Merrill G F, Downey H F, Jones C E
Am J Physiol. 1986 Apr;250(4 Pt 2):H579-83. doi: 10.1152/ajpheart.1986.250.4.H579.
The hypothesis that adenosine mediates the coronary vasodilatory response to hypoxia was tested by determining if intracoronary infusion of the adenosine degrading enzyme, adenosine deaminase (ADA), would attenuate this response. Efficacy of ADA was also evaluated by examining its effect on the coronary responses to exogenous adenosine and to 20-s myocardial ischemia. Experiments were conducted in 14 anesthetized, open-chest dogs ventilated 3-5 min with 3% O2-5% CO2-92% N2 to induce systemic hypoxia. Under control, pre-ADA conditions, hypoxia (arterial PO2 19 +/- 2 mmHg) caused left anterior descending (LAD) coronary blood flow to increase from 100 +/- 12 to 382 +/- 47 ml X min-1 X 100 g-1 (+282%). After infusion of ADA (5 U X kg-1 X min-1 for 8-10 min) into the LAD, equally severe hypoxia (arterial PO2 18 +/- 3 mmHg) caused a significantly smaller increase in LAD flow, 79 +/- 9 to 234 +/- 41 ml X min-1 X 100 g-1 (+195%). Oxygen consumption in the LAD perfusion field was unchanged by hypoxia before ADA but fell significantly during hypoxia after ADA. ADA also attenuated significantly the coronary vasodilatory response to exogenous adenosine and to 20-s ischemia. The results of this investigation demonstrate a significant role of adenosine in the coronary vasodilatory response to systemic hypoxia.
通过测定冠状动脉内注入腺苷降解酶腺苷脱氨酶（ADA）是否会减弱这种反应，来检验腺苷介导冠状动脉对缺氧的血管舒张反应这一假说。还通过检查其对冠状动脉对外源性腺苷和20秒心肌缺血反应的影响，来评估ADA的功效。实验在14只麻醉开胸犬身上进行，用3% O₂-5% CO₂-92% N₂通气3 - 5分钟以诱导全身性缺氧。在对照、ADA注入前的条件下，缺氧（动脉血氧分压19±2 mmHg）使左前降支（LAD）冠状动脉血流量从100±12增加到382±47 ml·min⁻¹·100 g⁻¹（增加282%）。向LAD注入ADA（5 U·kg⁻¹·min⁻¹，持续8 - 10分钟）后，同样严重的缺氧（动脉血氧分压18±3 mmHg）使LAD血流量的增加显著减小，从79±9增加到234±41 ml·min⁻¹·100 g⁻¹（增加195%）。在ADA注入前，缺氧对LAD灌注区域的氧消耗没有影响，但在ADA注入后缺氧期间氧消耗显著下降。ADA还显著减弱了冠状动脉对外源性腺苷和20秒缺血的血管舒张反应。本研究结果表明腺苷在冠状动脉对全身性缺氧的血管舒张反应中起重要作用。
