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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 To investigate the regulatory effect of nitric oxide and endothelin-1 on myocardial blood flow during hypoxia. Methods The rats were randomly divided into two groups: Placenta group and acute hypoxia group. The myocardial blood flow was measured by 99mTc labeled toad red blood cells. The levels of NO2-, ET-1 ), And the activity of nitric oxide synthase (NOS) was measured by dual-wavelength spectrophotometry. Results Acute hypoxia resulted in a significant decrease of blood flow in left and right ventricular myocardium, NO2-, ET-1 and NOS activity in plasma and myocardium (P <0.05) and vascular resistance and myocardial ET-1 / NO2- ratio in left and right ventricles P <0.05), hematocrit (Hct) and ventricular weight index no significant change. Conclusions In acute hypoxia, the blood flow of left and right ventricular myocardium is increased. ET-1 / NO is involved in the regulation of myocardial blood flow during acute hypoxia, with the vasodilator effect of NO being dominant.