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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。
Aims: This article aims to investigate the regulation of nitric oxide and endothelin-1 on myocardial blood flow during hypoxia. Methods: The rats were randomly divided into plain group and acute hypoxia group. The myocardial blood flow was measured by 99m Tc labeled toad red blood cells. The plasma and myocardial NO-2 and endothelin-1 levels were measured by Gess method and radioimmunoassay. ET-1), and the activity of nitric oxide synthase (NOS) was measured by dual-wavelength spectrophotometry. Results: Acute hypoxia caused left ventricular myocardial blood flow, NO-2, ET-1 and NOS activities in left ventricle and right ventricle increased significantly (P <0.05), left ventricular myocardial vascular resistance and myocardial ET-1 / NO2 ratio decreased significantly (P <0.05), Hct and ventricular weight index no significant change. CONCLUSION: In acute hypoxia, left ventricular and right ventricular myocardial blood flow increases. ET-1 and NO participate in the regulation of myocardial blood flow in the process of implicit hypoxia.