心肌脂质过氧化与急性低压缺氧关系的实验研究

本文采用低压舱模拟7500m高空停留30min,造成体内重度缺氧.对39只成熟健康Wistar大鼠进行了心肌组织脂质过氧化及心肌酶学改变的观察.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,心肌酶活力显著增高.以上结果表明,急性低压缺氧对心肌有明显损伤,心肌的潜在抗氧化能力下降.但心肌脂质过氧化反应并无明显增强.结果表明,心肌损伤与脂质过氧化无明显相关.心肌酶活力明显增高的原因,可能是急性缺氧对心肌细胞直接作用的结果.

Laboratory investigation of the relationship between myocardial lipid peroxidation and acute hypobaric hypoxia.

SeGSHpx. MDA, SeGSHpx/MDA and various kinds of myocardial enzymes were measured in 30 adult healthy Wistar rats by staying at 7500m. for 30 mm. in a hypobaric chamber in order to observe the effect of acute hypoxia upon the myocardium and if there is any relationship between lipid peroxidation and myocardial damage. The results showed that after acute hypoxia, the activity of myocardial SeGSHpx and SeGSH-px/MDA ratio was decreased, the myocardial enzymes such as CPK, CK-B, LDH, a-HBD and AST weresignificantly increased, but the myocardial MDA content was decreased. Above results suggested, that acutehypobaric hypoxia was harmful to the myocardium, the potential anti-oxidative ability of the myocardium wasdecreased. but there was no intimate relationship between lipid peroxidation and myocardial damage. The pathogenesis of myocardial damage due to acute hypobaric hypoxia might be the direct results of acute hypoxia upon myocardial cells.