Trimarco B, Chierchia S, Ricciardelli B, Cuocolo A, Volpe M, Saccá L, Condorelli M
Am J Physiol. 1984 May;246(5 Pt 2):H664-70. doi: 10.1152/ajpheart.1984.246.5.H664.
Experiments were performed to determine the effects of digitalis-induced stimulation of cardiac receptors on the coronary circulation. In chloralose-anesthetized dogs, left circumflex coronary artery was perfused at constant flow, and heart rate was maintained constant by electric pacing. Ouabain injection in the perfused coronary artery produced a significant decrease in coronary perfusion pressure. Epicardial application of lidocaine completely blocked the reflex response. Vagotomy also prevented this reflex response. Sympathetic blockade with intravenous guanethidine or intracoronary phentolamine partially reduced the reflex coronary vasodilatation. Intracoronary atropine also partially reduced the coronary vasodilator response to ouabain. The combined administration of guanethidine and atropine completely abolished the coronary reflex response. These data demonstrate that ouabain can evoke reflex coronary vasodilation by stimulating cardiac receptors. This reflex response is mediated by activating cholinergic vasodilator fibers and inhibiting sympathetic vasoconstrictor fibers.
进行实验以确定洋地黄诱导的心脏受体刺激对冠状动脉循环的影响。在氯醛糖麻醉的犬中,左旋冠状动脉以恒定流量灌注,通过电起搏使心率保持恒定。向灌注的冠状动脉注射哇巴因导致冠状动脉灌注压显著降低。在心外膜应用利多卡因可完全阻断反射反应。迷走神经切断术也可防止这种反射反应。静脉注射胍乙啶或冠状动脉内注射酚妥拉明进行交感神经阻滞可部分降低反射性冠状动脉扩张。冠状动脉内注射阿托品也可部分降低对哇巴因的冠状动脉扩张反应。胍乙啶和阿托品联合给药可完全消除冠状动脉反射反应。这些数据表明,哇巴因可通过刺激心脏受体引起反射性冠状动脉扩张。这种反射反应是通过激活胆碱能血管舒张纤维和抑制交感缩血管纤维介导的。