| Project/Area Number |
08457012
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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 |
General physiology
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| Research Institution | Kagawa Medical University (1997)
Osaka University (1996) |
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Principal Investigator |
KOSAKA Hiroaki Medical University Dept.of Physiology 2, Professor, 医学部, 教授 (60158897)
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| Co-Investigator(Kenkyū-buntansha) |
YONEYAMA Hirohito Kagawa Medical University Dept.ofPhysiology 2, Assitant Professor, 医学部, 助手 (80294750)
SEIYAMA Akitoshi Osaka University Medical School, Dept.of Physiology 1, Assitant Professor, 医学部, 助手 (70206605)
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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 |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1996: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | nitric oxide / hemoglohin / oxygen relrease / ESR / EPR / nitroglycerin / isosobide dinitrate / angina / 一酸化窒素 |
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| Research Abstract |
The effect of nitroglycerin on oxygen (O2) release in microcirculation was investingated by examining single, unbranched hepatic sinusoids of rats using dual-spot microspectroscopy. Nitroglycerin significantly increased O2 selease from erythrocytes flowing in the sinusoids. Differences in O2 saturation of hemoglobin per unit length of the sinusoid were significantly enhanced, while there were no significant changes in erythrocyte velocity, hemoglobin (Hb) concentration, and oxyhemoglobin flow into the sinusoids, as well as regional hepatic blood flow measured with a laser tissue blood flow meter. No change was noted for hepatic O2 consumption measured in isolated liver perfused with Hb-free oxygenated buffer. Isosorbide denitrate showed a similar but slower effect. These findings suggest that nitroglycerin and isosorbide dinitrate enhance O2 release from erythrocytes without significantly increasing tissue blood flow. In vitro study revealed O2 affinity was significantly decreased in blood taken from rats treated with nitroglycerin. It contained NO bound to Hb a subunit alone. It is possible that breaking or stretching of the NO heme iron-proximal histidine bond during organ circulation triggered the decrease in O2 affinity, while the O2 affinity was recovered in lung by restoring the bond. These results should operate when cytokines induce NO synthase in vascular system during such events as inflammation.
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