1994 Fiscal Year Final Research Report Summary
Characterization of Myocardial Ischemia in Shock by NADH Fluorescence
| Project/Area Number |
05670633
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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 | Keio University |
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Principal Investigator |
HORI Shingo Keio University, School of Medicine, Associate Professor, 医学部, 助教授 (80129650)
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| Co-Investigator(Kenkyū-buntansha) |
ADACHI Ken Keio University, School of Medicine, Director, 医学部, 助手 (50231931)
MIYAZAKI Koji Keio, University, School of Medicine, Director, 医学部, 助手 (90219759)
INOUE Soushin Keio University, School of Medicine, Director, 医学部, 助手 (10193591)
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| Project Period (FY) |
1993 – 1994
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| Keywords | shock / NADH / myocardial ischemia / coronary circulation / cathecolamine / NO / right ventricle / L-NAME |
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| Research Abstract |
To clarify the characteristics of myocardial ischemia in the shock, hypotension was experimentally induced in the canine model by adjusting the level of the reservoir connected to the subclavian artery. The beating hearts were rapidly cross-sectioned and freeze-clamped in situ to obtain frozen heart slices. When aortic mean pressure was lowered to 40 mmHg or less, NADH fluorescence photography provided visualization of myocardial ischemia which was localized dominantly in the subendocardium. Coronary blood flow was reduced depending on the low coronary perfusion pressure and also the work of the ventricle in the shock, however, coronary reserve was maintained as shown by stable coronary resistance, endocardial epicardial tissue flow ratio in the left ventricle, and preservation of reactive hyperemia following coronary occlusion. Augmented sympathetic tone, indicated by elevated plasma epinephrine and norepinephrine concentrations, is likely to take a significant role to constrict coronary vessels in the shock.
Right ventricle was also involved in myocardial ischemia simultaneously with the left ventricle, e.g.myocardial ischemia was visualized in the right ventricle when aortic pressure was at 40 mmHg or less.
Pretreatment with L-NAME increased ischemic area in the shock, and coronary blood flow in the shock was further reduced following L-NAME administration. It is indicated that both vasoconstricting and vasodilating effect s of vasoactive substances released in the shock take significant roles to generate myocardial ischemia in the shock. Cathecolamines and NO are possible candidates to affect coronary circulation in the shock.
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