【摘要】 目的 :探讨长期心理应激在老龄鼠心肌脂质过氧化形成和心肌超微结构损伤中的作用。方法 :观察经为期 6周的多相性应激源 (限制、旋转、拥挤 )刺激后 ,青龄鼠 (1 5月龄 )和老龄鼠 (15月龄 )心肌脂质过氧化物 (LPO)含量和超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH -PX)活性 ,以及心肌天门冬酸转氨酶 (AST)、乳酸脱氢酶 (LDH)、肌酸磷酸激酶 (CPK)活性的变化 ,观察电镜下心肌超微结构的改变。结果 :与青龄鼠比较 ,老龄鼠心肌LPO含量较高 ,SOD活性较低 ,LDH和CPK活性也较低 (P均 <0 0 5 ) ;慢性多相性应激后 ,老龄鼠心肌LPO含量进一步增高 ,SOD活性进一步降低 ,GSH -PX活性也下降 (均P <0 0 5 ) ;电镜下老龄鼠心肌细胞线粒体、肌质网等膜结构损伤加重 ,青龄鼠心肌SOD活性增高 (P <0 0 5 ) ,其心肌细胞未见明显病理改变。结论 :外界环境中心理应激源的长期刺激可能促进老龄鼠心肌脂质过氧化的形成和心肌超微结构破坏更多还原

【Abstract】 Objective: To investigate the effects of long term psychological stress on lipid peroxidation formation and ultrastructure in myocardium of aged mice. Methods: Lipid peroxidate (LPO) content, superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities and aspartate aminotransferase (AST), lactic dehydrogenase (LDH), creatine phosphokinase (CPK) activities were measured in myocardium of young (1.5 month) and aged (15 month) KM mice exposed to multiple stressors (restrain, rotation, crowding) for 6 weeks. Changes of myocardial ultrastructure were observed. Results: LPO content in myocardium was higher in the aged mice than in the young control mice, and SOD, LDH, CPK activities were lower in the former than in the latter (p<0.05). The aged stressed mice showed a significant increase in LPO content and decrease in SOD, GDH-PX activities in myocardium (p<0.05), while the young stressed mice showed a marked increase in SOD activity in myocardium (p<0.05). Profound injury changes in biomembrane, such as mitochondria and sarcoplasmic reticulum of myocardial ultrastructure were found in the aged stressed mice. In the young stressed mice, however, such changes were not found. Conclusions: The effects of aging on lipid peroxidation formation and ultrastructure damage in mice myocardium can be aggravated by long term exposure of the animals to psychological stressors from their external environment.更多还原