| Project/Area Number |
11671331
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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 |
Thoracic surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
MORITA Shigeki Faculty of Medicine, Kyushu University Ass. Prof, 医学部・附属病院, 講師 (70243938)
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| Co-Investigator(Kenkyū-buntansha) |
TOMINAGA Ryuuji Faculty of Medicine, Kyushu University Ass. Prof, 大学院・医学研究院, 助教授 (70136464)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | Brain death / Coronary artery / Coronary flow reserve / Endothelium / Cardiac function / 血管内皮機能 |
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| Research Abstract |
Background : Massive catecholamine release after brain death is thought to be one of the most important causes to cardiac dysfunction after heart transplantation. However, the exact mechanism for cardiac failure in brain-dead heart has not been fully elucidated. The aim of this study was to investigate the response of coronary artery to vasodilator and their contribution to hemodynamic deterioration using canine brain death model.
Methods: Brain death was induced by rapid inflation of a subdurally placed balloon catheter. Hemodynamic measurements including assessment of left ventricular contractility using pressure-volume relations and biochemical analysis of blood samples was performed in 7 dogs. Coronary flow reserve was assessed by endothelium-dependent (acetylcholine ; Ach) and -independent (sodium nitroprusside ; SNP) coronary vasodilation in 8 dogs.
Results: Hyperdynamic response was observed transiently after induction of brain death followed by decreases in arterial pressure, cardiac output and coronary blood flow. Left ventricular contractility was deteriorated at 60-minute after brain death. Coronary flow reserve both by Ach and SNP were significantly impaired at 30- and 60-minute after brain death (Ach 3μg 320.5 % to 189.1 % and 202.8 % ; SNP 100μg 255.6 % to 145.8 % and 153.5 %). Coronary resistance ratios were significantly increased at 30- and, 60-minute after brain death.
Conclusions : Impairement of coronary flow reserve and left ventricular function was observed in brain-dead canine heart. This impaired coronary circulation could be a disadvantage of preservation and recovery of cardiac dysfunction.
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