1989 Fiscal Year Final Research Report Summary
Free Radicals and Metabolic State of the Reperfused Myocardium
| Project/Area Number |
63570413
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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 | TOKAI UNIVERSITY |
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Principal Investigator |
OKINO Haruka TOKAI Univ. Dept of Physiology, Professor, 医学部, 教授 (60055689)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIMORI Kohji TOKAI Univ. Dept of Physiology, Research Associate, 医学部, 助手 (60184636)
NAKAZAWA Hiroe TOKAI Univ. Dept of Physiology, Associate Professor, 医学部, 助教授 (20110885)
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| Project Period (FY) |
1988 – 1989
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| Keywords | Reperfusion Injury / Metabolism / Myocardium / Free Radicals |
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| Research Abstract |
Oxygen-derived radicals have recently been implicated as important agents in causing tissue damage in myocardial ischemia and reperfusion injury. However, there is no appropriate technique for the direct measurement of the generation of these radicals, since oxygen-derived radicals are extremely reactive and have short life spans. The purposes of this study are 1) to directly evaluate oxygen derived radicals in myocardium using electron spin resonance (ESR) spectroscopy, 2) to evaluate radical scavenger contents of the myocardium subjected to reperfusion injury 3) to show the efficacy of radical scavengers in reperfused canine hearts, and 4) to correlate the energy levels and pH in the reperfused myocardium to the severity of vascular impairment.
RESULTS: 1) Using 20 open chest canine hearts and isolated retro-perfused rat hearts the myocardium was freeze-clamped with precooled tongs immediately after reperfusion and free radicals existing in the samples were measured using electron spi
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n resonance spectroscopy (ESR) at -196 C. The freeze-trapping method failed of demonstrating O_2- probably due to low detection range of this method, however, the presence of coenzyme Q_<10> radical in the myocardium has been demonstrated. 2) Using canine hearts, SOD activities in myocardium rendered ischemia for 3 hours or reperfused after 90 min of ischemia were evaluated. SOD activities revealed 21-22 units/mg prot which remained in the same range of that in normal myocardium. 3) In 20 open chest dogs, hearts were subjected to a 90 min period of ischemia by LAD occlusion followed by 60 min reperfusion. In the group which received SOD (15000 U/kg) demonstrated less injury than the group without SOD in all parameters of cardiac functions and area of necrosis. 4) In 25, perfused hearts, myocardial high energy phosphate and pH were monitored by ^<31>P-NMR spectra during ischemia and reperfusion. Coenzyme Q_<10> radical in myocardium, an indicator of tissue redox state, was low in hearts which demonstrated heterogeneous pH and low ATP levels. Less
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Research Products
(16 results)
