| Project/Area Number |
05670639
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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 |
Circulatory organs internal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
IMANISHI Sunao Kanazawa Medical University, Department of Physiology, Professor, 医学部, 教授 (90108689)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | human atrial muscle / partial depolarization / intracellular Na^+ activity / Na^+ -selective electrode / voltage clamp / 膜のNa^+透過性 / 細胞内ナトリウムイオン活性 / 膜電位固定 |
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| Research Abstract |
Diseased human atrial fibers are characterized by low levels of resting membrane potential(Vm). As a mechanism involved in such depolarization we have investigated the possibility of an increase in Na^<<minus-plus>> permeability to the resting membrane (P_<Na>). With increased resting P_<Na>, the intracellular Na^+ activity (a_<Na>) should be expected to increase. In the present experiment both a_<Na> and Vm were recorded simultaneously using double-barreled Na^+-selective microelectrodes. The Vm averaged -44.1<plus-minus>5.0mV (mean<plus-minus>SD,n=9) as be expected and the a_<Na>,6.9<plus-minus>1.7mM under normal Tyrode solution containing 5.4mM-K^+. The a_<Na> value was within physiological levels, suggesting that the low Vm is not due to increased P_<Na>. But the partial depolarization as seen in diseased human preparations may possibly accelerate extrusion of intracellular Na^+, with consequent decreases in a_<Na>. So we tried to measure a_<Na> under the condition of membrane voltage clamp using single sucrose gap method. The a_<Na> value obtained was 7.8mM at the Vm of about-60mV and 8.6mM at about -80mV,though the voltage control was incomplete. Thus, the low Vm observed in diseased human atrial muscle may not be attributed to increased P_<Na> of the resting membrane. Further studies into mechanisms underlying the low Vm of the human specimen are necessary.
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