Kirshenbaum L A, Singal P K
Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Man., Canada.
Can J Physiol Pharmacol. 1992 Oct;70(10):1330-5. doi: 10.1139/y92-186.
Because hypertrophied rat hearts display an increase in antioxidant enzyme activities and because hypoxia-reoxygenation injury is known to involve free radicals, we tested the hypothesis that the hypertrophied heart may be more resistant to this type of injury. Hypertrophied rat hearts after 10 weeks of chronic pressure overload showed elevated superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) activities and a decrease in lipid peroxidation as indicated by malondialdehyde (MDA) content. Glucose-free hypoxia for 15 min resulted in a complete failure of developed tension and about 200% increase in resting tension in both hypertrophied and sham control groups (p < 0.05). Upon reoxygenation for up to 30 min, hypertrophied hearts recovered developed tension to 60% and resting tension was higher by only 80% of prehypoxic values. In contrast, sham hearts showed only a 25% recovery of developed tension, whereas resting tension remained 130% higher than prehypoxic control values. During hypoxia, the SOD activity was significantly reduced in both sham and hypertrophied groups, whereas GSHPx was reduced only in the sham group. Upon reoxygenation there was no further change in these enzyme activities. Both the SOD and GSHPx activities in the hypertrophied group remained significantly higher than the corresponding reoxygenated sham hearts. During hypoxia, there was no apparent change in MDA content in either the sham or hypertrophied hearts. However, reoxygenation resulted in a significant increase in MDA content in both sham and hypertrophied hearts, but the MDA content was significantly less in the hypertrophied group (p < 0.05). It is suggested that maintenance of an adequate endogenous antioxidant reserve during hypoxia may be important in recovery upon reoxygenation.
由于肥大的大鼠心脏显示抗氧化酶活性增加，且已知缺氧-复氧损伤涉及自由基，我们检验了以下假设：肥大的心脏可能对这种类型的损伤更具抵抗力。慢性压力超负荷10周后的肥大大鼠心脏，超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSHPx）活性升高，丙二醛（MDA）含量表明脂质过氧化作用降低。在肥大组和假手术对照组中，无糖缺氧15分钟导致舒张张力完全丧失，静息张力增加约200%（p<0.05）。复氧长达30分钟后，肥大心脏的舒张张力恢复到60%，静息张力仅比缺氧前值高80%。相比之下，假手术心脏的舒张张力仅恢复25%，而静息张力仍比缺氧前对照值高130%。在缺氧期间，假手术组和肥大组的SOD活性均显著降低，而GSHPx仅在假手术组降低。复氧后这些酶活性没有进一步变化。肥大组的SOD和GSHPx活性仍显著高于相应的复氧假手术心脏。在缺氧期间，假手术心脏和肥大心脏的MDA含量均无明显变化。然而，复氧导致假手术心脏和肥大心脏的MDA含量均显著增加，但肥大组的MDA含量显著较低（p<0.05）。提示缺氧期间维持足够的内源性抗氧化储备可能对复氧后的恢复很重要。
