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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
Objective: To investigate the role of long-term psychological stress in the formation of myocardial lipid peroxidation and myocardial ultrastructure in aged rats. Methods: The levels of myocardial lipid peroxides (LPO) in young rats (15 months old) and aged rats (15 months old) were measured after a six-week-long heterogeneous stressor (restraint, rotation and crowding) And superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) activity, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine phosphokinase (CPK) Changes in activity, observed under electron microscopy myocardial ultrastructure changes. Results: Compared with the young rats, LPO content was higher, SOD activity was lower and the activities of LDH and CPK were lower in old rats (P <0.05). After chronic multiphasic stress, LPO content in the aged rats (P <0 05). The damage of mitochondria membrane and sarcoplasmic reticulum and other membrane structures in aged rats were aggravated under electron microscope, while the activity of SOD in young rats increased (P <0. 05) 0 5), no obvious pathological changes of myocardial cells. CONCLUSION: Long-term stimulation of psychological stressors in the external environment may promote the formation of myocardial lipid peroxidation and myocardial ultrastructure damage in aged rats