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作 者:周玉峰[1] 万强[1] 谢增柱[1] 刘福玉[1] 廖为公
机构地区:[1]第三军医大学基础部,400038
出 处:《高原医学杂志》1999年第3期21-24,共4页Journal of High Altitude Medicine
摘 要:目的:本文旨在探讨一氧化氮和内皮素-1 在缺氧时对心肌血流量的调节作用。方法:大鼠随机分为平原组和急性缺氧组,用99m Tc标记蟾蜍红细胞测定心肌血流量,用Gess法和放免法分别测量血浆和心肌NO-2 、内皮素-1(endothelin-1,ET-1)含量、用双波长分光光度法测量一氧化氮合酶(nitric oxide synthase,NOS)活性。结果:急性缺氧导致左、右心室心肌血流量、血浆和心肌NO-2 、ET-1含量、NOS活性明显增高(P< 0.05),左、右心室心肌血管阻力和心肌ET-1/NO2 比值明显下降(P< 0.05),Hct及心室重量指数无明显变化。结论:急性缺氧时,左、右心室心肌血流量增加,ET-1、NO参与隐性缺氧时心肌血流量的调节,以NO的扩血管作用为主。The article was to investigate the roles of nitric oxide(NO)and endothelin 1(ET-1)in regulation of myocardial blood flow(MBF)during acute hypoxia.Methods:Rats were divided into normoxic group(Control)and acute hypoxia group(AH),MBF were measures with 99m TC radiolabelled toad RBC,the changes of myocardial NO - 2、ET 1 contents,nitric oxide synthase(NOS)activity were observed.Results:Acute hypoxia caused an increase in left and right ventricular MBF,myocardial NO - 2、ET 1 contents and NOS activity,but myocardial vascular resistance,the ratio of ET 1/NO - 2 in the left and right ventricle were decreased,as compared with the control group.Conclusions:NO and ET 1 may be involved in the regulation of MBF in acute hypoxia,but the NO-dependent vasodilation was stronger than the ET 1 dependent vasoconstriction.
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