1997 Fiscal Year Final Research Report Summary
THE EFFECT OF VOLATILE ANESTHETICS ON MUSCARINIC ACETYLCHOLINE RECEPTOR SIGNAL TRANSDUCTION SYSTEM IN RAT ATRIUM
| Project/Area Number |
08671743
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
SERA Akihiko Hiroshima University Medical Hospital, Research Associate, 医学部・附属病院, 助手 (30243570)
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| Co-Investigator(Kenkyū-buntansha) |
AZUMA Toshiharu Hiroshima University Medical Hospital, Research Associate, 医学部・附属病院, 助手 (60284197)
YUGE Osahumi Hiroshima University School of Medicine, Professors, 医学部, 教授 (40034128)
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| Project Period (FY) |
1996 – 1997
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| Keywords | volatile anesthetics / muscarinic receptor / receptor assay |
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| Research Abstract |
The effects of sevoflurane and isoflurane on the muscarinic acetylecholine receptor (mAchR) system, consisting of the recepyor, inhibited guanine nucleotide binding protein (Gi), and adenylate cyclase (AC), were studied in rat atrial membrane. The receptor studies were performed by using the 3-quinuclidinyl benzilate ([3H] QNB) binding method. Nonspecific binding was determined in the presence of (-) AF-DX116.
The mAchR binding capacity determined by the maximum number of binding sites (Bmax) and the dissociation constant (Kd) for [3H] QNB were calculated. Cyclic adenosine monophosphate (cAMP) production rate was measured as cAMP generation stimulated by isoprotelenoll. We observed Kd for [3H] QNB increased in a volatile anesthetics concentration-dependent manner, wheares Bmax remained on changed. Sevoflurane strongly depressed Kd at the same concentration than isoflurane. As for cAMP production rate, sevoflurane decreased it than isoflurane. We speculated that isoflurane might be severely depress mAch signal transduction system by regucing ligand-receptor bindings than sevoflurane.
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