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目的:观察慢性持续性温和刺激、间断强刺激制作的老龄大鼠“郁证”模型心血管活性物质一氧化氮(NO)、内皮素-1(ET-1)水平及胸主动脉超微结构的改变。方法:Wistar老龄大鼠共24只,随机分为空白对照组、间断强刺激干预组、慢性持续性温和刺激干预组。适应性喂养后,分别给予两组刺激干预组大鼠慢性持续性温和刺激和间断高强度刺激(均包括冰水游泳、热刺激、禁食、禁水、夹尾、昼夜颠倒、高速水平摇晃、频闪灯照射等,但程度及频次不同)。之后观察大鼠体重变化、糖水偏嗜度等一般情况;检测血管活性物质(NO、ET-1)水平;电镜下观察胸主动脉超微结构变化。结果:分别给予慢性持续性温和刺激、间断强刺激56 d后,两组不同刺激干预组与空白对照组比较,体重上升幅度、糖水偏嗜度均有降低趋势,但无明显差异(P>0.05)。两组不同刺激干预组与空白对照组比较,慢性持续性温和刺激干预组NO水平明显升高(P<0.05);慢性持续性温和刺激干预组ET-1水平明显升高(P<0.05)。电镜下观察胸主动脉超微结构发现:空白组及慢性持续性温和刺激干预组胸主动脉超微结构未见明显变化。间断强刺激干预组胸主动脉线粒体、内皮细胞发生了改变。结论:慢性持续性温和刺激制作的“郁证”老龄大鼠模型心血管活性物质(NO、ET-1)表达的改变更明显,而间断高强度制作的“郁证”老龄大鼠模型则可出现主动脉内皮的损伤。
Objective: To observe the levels of nitric oxide (NO), endothelin-1 (ET-1) and the content of thoracic aorta in aged rats with chronic persistent mild stimulation and intermittent strong stimulation Microstructure changes. Methods: Twenty-four Wistar old rats were randomly divided into blank control group, intermittent strong stimulation group and chronic persistent mild stimulation group. After adaptive feeding, the rats in both groups were stimulated with chronic persistent mild stimulation and intermittent high-intensity stimulation (including ice water swimming, thermal stimulation, fasting, water forbidden, pinching tail, circling day and night, shaking at high speed, Strobe light irradiation, but the degree and frequency of different). The changes of body weight, glycemic index and so on were observed. The levels of NO and ET-1 were measured. The ultrastructure of thoracic aorta was observed under electron microscope. Results: After chronic persistent mild stimulation and intermittent stimulation for 56 days, weight gain and glyphosate bias both decreased compared with the control group, but there was no significant difference (P> 0.05 ). Compared with the blank control group, the levels of NO in the chronic stimulation group and the chronic stimulation group were significantly increased (P <0.05); ET-1 level was significantly increased in the chronic persistent mild stimulation group (P <0.05). The ultrastructure of thoracic aorta was observed under electron microscope. The ultrastructure of thoracic aorta in blank group and chronic persistent mild stimulation group showed no significant changes. Intermittent strong stimuli intervention thoracic aorta mitochondria, endothelial cells have changed. CONCLUSION: The changes of the expression of cardiovascular activity substance (NO, ET-1) in aging rat model with chronic persistent mild stimulation are more obvious, while the intermittent high- Aortic endothelial injury can occur in murine models.