Project/Area Number |
10671434
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
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Research Institution | Sapporo Medical University |
Principal Investigator |
MATSUMOTO Maki Sapporo Medical University, School of Medicine, Dept. of Anesthesiology, Lecturer, 医学部, 講師 (00173914)
|
Co-Investigator(Kenkyū-buntansha) |
KANAYA Noriaki Sapporo Medical University, School of Medicine, Dept. of Anesthesiology, Lecturer, 医学部, 講師 (10244344)
NAKAE Yuri Sapporo Medical University, School of Medicine, Dept. of Anesthesiology, Assistant, 医学部, 助手
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Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
Keywords | Intracellular CaィイD12+ィエD1 concentration / Myofilament CaィイD12+ィエD1 sensitivity / Morphine / Opioid receptor / Cardiac contractility |
Research Abstract |
(1) We investigated the effect of morphine on intracellular CaィイD12+ィエD1 concentration ([CaィイD12+ィエD1]i) and left ventricular pressure (LVP) relationship in intact beating hearts isolated from guinea pigs, and using specific κ-,δィイD21ィエD2-, and δィイD22ィエD2-, opioid antagonists, which opioid stimulation is related to the direct cardiac effect of morphine . Morphine (1μM) decreases available without decreasing [CaィイD12+ィエD1]i cardiac contraction, and it enhances myofilament CaィイD12+ィエD1 sensitivity in intact beating hearts. The decrease of CaィイD12+ィエD1 transients induced by morphine would be mainly cause by δィイD21ィエD2-, and δィイD22ィエD2-opioid stimulation, but not κ opioid stimulation. (2) δィイD21ィエD2-opioid agonist (TAN-67, 1μM) decreased both LVP and [CaィイD12+ィエD1]i, but not LVP. The cardiac effects induced by δィイD21ィエD2-, and δィイD22ィエD2-antagonist, respectively. The δィイD21ィエD2-, and δィイD22ィエD2-agonists caused a leftward shift in the curve of developed LVP as a function of available [CaィイD12+ィエD1]i, and it was indicated that these agonists enhanced myofilament CaィイD12+ィエD1 sensitivity. (3) Propofol decreases available [CaィイD12+ィエD1]i without decreasing cardiac contraction, and it enhances myofilament CaィイD12+ィエD1 sensitivity in intact beating hearts at clinical concentrations. The inhibition of available [CaィイD12+ィエD1]i by propofol may be mainly mediated by an impairment of sarcoplasmic reticulum CaィイD12+ィエD1 handling rather than the sarcolemmal L-type CaィイD12+ィエD1 current.
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