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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。
Objective: To investigate the effects of long-term smoking on pulmonary arterial pressure and nitric oxide synthase in rats. Methods: Forty male Sprague-Dawley rats were randomly divided into smoking group and control group. The smoking group was exposed to the cigarette smoke for 6 hours a day, and the mean pulmonary artery pressure (m PAP, NO, c NOS and iNOS. Results: The m PAP in smoking group was significantly higher than that in control group. The serum NO concentration was significantly lower than that in control group. The average value of c NOS in smoking group was significantly lower than that in control group. In smoking group, the iNOS The average absorbance value was significantly higher than the control group. Conclusion: The smoke may cause the formation of pulmonary hypertension, inhibit the expression of c NOS in pulmonary arterioles and promote the expression of i NOS in pulmonary arterioles, which may be one of the important mechanisms.