| Project/Area Number |
04670554
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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 | School of Medicine, Keio University |
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Principal Investigator |
KOBARI Masahiro School of Medicine, Keio University, Assistant, 医学部・内科, 助手 (30162035)
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| Co-Investigator(Kenkyū-buntansha) |
SHINOHARA Tamotsu School of Medicine, Keio University, 医学部・内科, 助手 (50138004)
TANAHASHI Norio School of Medicine, Keio University, 医学部・内科, 講師 (10124950)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1993: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1992: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Cardiac arrest / Cerebral blood flow / Cerebral blood volume / Cerebral ischemia / Delayd hypoperfusion / Microcirculation / Photoelectric method / Reactive hyperemia / 脳循環 / 脳血流量 / 遅発性低潅流 |
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| Research Abstract |
Cerebral hemodynamic changes during and following cardiac arrest of various dutation were examined in cats. Animals were anesthetized with alpha-chloralose and urethane, and were artificially ventilated. Local cerebral blood volume (CBV), mean transit time of blood (MMT), and local cerebral blood flow (CBF) in the crtex were measure by our photoelectric method. After thoracotomy, cardiac arrest was induced by applytin electric fibrillator to the heart.
Immediately after termination of cardiac arrest of 10-s, 30-s, and 3-min duration, CBV was transiently increased (reactive hyperemia). The critical time for the appearance of reactive hyperemia was less than 10 s. Duration of the reactive hyperemia was dependent on the duration of cardiac arrest. In the 30-s and 3-min cardiac arrest group, CBF was temporarily recovered after termination of cardiac arrest, but showed continuous reducsions for 3hrs (delayd hypoperfusion). The critical time for the advent of posischemic hypoperfusion was between 10 and 30 s. Adenosine appeared to be involved in the appearance of reactive hyperemia
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