缺氧时ET-1、NO、TXA_2、PGI_2的变化及对心肌血流量的调节作用  

Roles of nitric oxdire,enddothelin-1,thromboxane A2 and prostacyclin regulation of myocardial bood flow during acute hypoxia

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：《中国实验诊断学》2010年第10期1518-1520,共3页Chinese Journal of Laboratory Diagnosis

摘　　要：目的本文旨在探讨ET-1、NO、TXA2和PGI2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法测量NO-、用放免法分别测量ET-1、TXA2、PGI2的含量。结果急性缺氧导致左、右心室心肌血流量、心肌NO2-、ET-1、血浆TXB2含量、TXB2/6-keto-PGF1ɑ比值明显增高(P<0.05),左、右心室心肌血管阻力、ET-1/NO2-比值明显下降(P<0.05),血浆6-keto-PGF1ɑ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、TXA2/PGI2参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）、enothelin-1（ET-1）、thromboxane A2（TXA2） and prostacyclin （PGI2） in regulation of myocardial blood flow（MBF） during acute hypoxia.Methods Rats were divided into normoxic group（Control） and acute hypoxia（AH）,MBF wre measures with 99m Tc radiolabelled toad RBC,the changes of myocardial NO-2、ET-1 contents and plasm TXB2、6keto-PGF1ɑ contents were observed.Results Acute hypoxia caused an increase in left and right ventricular MBF、myocardial NO-2、ET-1contents、plasm TXB2 contents and the ratio of TXB2/6-keto-PGF1ɑ,myocardial vascular resistance and the ratio of ET-1/ NO-2 in the left and right ventricle were decreased,but plasm 6-keto-PGF1ɑ weren＇t changed,as compared with the control group.Conclusion NO/ET-1、TXA2 /PGI2 may be involved in the regulation of MBF in acute hypoxia,but the NO-dependent vasodilation was stronger than the ET-1、TXA2-dependent vasoconstriction.

关 键 词：大鼠 缺氧 心肌血流量 一氧化氮 内皮素-1 血栓素A2 前列环素 

分 类 号：R285.5[医药卫生—中药学]