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고압산소 전처치의 심근 항산화효소 활성 증가 및 허혈-재관류손상 보호 효과
Pretreatment of Hyperbaric Oxygenation Increases the Activities of Myocardial Antioxidant Enzymes and Protects the Ischemia-Reperfusion Injury of the Heart

오동진   (한림대학교 의과대학 내과학교실UU0001493  ); 김영훈   (서울대학교 의과대학 약리학교실UU0000691  ); 김찬형   (서울대학교 의과대학 약리학교실UU0000691  ); 박종완   (서울대학교 의과대학 약리학교실UU0000691  ); 김명석   (서울대학교 의과대학 약리학교실UU0000691  );
  • 초록

    Myocardial ischemia-reperfusion injury is known to be mediated by reactive oxygen species. The myocardial cell is equipped with endogenous antioxidant defensive system which can be adaptively stimulated by various oxidative stress. It is postulated that an increased oxygen partial pressure induced by hyperbaric oxygenation impose an oxidative stress on the cells, resulting alterations in the endogenous antioxidant system. In this study we investigated the effect of hyperbaric oxygenation on the activities of myocardial antioxidant enzymes and observed whether the hyperbaric oxygenation could protect the ischemia-reperfusion injury of heart. Rats or rabbits were pretreated with hyperbaric $oxygenation(2{\sim}3\;atm\;O_2/1{\sim}3\;hrs/1{\sim}10\;days)$ . The changes in activities of major antioxidant enzymes(superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phasphate dehydrogenase), functional recovery and infarct size were observed in the experimentally induced ischemia-reperfused hearts. In the hearts isolated from rats pretreated with $2\;atm\;O_2/1{\sim}2\;hrs$ for 5 days, the functional recovery after reperfusion(20 min) following global ischemia(25 min) was significantly increased without any observable oxygen toxicity. Lactate dehydrogenase release was also significantly reduced in this hyperbaric oxygenated rat hearts. In in vivo regional ischemia(30 min) model of rabbit hearts, pretreatrment with $2\;atm\;O_2/1\;hr$ for 5 days significantly limited the infarct size. Among the myocardial antioxidant enzymes of rat hearts pretreated with the hyperbaric oxygenation, the activities of catalase, superoxide dismutase and glucose-6-phosphatase dehydrogenase were increased, while those of glutathione peroxidase and reductase were not changed. There were lethal cases in the groups of rats exposed to 3 atm $3\;atm\;O_2/2{\sim}3\;hrs$ for 5 days. A lipid-peroxidation product, rnnlondialdehyde was increased in brains and livers of the rats exposed to $2\;atm\;O_2/2{\sim}3\;hrs/5\;days\;and\;3\;atm\;O_2/1\;hr/5days$ . The present results suggest that the pretreatment of hyperbaric oxygenation can protect the post-ischemic rererfused hearts in association with a stimulation of the activities of myocardial antioxidant defensive enzymes, and that the hyperbaric oxygenation of $2\;atm\;O_2/1\;hr$ for 5 days would be a safe condition which does not produce any oxygen toxicity.


  • 주제어

    Hyperbaric oxygen .   Ischemia-reperfusion injury .   Myocardial antioxidant enzyme.  

 저자의 다른 논문

  • 오동진 (2)

    1. 1995 "실험견에서 Metoprolol 약리효과의 약동/력학적 검토" The Korean journal of pharmacology : official journal of the Society of Pharmacology, Republic of Korea 31 (2): 251~259    
    2. 1999 "냉동절제 없이 시행한 Maze III 술식의 조기 결과" 大韓胸部外科學會誌 = The Korean journal of thoracic and cardiovascular surgery 32 (3): 255~261    
  • 김영훈 (6)

  • Park, Jong-Wan (13)

  • 김명석 (38)

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