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目的：本研究通过大鼠在慢性间断性缺氧状态下，持续给予L-精氨酸灌饲，动态观察其对大鼠肺循环和体循环的影响;方法：将大鼠随机分为三组：单纯缺氧组、缺氧给药组与正常对照组。用微导管插管分别测定各组大鼠的肺动脉与体循环的收缩压和舒张压;结果：单纯缺氧组与缺氧给药组的肺动脉压均高于正常对照组，除给药组第4周的肺动脉压外，均有显著性差异（P＜0.01、P＜0.05）。体循环压力各组间均无显著性差异（P＞0.05）。单纯缺氧组肺动脉压随缺氧时间延长而逐渐升高;缺氧给药组肺动脉压在第3周时明显下降，与单纯缺氧组比较有显著性差异（P＜0.01）;结论;内皮细胞是通过释放内皮衍生舒张因子（EDRF）而发挥调节肺血管张力的作用，机体急性缺氧时EDRF合成酶受到抑制，使内皮细胞EDRF释放减少，使肺血管收缩。L-精氨酸作为EDRF的合成前体，对缺氧性的肺血管收缩有一定抑制作用。给予L-精氨酸的补充，其作用的发挥有赖于内皮细胞结构和功能的完整。
OBJECTIVE: In this study, L-arginine was continuously fed into rats by chronic intermittent hypoxia to observe its effects on pulmonary circulation and systemic circulation. Methods: The rats were randomly divided into three groups: simple Hypoxia group, hypoxia group and normal control group. Pulmonary arterial and systemic systolic and diastolic blood pressure were measured by microcatheter cannulation. Results: Pulmonary arterial pressure was significantly higher in hypoxia group and hypoxia group than in control group Week pulmonary artery pressure, there was a significant difference (P <0.01, P <0.05). There was no significant difference between the groups in systemic pressure (P> 0.05). In hypoxia group, pulmonary arterial pressure gradually increased with the prolongation of hypoxia; pulmonary arterial pressure in hypoxia group decreased significantly at the third week, which was significantly different from that in the hypoxia group (P <0.01); Conclusions; Endothelium Cells release the endothelial-derived relaxing factor (EDRF) play a role in the regulation of pulmonary vascular tension, the body acute hypoxia EDRF synthase was inhibited, so that endothelial cell release of EDRF, the pulmonary vasoconstriction. As a synthetic precursor of EDRF, L-arginine has a certain inhibitory effect on hypoxic pulmonary vasoconstriction. Given L-arginine supplement, its role depends on the endothelial cell structure and function of integrity.