Feigl E O
Circ Res. 1975 Jul;37(1):88-95. doi: 10.1161/01.res.37.1.88.
The effect of sympathetic alpha-receptor coronary vasoconstriction on myocardial oxygen tension was studied in open- and closed-chest, chloralose-anesthetized dogs. Blood oxygen tension in the coronary sinus and blood flow in the circumflex coronary artery were continuously measured in a three-part experiment. With stimulation of the left stellate ganglion (15 Hz, 3 msec, 4-7 v, 90-second train) under vagotomy control conditions (part 1), heart rate, blood pressure, and coronary blood flow increased, but coronary sinus oxygen tension decreased from 19 mm Hg to 15 mm Hg. In part 2, beta-receptor blockade with propranolol (2.0 mg/kg. iv) in the same dogs blunted the positive inotropic and chronotropic effects of sympathetic stimulation; coronary alpha-receptor vasoconstriction was unmasked, and coronary sinus blood oxygen tension fell from 17 mm Hg to 11 mm Hg. Since increases in oxygen metabolism were blunted, it appeared that the decrease in coronary sinus oxygen tension was caused by alpha-receptor coronary artery vasoconstriction. This hypothesis was tested in part 3 by the addition of alpha-receptor blockade with Dibozane (3.0 mg/kg, iv). Sympathetic stimulation no longer resulted in a change in either coronary vascular resistance or coronary sinus oxygen tension. These results indicate that the fall in oxygen tension during beta-receptor blockade in part 2 was due to alpha-receptor coronary vasoconstriction. Thus, myocardial oxygen tension may be regulated by coronary sympathetic vasomotion as well as by myocardial oxygen metabolism and local vascular control mechanisms.
在氯醛糖麻醉的开胸和闭胸犬中，研究了交感α受体冠状动脉收缩对心肌氧张力的影响。在一个分为三个部分的实验中，持续测量冠状窦中的血氧张力和左旋冠状动脉中的血流。在迷走神经切断控制条件下（第1部分），刺激左侧星状神经节（15Hz，3毫秒，4 - 7伏，90秒串刺激），心率、血压和冠状动脉血流量增加，但冠状窦氧张力从19mmHg降至15mmHg。在第2部分中，用普萘洛尔（2.0mg/kg，静脉注射）对同一只犬进行β受体阻断，减弱了交感刺激的正性肌力和变时作用；冠状α受体血管收缩被揭示出来，冠状窦血氧张力从17mmHg降至11mmHg。由于氧代谢增加被减弱，似乎冠状窦氧张力的降低是由α受体冠状动脉收缩引起的。在第3部分中，通过静脉注射地布宗（3.0mg/kg）添加α受体阻断来检验这一假设。交感刺激不再导致冠状动脉阻力或冠状窦氧张力发生变化。这些结果表明，第2部分中β受体阻断期间氧张力的下降是由于α受体冠状动脉收缩所致。因此，心肌氧张力可能受冠状动脉交感血管运动以及心肌氧代谢和局部血管控制机制的调节。
