摘要
为探讨应激引发老年心脏损害的机制，本实验从自由基角度研究了应激对老年小鼠心肌营养性血流（ＮＢＦ），氧自由基（ＯＦＲ）浓度，超氧化物歧化酶（ＳＯＤ）活性及丙二醛（ＭＤＡ）含量的影响，结果发现：应激前老年组与青年组相比，心肌ＮＢＦ（８６Ｒｂ摄取率％）无显著差异（ｐ＜０．０５）；而心肌ＯＦＲ浓度（ｈｇ１１，ｍｍ）显著升高（７．１７±２．６６，３．８３±３．５６，Ｐ＜０．０５）；ＭＤＡ含量（ｎｍｏｌ／１００ｍｇ，心肌）显著增加（６１．５±６．７，４７．３±６．３，Ｐ＜０．０１）；ＳＯＤ活性（Ｕ／１００ｍｇ，心肌）则显著下降（１０１．４±９．２，１１８．２±１４．４，Ｐ＜０．０５），提示应激前老年心肌已经存在失衡的自由基反应。与应激前水平相比，应激后老年组ＮＢＦ摄取率显著下降（１．６６±０．３２，１．０６±０．１７，Ｐ＜０．００１），ＯＰＲ浓度进一步显著上升（７．１７±２．６６，１０．５±２．９５，Ｐ＜０．０５），ＭＤＡ含量进一步显著增加（６１．５±６．７，７３．５±５．９，Ｐ＜０．０１），而ＳＯＤ活性则进一步下降（１０１．４±９．２，９０．３±８．１，Ｐ＜０．０５）。提示应激可导致老年心肌供血不足并使已经失衡的自由?
Effects of stress on myocardial nutritional blood flow (NBF), oxygen free radical (OFR)concentration, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content of aged mice were studied for exploring the mechanism by which the aged heart is damaged by stress reaction. Results (x±s) are as follows:(1) Before stress there was no difference in NBF between the elderly group (EG) and young control group (YG). OFR concentration and MDA content of EG were significantly higher than those of YG (OFR: 7. 17±2.66 vs 3.83±3.56, P<0.05; MDA:61.5±6.7 vs 47.3±6.3, P<0.01), while SOD activity of EG was lower than that of YG (101.4±9.2 vs 118.2±14.4, P<0.05), suggesting that imbalance of free radical reaction had already existed in the aged heart before stress.(2) After stress, compared with the pre-stress level of the EG itself, the NBF of EG decreased significantly (1.66±0.32 vs 1.06±0.17, P<0.001), the OFR concentration rose (7.17±2.66 vs 10.5±2.95, P<0.05), the MDA content increased (61.5±6.7 vs 73.5±5.9, P<0.01), while the SOD activity decreased (101.4±9.2 vs 90.3±8.1, P<0.05), suggesting that stress can give rise to myocardial ischemia and deteriorate the disturbed free radical reaction in the aged heart.
出处
《中国应用生理学杂志》
CAS
CSCD
1994年第3期221-224,共4页
Chinese Journal of Applied Physiology
基金
国家自然科学基金
关键词
应激
氧自由基
心脏病
老年人
stress
aged mice
nutritional blood flow
oxygen free radical
superoxide dismutase
malondialdehyde
