缺氧时心肌血流量的变化及一氧化氮和内皮素-1的调节作用

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。

Roles of nitric oxide and endothelin-1 in regulation of myocardial bood flow during acute hypoxia

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.