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观察了急性缺氧和慢性间断性缺氧兔心肌血流量、心肌组织中腺苷和ｃＧＭＰ含量的变化及Ｎ￣ω－ＮＯ３－Ｌ－精氨酸（Ｌ－ＮＡ）阻断一氧化氮（ＮＯ）生成后的影响。结果表明，急性缺氧兔心肌血流量增加，心肌组织中腺苷和ｃＧＭＰ含量增高；静脉输入Ｌ－ＮＡ后，心肌血流量减少，同时心肌组织中ｃＧＭＰ含量降低，腺苷含量进一步增高。慢性缺氧免心肌血流量无明显变化，红细胞压积（Ｈｃｔ）增高；抑制ＮＯ合成后，右室心肌血流量减少，左室心肌血流量无明显变化。说明ＮＯ和腺苷均参与急性缺氧时冠状血管扩张机制；ＮＯ参与慢性缺氧兔心肌血管基础张力调节。
Acute hypoxia and chronic intermittent hypoxia were observed myocardial blood flow, myocardial tissue adenosine and cGMP content changes and N ~ ω-NO3-L-arginine (L-NA) block the nitric oxide (NO The effect after generation. The results showed that the myocardial blood flow of acute hypoxia increased and the content of adenosine and cGMP in myocardium increased. After L-NA infusion, the myocardial blood flow decreased and the content of cGMP in myocardium decreased and the content of adenosine increased further. Chronic hypoxia had no significant changes in myocardial blood flow and increased hematocrit (Hct). After inhibiting NO synthesis, the right ventricular myocardial blood flow decreased and left ventricular myocardial blood flow did not change significantly. NO and adenosine are involved in the mechanism of acute hypoxic coronary vasodilatation; NO involved in chronic hypoxic rabbit myocardium vascular tone.