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吸烟对大鼠肺动脉压和一氧化氮合酶的影响 被引量:3

The effect of cigarette smoke on the pulmonary artery pressure and Nitric oxide synthase
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摘要 目的 :探讨长期吸烟对大鼠肺动脉压及一氧化氮合酶的影响。方法 :SD雄性大鼠 40只 ,随机分为吸烟组和对照组 ,吸烟组暴露于点燃之烟卷 ,每日 6 h,于 9个月时检测吸烟组及对照组大鼠的肺动脉平均压 (m PAP)、血清一氧化氮 (NO)、肺动脉结构型一氧化氮合酶 (c NOS)和诱导型一氧化氮合酶 (i NOS)。结果 :吸烟组大鼠 m PAP明显高于对照组 ,血清 NO浓度与对照组相比明显减低 ,吸烟组肺细小动脉 c NOS平均吸光度值较对照组明显降低 ,吸烟组大鼠肺细小动脉 i NOS的平均吸光度值较对照组明显增高。结论 :烟雾可致肺动脉高压的形成 ,抑制肺细小动脉 c NOS表达、促进肺细小动脉 i NOS表达可能为其重要作用机制之一。 AIM: To investigate the effect of cigarette smoke on the pulmonary artery pressure and nitric oxide synthase. METHODS:Forty mature male rats were used to study the effect of long time cigarette smoke, the pulmonary artery pressure,NO in serum,cNOS and iNOS were measured in pulmonary artery smooth muscle cell. RESULTS:After 9 months exposure,the smoke rats′ mPAP and iNOS increased,while NO in serum and cNOS decreased. CONCLUSION: Smoke may be the cause of pulmonary hypertension, depressing the cNOS and increasing the iNOS may be one of the mechanism.
作者 栗艳 阎露
出处 《心脏杂志》 CAS 2001年第3期183-184,共2页 Chinese Heart Journal
关键词 吸烟 肺动脉压 一氧化氮合酶 cigarette smoke pulmonary artery pressure nitric oxide synthase
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参考文献4

  • 1Mcquillan LP,Leung GK,Marsden PA,et al.Hypoxia inhibits expression of eNOS via transcriptional and posttranscriptional mechanisms[].American Journal of Physiology.1994
  • 2Giaid A,Saleh D.Reduced expression of endothelial nitric oxide synthase in the lung of patients with pulmonary hypertension[].The New England Journal of Medicine.1995
  • 3Steudel W,Scherrer-Crosbie M,Bloch KD,et al.Sustained pulmonary hypertension and right ventricular hypertrophy after chronic hypoxia in mice with congenital deficiency of nitric oxide synthase 3[].The Journal of Clinical Investigation.1998
  • 4Smith JD,Mclean SD,Nakayama DK,et al.Nitric oxide causes apoptosis in pulmonary vascular smooth muscle cell[].Journal of Surgical Research.1998

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