| Project/Area Number |
01570494
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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 | Kyushu University |
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Principal Investigator |
YANAGA Takashi Kyushu Univ. Med. Inst. of Bioreg. Professor, 生体防御医学研究所, 教授 (80038702)
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| Co-Investigator(Kenkyū-buntansha) |
YANO Kenichi Kyushu Univ. Med. Inst. of Bioreg. Asist Prof., 生体防御医学研究所, 助手 (60230281)
HATA Tomoji Kyushu Univ. Med. Inst. of Bioreg. Asist Prof., 生体防御医学研究所, 助手 (90198739)
MAKINO Naoki Kyushu Univ Med. Inst. of Bioreg. Asso Pro., 生体防御医学研究所, 助教授 (60157170)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1989: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Reperfusion / Cardiac Damage / Free Radical / Calcium / Sodium / Freeradical Scavenger / Perfused Heart / Rat / 再潅流障害 / インタ-ワイキン1 / 腫瘍壊死因子 / 活性酸素消去剤 / ラット心臓 / Na^+ーK ATPaes / 活性酸素 / 潅流ラット心 / 膜脂質過酸化 / 心筋細胞膜 / 心筋カルシウム / 再灌流不整脈 / Na^+-K ATPase / 灌流ラット心 |
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| Research Abstract |
It is well known that cardiac dysfunction and serious ventricular arrhythmias were observed in hearts of reperfusion after ischemia in human or animal models. Those mechanisms still remain unknown in spite of many investigators in clinical and experimental studies. In the view of mechanisms of reperfusion induced arrhythmias (RA), oxygen free radicals (OFR) was now suggested to be one of arrhythmogenic factors. We have therefore examined whether the administration of OFR scavenger prior or to or during reperfusion could reduced the myocardial damage and inhibit the RA in the isolated rat hearts. The incidence of RA in the presence of scavengers was not different from that in the absence of those. However, the duration of RA was reduced when the addition of scavengers in perfusate. And, Na^+-K^+ ATPaseSince the disturbance of ion homeostasis is also considered to be a major cause in the electrical abnormalities and cardiac dysfunction in reperfused hearts, it was studied that the role o
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f Na ion during ischemia and reperfusion was examined by the intervention of Amiloride, which is a nonspecific inhibitor of Na^+-H^+ antiporter, on the occurrence of arrhythmias and on cardiac function in isolated rat hearts. Administration of Amiloride prior to ischemia decreased the incidence of arrhythmias at dose dependent manner. Similar results were obtained by perfusion with low Na concentration durig ischemia. It was seen under those interventions that tissue Na, Ca and malondialdehyde contents were significantly decreased in the reperfused rat hearts. Thus, it may be one of major causes on the occurrence of reperfusion arrhythmias because changes or disturbance of Na^+ and Ca^<2+> ion homeostasis during ischemia-reperfusion period were seen.
These results indicate that pathogenesis for reperfusion arrhythmias was different from cardiac dysfunction in reperfusion after ischemia in the present study. However, since OFR scavengers reduced the duration of reperfusion induced arrhythmias and also decreased lipid peroxidation of hearts, OFR may play an important role in the development of RA. By the way, disturbance of Ca ion and Na ion homeostasis may be contributed to cardiac dysfunction in reperfused heart after ischemia. Less
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