1999 Fiscal Year Final Research Report Summary
Endothelium-dependent and -independent responses of coronary arteriole to pulsatile mechanical stress in vivo
| Project/Area Number |
10670694
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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 |
Circulatory organs internal medicine
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| Research Institution | Kawasaki College of Allied Health Professions |
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Principal Investigator |
GOTO Masami Kawasaki College of Allied Health Professions, Dept. of Applied Medical Engineering, Professor, 臨床工学科, 教授 (50148699)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAMATSU Osamu Kawasaki College of Allied Health Professions, Dept. of Applied Medical Engineering, Assistant Professor, 臨床工学科, 講師 (50208849)
MATSUMOTO Takeshi Kawasaki College of Allied Health Professions, Dept. of Applied Medical Engineering, Associate Professor, 臨床工学科, 助教授 (30249560)
MOCHIZUKI Seiichi Kawasaki College of Allied Health Professions, Dept. of Applied Medical Engineering, Associate Professor, 臨床工学科, 助教授 (60259596)
KAJIYA Fumihiko Kawasaki Medical School, Dept. of Medical Engineering, Professor, 医学部, 教授 (70029114)
TACHIBANA Hiroyuki Kawasaki College of Allied Health Professions, Dept. of Applied Medical Engineering, Instructor, 臨床工学科, 助手 (00241216)
YADA Toyotaka Kawasaki Medical School, Dept. of Medical Engineering, Associate Professor (00210279)
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| Project Period (FY) |
1998 – 1999
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| Keywords | subendocardium / arteriole / mechanical stress / pulse pressure / myogenic regulation / vascular response / myocardial ischemia / microcirculation |
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| Research Abstract |
We organized this project in order to provide a better understanding of the physiological importance of the endothelium-dependent and -independent regulations of coronary arteriole under pulsatile mechanical stress. Followings are the major findings this project.
With aids of needle-probe CCD intravital microscopy and coronary perfusion system, we evaluated the behavior of the coronary arterioles in response to a reduction of coronary perfusion pressure. Pulsatile transmural pressure of the arterioles contributed to the arteriolar dilation in response to a decrease in coronary perfusion pressure. At the same time, diastolic time fraction increased when coronary flow was reduced by lowering perfusion pressure. These pulsation-related vasodilation and modulation of diastolic perfusion time can provide an important regulatory mechanism to match supply and demand of the myocardium at low perfusion pressure, especially in the subendocardium.
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