
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| Co-Investigator(Renkei-kenkyūsha) |
SHIMIZU Shuji 国立循環器病研究センター, 研究所, 特任研究員 (80443498)
LI Meihua 国立循環器病研究センター, 研究所, 特任研究員 (60443496)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 循環器・高血圧 / 薬理学 / 生理学 / 制御工学 / システム生理学 / メデトミジン / 迷走神経 / 動脈圧反射 |
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| Research Abstract |
Dexmedetomidine is a centrally acting alpha2-adrenergic agonist and is used for sedation in the intensive care units. Although it has a minimal effect on respiratory function, severe bradycardia and sinus arrest are occasionally observed. The aim of the present study was to examine which of the direct effect on the heart (peripheral effect) or the central vagal activation is responsible for such side effects of medetomidine. To evaluate efferent vagal activity, acetylcholine was measured through a microdialysis fiber implanted into the myocardial interstitium of anesthetized rabbits. Intravenous medetomidine administration increased myocardial interstitial acetylcholine concentration, which was abolished by vagotomy. These results indicate that medetomidine centrally activates the vagal nerve and can cause bradycardia and, in severe cases, sinus arrest.
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Research Products
(17 results)
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[Journal Article] Medetomidine, anα2-adrenergic agonist, activates cardiac vagal nerve through modulation of baroreflex control2012
Author(s)
Shimizu S, Akiyama T, Kawada T, Sata Y, Mizuno M, Kamiya A, Shishido T, Inagaki M, Shirai M, Sano S, Sugimachi M
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Journal Title
Circ J
Volume: 76(1)
Pages: 152-159
DOI
Peer Reviewed
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