Pretreatment of hyperbaric oxygenation increases the activities of myocardial antioxidant enzymes and protects the ischemia-reperfusion injury of the heart.
- Author:
Dong Jin OH
1
;
Young Hoon KIM
;
Chan Hyung KIM
;
Jong Wan PARK
;
Myung Suk KIM
Author Information
1. Department of Internal Medicine, Gangdong Sacred Heart Hospital, College of Medicine, Hallym University, Seoul 110-799 South Korea.
- Publication Type:Original Article
- Keywords:
Hyperbaric oxygen;
Ischemia-reperfusion injury;
Myocardial antioxidant enzyme
- MeSH:
Animals;
Brain;
Catalase;
Glucose-6-Phosphatase;
Glucose-6-Phosphate;
Glutathione Peroxidase;
Glutathione Reductase;
Heart*;
Hyperbaric Oxygenation*;
Ischemia;
L-Lactate Dehydrogenase;
Liver;
Malondialdehyde;
Oxidative Stress;
Oxidoreductases;
Oxygen;
Partial Pressure;
Rabbits;
Rats;
Reactive Oxygen Species;
Reperfusion;
Reperfusion Injury*;
Superoxide Dismutase
- From:The Korean Journal of Physiology and Pharmacology
1997;1(6):749-758
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 ~ 3 atm O2/1 ~ 3 hrs/1 ~ 10 days). The changes in activities of major antioxidant enzymes(superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate 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 O2/1 ~ 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, pretreatment with 2 atm O2/1 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 O2/2 ~ 3 hrs for 5 days. A lipid-peroxidation product, malondialdehyde was increased in brains and livers of the rats exposed to 2 atm O2/2 ~ 3 hrs/5 days and 3 atm O2/1 hr/5 days. The present results suggest that the pretreatment of hyperbaric oxygenation can protect the post-ischemic reperfused hearts in association with a stimulation of the activities of myocardial antioxidant defensive enzymes, and that the hyperbaric oxygenation of 2 atm O2/1 hr for 5 days would be a safe condition which does not produce any oxygen toxicity.
