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作 者:周玉峰[1] 黄梅[2] 邓聪颖[1] 汤立新[1]
机构地区:[1]中国人民解放军第324医院神经外科,重庆400020 [2]重庆通信学院门诊部,重庆400035
出 处:《热带医学杂志》2011年第6期644-646,共3页Journal of Tropical Medicine
摘 要:目的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99mTc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NO2-、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氧合酶(nitric oxide synthase,NOS)活性。结果急性缺氧导致左右心室心肌血流量、血浆和心肌血NO2-、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),血球压积(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参与了急性缺氧时心肌血流量的调节,以NO的扩血管作用为主。Objective The article was to investigate the roles of nitric oxide (NO) and enothelin-1 (ET-1) in regulation of myocardial blood flow (MBF) during acute hypoxia. Methods Rats were divided into normoxic group (Control) and acute hypoxia(AH) group. MBF was measured with 9^mTc radiolabelled toad red blood cell. The changes of myocardial NO2- and ET- 1 contents, nitric oxide synthase (NOS) activity were observed. Results Acute hypoxia caused an increase in left and right ventricular MBF, myocardial NO2-, ET- 1 contents and NOS activity, but myocardial vascular resistance, the ratio of ET- I/ NO2- in the left and right ventricle were decreased, as compared with the control group. Conclusions NO and ET-I may be involved in the regulation of MBF in acute hypoxia, but the NO-dependent vasodilation was stronger than the ET-1-dependent vasoconstriction.
分 类 号:R540.47[医药卫生—心血管疾病]
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