Schulz R, Guth B D, Heusch G
Abteilung für Herz-und Kreislaufphysiologie, Universität Düsseldorf, Federal Republic of Germany.
Cardiovasc Drugs Ther. 1989 Mar;3(1):43-56. doi: 10.1007/BF01881528.
Distal to a coronary stenosis, resting myocardial blood flow and function can be maintained by a compensatory dilation of the poststenotic vascular bed and an increased collateral blood flow from adjacent coronary vessels. Under this condition, electrical stimulation of cardiac sympathetic nerves, as well as their activation during sympathoexcitatory reflexes and exercise, induces a poststenotic alpha 2-adrenoceptor-mediated coronary constriction and a beta-adrenoceptor-mediated, tachycardia-related redistribution of blood flow away from the ischemia myocardium. Thus, activation of cardiac sympathetic nerves can precipitate poststenotic myocardial ischemia. In experimental studies in anesthetized, vagotomized dogs, as well as in conscious, chronically instrumented dogs, selective alpha 2-adrenoceptor antagonists and calcium-channel blockade with nifedipine were able to attenuate the sympathetically induced poststenotic myocardial ischemia. Beta-adrenoceptor blockade with atenolol was only proven beneficial as long as there was a heart-rate reduction. Conversely, a specific bradycardic agent (ULFS-49) also exerted beneficial effects. Myocardial ischemia can activate cardiac sympathetic afferents and then, by a spinal reflex, can in turn activate sympathetic efferents and aggravate the severity of myocardial ischemia. This vicious cycle could be interrupted by segmental epidural anesthesia with procaine as well as by blockade of sympathoexcitation at the central nervous level with clonidine in anesthetized dogs.
在冠状动脉狭窄的远端，静息心肌血流和功能可通过狭窄后血管床的代偿性扩张以及相邻冠状动脉侧支血流增加得以维持。在此情况下，心脏交感神经的电刺激，以及在交感兴奋反射和运动期间它们的激活，会诱发狭窄后α₂肾上腺素能受体介导的冠状动脉收缩以及β肾上腺素能受体介导的、与心动过速相关的血流从缺血心肌重新分布。因此，心脏交感神经的激活可引发狭窄后心肌缺血。在麻醉、迷走神经切断的犬类实验研究以及清醒、长期植入仪器的犬类实验中，选择性α₂肾上腺素能受体拮抗剂和硝苯地平的钙通道阻滞能够减轻交感神经诱导的狭窄后心肌缺血。只要心率降低，阿替洛尔的β肾上腺素能受体阻滞才被证明有益。相反，一种特定的心动过缓药物（ULFS - 49）也发挥了有益作用。心肌缺血可激活心脏交感传入神经，然后通过脊髓反射，进而激活交感传出神经并加重心肌缺血的严重程度。在麻醉犬中，普鲁卡因的节段性硬膜外麻醉以及可乐定在中枢神经水平对交感兴奋的阻滞可中断这种恶性循环。
