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为了观察急性重度低压缺氧对心肌脂质过氧化及心肌酶学的影响，对３９只成年健康Ｗｉｓｔａｒ大鼠急性低压缺氧实验。结果发现，急性缺氧后心肌组织中硒谷胱甘肽过氧化物酶（ＳｅＧＳＨｐｘ）活性明显降低，丙二醛（ＭＤＡ）含量减少，ＳｅＧＳＨｐｘ／ＭＤＡ比值下降。结果提示，急性低压缺氧后，心肌组织中的脂质过氧化反应并无明显增强，仅有心肌的潜在抗氧化能力降低。另外，急性低压缺氧后，心肌酶活力显著增高，说明急性低压缺氧对心肌有一定损伤作用。鉴于心肌脂质过氧化反应无明显增强，提示心肌损伤与脂质过氧化无明显相关。心肌酶活力增高的原因，可能是急性缺氧对心肌细胞直接作用的结果。
In order to observe the effects of acute severe hypobaric hypoxia on myocardial lipid peroxidation and myocardial enzymology, 39 adult healthy Wistar rats were subjected to acute hypobaric hypoxia. The results showed that after acute hypoxia, the activity of SeGSHpx in myocardium was decreased, MDA content and SeGSHpx / MDA ratio decreased. The results suggest that acute hypobaric hypoxia, myocardial lipid peroxidation did not significantly enhanced, only the potential of myocardial antioxidant capacity decreased. In addition, acute hypobaric hypoxia, myocardial enzyme activity was significantly higher, indicating that acute hypoxia hypoxia has a certain role in myocardial injury. In view of myocardial lipid peroxidation was no significant increase, suggesting that myocardial injury and lipid peroxidation was not significantly correlated. Increased myocardial enzyme activity may be the result of a direct effect of acute hypoxia on cardiomyocytes.