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作 者:陈成水[1] 郑禄珍[2] 龚永生[2] 陈静炯[2] 陈少贤[1]
机构地区:[1]温州医学院附属第一医院肺科 [2]温州医学院附属第一医院肺心病研究室
出 处:《中国临床药理学与治疗学》2003年第5期554-556,共3页Chinese Journal of Clinical Pharmacology and Therapeutics
摘 要:目的 :探讨慢性缺O2 高CO2 性肺动脉高压形成中 ,一氧化氮 (NO)的作用及其对内皮素释放的影响。方法 :取雄性SD大鼠 2 9只 ,分 4组 :对照组 ,缺O2 高CO2 组 ,缺O2 高CO2 +L 精氨酸组 (L Arg) ,缺O2 高CO2 +NW 硝基 L 精氨酸甲酯 +L 精氨酸组(L NAME)。除对照组外其他组动物置入常压低O2高CO2 舱内饲养 ,每天 1 0h,共 3 0d。到规定时间分别测定其肺动脉压力和血浆内皮素 1 (ET 1 )含量 ,并分析肺动脉压力和血浆ET 1含量的相关性。结果 :缺O2 高CO2 组及L NAME组肺动脉平均压(mPAP)均高于对照组 (P <0 .0 0 1 )及L Arg组 (P <0 .0 5 ,0 .0 1 ) ;但缺O2 高CO2 组与L NAME组之间mPAP无统计学差异 ;L Arg组mPAP显著高于对照组 (P <0 .0 5 )。缺O2 高CO2 组血浆ET 1与L NAME组比较无统计学差异 ,但两组均高于对照组(P <0 .0 5 )及L Arg组 (P <0 .0 5 ) ;L Arg组与对照组血浆ET 1则无统计学差异。相关分析显示mPAP与血浆ET 1含量之间呈正相关 (r =0 .768,P <0 .0 5 )。结论 :NO前体物L 精氨酸通过NO抑制ET 1释放 ,调节慢性缺O2 高CO2 性肺动脉高压。AIM: To investigate the role of nitric oxide (NO) in development of pulmonary artery hypertension and the effects of NO on the release of endothelin 1 (ET 1) in rats with pulmonary hypertension and with chronic hypoxia and hypercapnia. METHODS: Twenty nine rats were divided into four groups: the control group; the hypoxia hypercapnia group; the hypoxia hypercapnia group +L Arg group (L Arg), intraperitoneal injection of L Arg (500 mg·kg -1 ) every day for 1 month and the hypoxia hypercapnia group +L Arg+L NAME group (L NAME), intraperitoneal injection of L Arg (500 mg·kg -1 ) and L NAME (5 mg·kg -1 ) every day for 1 month. All these rats except those in the control group were exposed to hypoxia hypercapnia 10 hours each day for 1 month. Mean pulmonary artery pressure (mPAP) and ET 1 in plasma were detected in these rats. And the relationship between mPAP and ET 1 was analyzed. RESULTS: The values of mPAP in the hypoxia hypercapnia group and L NAME groups were higher than those in the control group (P< 0.001 ) and L Arg (P< 0.05 , or 0.01 ) groups; the value of mPAP in the L Arg group was higher than that in the control group (P< 0.05 ). There was no difference in ET 1 between the hypoxia hypercapnia group and the L NAME group (P> 0.05 ), and the same between the L Arg group and the control group (P> 0.05 ). But the levels of ET 1 were higher in the hypoxia hypercapnia group and L NAME groups than those in the control group (P< 0.001 ) and L Arg groups (P< 0.05 , or 0.01 ). There was positive correlation between mPAP and ET 1 (r= 0.768 , P< 0.05 ). CONCLUSION: NO can inhibit the release of ET 1, and downregulate the pressure of pulmonary artery in rats with chronic hypoxica and hypercapnica.
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