2002 Fiscal Year Final Research Report Summary
Basic Fibroblast growth factor improves high energy phosphate metabolism in the ischemic myocardium in rabbits
| Project/Area Number |
11670719
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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 | Kinki University |
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Principal Investigator |
ISHIKAWA Kinji Kinki University, Professor, 医学部, 教授 (10088536)
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| Co-Investigator(Kenkyū-buntansha) |
TANIWA Takaaki Kinki University, Assistant, 医学部附属病院, 助手 (60340775)
KIMURA Akio Kinki University, Assistant Professor, 医学部, 講師 (80309278)
MIYATAKA Masaru Kinki University, Assistant Professor, 医学部, 講師 (40309282)
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| Project Period (FY) |
1999 – 2002
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| Keywords | Basic fibroblast growth factor / Angiogenesis / Ischemic myocardial metabolism / Acute myocardial infarction / ^<31>P-NMR / Myocardial salvage / Infarct size / Cardioprotective effect |
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| Research Abstract |
Basic fibroblast growth factor (bFGF) has been shown effective in the treatment of chronic iscnemic myocardium as well as in acute myocardial infarction. The beneficial role to limit infarct size following abrupt coronary occlusion can not be attributable solely to angiogenesis and myocardial salvage independent of angiogenesis or cardioprotective effect of bFGF has been proposed. We hypothesized that bFGF may modify high energy phosphate metabolism in the ischemic myocardium to extend cell survival and prolong myocardial survival. In 17 Japanese white rabbits, the heart was perfused with Langendorff preparation and adenosine triphosphate (ATP), creatine phosphate (CrP) and inorganic phosphate (Pi) were measured every 5 min using ^<31>P-NMR during 10 min basal state, 20 min global ischemia following by 60 min postischemic reperfusion. In 8 of these, bFGF 100 μg was injected in the perfusate 1 min prior to the global ischemia. ATP was higher during postischemic reperfusion in bFGF-treated heart.
In conclusion, bFGF was effective to maintain ATP higher in the postischemic myocardium. This effect may contribute to limit infarct size in the acute myocardial infarction.
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