1999 Fiscal Year Final Research Report Summary
Micromechanics Control of Coronary Circulation
| Project/Area Number |
10044330
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| Research Category |
Grant-in-Aid for Scientific Research (A).
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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 Engineeering, Kawasaki Medical School, Professor, 医学部, 教授 (70029114)
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| Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Motoaki Cardiovascular Science, Tokyo Women's Medical College, Professor, 医学部, 教授 (60010914)
SUGA Hiroyuki Medical School, Physiology II, Okayama University, Professor, 医学部, 教授 (90014117)
OGASAWARA Yasuo Medical Engineeering, Kawasaki Medical School, Associate Professor, 医学部, 助教授 (10152365)
GOTO Masami Medical Electronics, Kawasaki College of Allied Health Professions, Professor, 臨床工学科, 教授 (50148699)
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| Project Period (FY) |
1998 – 1999
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| Keywords | coronary microcirculation / blood flow regulation / mechanical stress / myocardial ischemia / molecular flow tracer / vascular response / 血管反応 |
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| Research Abstract |
We organized this interdisciplinary project in order to provide a better understanding of the regulation of coronary microcirculation from a viewpoint of mechanoenergetic interaction between coronary vessels and myocardium. Followings are the major findings from 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. Pulsatilet ransmural pressure of the arterioles may contribute to the arteriolar dilation in response to a decrease in coronary perfusion pressure. Endothelium-derived hyperpolarizing factor contributes mainly to the dilation of the smaller coronary arteriole, while nitric oxide of the lager coronary arteriole and the smaller artery. When these mechanisms are inhibited, adenosine and Pco2 may play compensatory role in the coronary arteriolar dilation.
Diastolic time fraction increased when coronary flow was reduced by lowering perfusion pressure. Modulation of the diastolic time fraction can provide an important regulatory mechanism to match supply and demand of the myocardium when vasodilatory reserve is exhausted.
Evaluation of mechanical cardiovascular coupling using the wave intensity is sensitive to the change in cardiac performance and may be applicable to the evaluation of the mechanical effects to the coronary circulation.
Micro-imaging of the blood flow distribution at capillary level using molecular flow tracer is useful for evaluating mechanoenergetic regulation of coronary microcirculatiom. Β1-Adrenoceptor blockade reduced microheterogeneity of the subendocardial perfusion.
Nitric oxide donor suppressed the flow (shear stress)-induced production of nitric oxide. Tetrahydrobiopterin may counteract the nitric oxide donor-mediated suppression. Gap junctions may play a role in heterocellular communication in the microvascular regulation.
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