Interaction between coronary arterial microvessels and cardiac muscles : Analysis during myocardial ischemia and tachcardia.
| Project/Area Number |
08670752
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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 | Tohoku University |
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Principal Investigator |
KOMARU Tatsuya Tohoku University School of Medicine, The First Department of Ineternal Medicine Research Associate,, 医学部, 助手 (30261530)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | microvessels / coronary circulation / myocardial ischemia / G protein / signal transduction / vasodilation / Pertussis toxin / microcirculation / 虚血 / 頻拍 / 筋原性張力 / 冠血流自己調節 / 代謝性因子 |
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| Research Abstract |
We have established an experimental model to analyze the interaction between cardiac muscle and coronary microcirculation. In that model, excised coronary arterial microvessels and beating hearts were contacted and they could be controlled independently. The coronary arterial microvessel (inner diameter 127-296 mum) was excised from male Japanese white rabbits and was cannulated into a polyethylene tube (outer diameter - 100 mum). When they were immeraed into the water bath with warmed and oxygenated physiological salt solution intrinsic vascular tone was observed without and pharmacological preconstriction. Thereafter, those microvascular preparations were gently embedded onto the surface of beating canine left ventricle perfused by the left anterior descending artery (LAD). The excised microvessels (n=9) on the beating heart were observed by intravital microscope equipped with a floating objective. Changes in the microvascular diameter during the occlusion of LAD was measured with vi
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deomanipulator. The microvessels started to dilate right after the induction of the myocardial ischemia, and the dilation attained significant in 2 minutes (8 (]SY.+-。[)) 2 %). In four minutes, the dilation attained maximum (12 (]SY.+-。[)) 3 %). Subsequently, the diameter began to decrease, and the diameter returned to control level in 30 minutes (1 (]SY.+-。[) 3 %). The transient dilation offers two possibilities in terms of mechanism. First, the dilatory signal from ischemic myocardium may be transient. Second, the vasomotor signals from ischemic myocyte may consist of two components, namely, both vasodilator and constrictor signals which are released sequentially. As some vessels constricted markedly in the later phase of ischemia, the second mechanism is more likely. The experiment to investigate the sensitivity of the vasomotor signal from ischemic heart muscle to pertussis toxin is under way. Although we need to do more experiment, pertussis toxin tended to inhibit the dilation of microvessels during myocardial ischemia. The study using adenosine blocker is planned. Less
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Report
(3 results)
Research Products
(30 results)
