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郝文君, 白小涓. 兔动脉粥样硬化不同阶段一氧化氮及合酶观察[J]. 中国公共卫生, 2005, 21(4): 444-446. DOI: 10.11847/zgggws2005-21-04-36
引用本文: 郝文君, 白小涓. 兔动脉粥样硬化不同阶段一氧化氮及合酶观察[J]. 中国公共卫生, 2005, 21(4): 444-446. DOI: 10.11847/zgggws2005-21-04-36
HAO Wenjun, BAI Xiaojuan. Observation of rabbit nitric oxide and its synthase in different phases of atherosclerosis[J]. Chinese Journal of Public Health, 2005, 21(4): 444-446. DOI: 10.11847/zgggws2005-21-04-36
Citation: HAO Wenjun, BAI Xiaojuan. Observation of rabbit nitric oxide and its synthase in different phases of atherosclerosis[J]. Chinese Journal of Public Health, 2005, 21(4): 444-446. DOI: 10.11847/zgggws2005-21-04-36

兔动脉粥样硬化不同阶段一氧化氮及合酶观察

Observation of rabbit nitric oxide and its synthase in different phases of atherosclerosis

  • 摘要:
      目的   探讨一氧化氮(NO)及其合酶(NOS)在动脉粥样硬化(AS)病程中的变化.
      方法   在高胆固醇饮食基础上建立兔AS模型.在实验不同阶段, 观察各组兔主动脉壁NOS活力、NO含量、全血超氧化物歧化酶(SOD)活力及血清脂质浓度的变化, 并进行病理形态学观察.
      结果   模型组血清总胆固醇(TC)、低密度脂蛋白胆固醇(LDLC)、甘油三酯(TG)的浓度、主动脉壁NOS活力及NO含量均高于对照组(P < 0.01), 全血SOD活力则明显低于对照组(P < 0.01).模型组内比较显示NOS活力及NO含量于实验16周达峰值, 此后呈下降趋势; 全血SOD活力逐渐下降, 各阶段差异有统计学意义(P < 0.05).
      结论   在AS发生、发展过程中, 动脉壁NOS活力增强, NO合成增多, 并于纤维斑块期达峰值.

     

    Abstract:
      Objective   To observe the changes of nitric ox ide(NO)and its synthase in the pathogenesis of atherosclero sis.
      Methods   36 male New Zealand white rabbits were divided into control group and model group(fed with 1% cholesterol and 2% pig oil)at random.At the time of 8, 16, 24 weeks, serum lipid concentrations Nitric ox ide synthase(NOS)activity, NO production and blood superox ide dismutase(SOD)activity were detected, and pathologic changes were observed.
      Results   Compared with control group, serum TC, LDLC concentrations, aortic NOS activity and NO production in model group in creased(P < 0.01), but SOD activity decreased markedly(P < 0.01).In model groups, TC, LDLC concentrations increased, SOD activity decreased gradually with the progress of experiment(P < 0.05), NOS activity and NO production reached the peak at 16 weeks.
      Conclusion   With the progress of atherosclerosis, NOS activity and NO production were enhanced, and they reached the peak at the phase of fiberous plaque.

     

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