| Project/Area Number |
09480259
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
KAJIYA Fumihiko Medical Engineering, Kawasaki Medical School, Professor, 医学部, 教授 (70029114)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJIOKA Katsuhiko Medical Engineering, Kawasaki Medical School, Professor, 医学部, 教授 (30163801)
YADA Toyotaka Medical Engineering, Kawasaki Medical School, Assistant Professor, 医学部, 講師 (00210279)
OGASAWARA Yasuo Medical Engineering, Kawasaki Medical School, Associate Professor, 医学部, 助教授 (10152365)
SARUTA Takao Medical Engineering, Keio University, Professor, 医学部, 教授 (70051571)
GOTO Masami Medical Engineering, Kawasaki College of Allied Health Professions, Professor, 臨床工学科, 教授 (50148699)
HAYASHI Kohichi Medical Engineering, Keio University, Assistant Professor (80164937)
仲本 博 川崎医科大学, 医学部, 助手 (10299183)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥10,100,000 (Direct Cost: ¥10,100,000)
Fiscal Year 1999: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1997: ¥3,800,000 (Direct Cost: ¥3,800,000)
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| Keywords | Subendocardial Arterioles / Coronary Slosh Phenomenon / High-speed CCD Intravital microscope / Niobium microsphere / Vascular Pulsation / 高血圧肥大心 / 冠予備 / 心内膜側冠細動脈 / 心筋虚血 / 内皮依存性血管拡張反応 / 内皮非依存性血管拡張反応 / ACE阻害剤 |
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| Research Abstract |
Time sequential changes in endothelium-dependent and -independent vasodilator mechanisms on subendocardial arterioles (Emdo-A) were studied in hypertensive canine hearts (2-clip and 2-kidney model). The diameter of Endo-A and subepicardial (Epi-A) arterioles (<110 μm) was measured using a high-speed CCD intravital microscope. We also visualized the blood velocities in the subendocardial microcirculation with a light marker (niobium microsphere). Vascular responses to acetylcholine (Ach, 1μg/kg, ic) and papaverine (Papa, 1mg, ic) were compared in normotensive (N, left ventricular wall thickness : LVWT=9mm, n=7) and hypertensive (4w-HT, LVWT=12mm, m=8, p<0.01, vs N : 12w-HT, LVWT=14mm n=3, p<0.01, vs N) hearts. Percent increase of end-diastolic diameter of Endo-A in both 4w- and 12w-HT after Ach was smaller than that of N (4w, p<0.05 and 12w, p<0.001). The vasodilation of Endo-A after Papa was impaired in 12w-HT (p<0.01), but that of Epi-A was not. The blood velocity waveform in a subendocardial arteriole exhibited a forward flow exclusively during diastole and a twopeaked reverse flow during systole. This velocity waveform implies that a part of the diastolic forward flow moved back during systole and we called this wastful back and forth flow as "coronary slosh phenomenon" which increased in HT.
In conclusion, in an early stage of HT (4w-HT), the endothelium-dependent response of Endo-A was impaired. In the later stage (12w-HT), both the endothelium-dependent and independent responses of Endo-A were impaired. These time sequential changes may be related with the degree of decreased subendocardial coronary flow reserve in progression of LVH. The coronary slosh phenomenon which increased in FIT may be important to understand the clinically well-known higher incidence of ischemia in the subendocardium.
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