Korean J Physiol Pharmacol.  1997 Dec;1(6):749-758.

Pretreatment of hyperbaric oxygenation increases the activities of myocardial antioxidant enzymes and protects the ischemia-reperfusion injury of the heart

• Oh DJ
• Kim YH
• Kim CH
• Park JW
• Kim MS

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.

Keyword

Hyperbaric oxygen; Ischemia-reperfusion injury; Myocardial antioxidant enzyme

MeSH Terms

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
Catalase
Glucose-6-Phosphatase
Glucose-6-Phosphate
Glutathione Peroxidase
Glutathione Reductase
L-Lactate Dehydrogenase
Malondialdehyde
Oxidoreductases
Oxygen
Reactive Oxygen Species
Superoxide Dismutase