Eckberg D L
Med Hypotheses. 1984 Dec;15(4):421-32. doi: 10.1016/0306-9877(84)90158-0.
Beta-adrenergic blocking drugs prolong lives of post-infarction patients primarily by preventing sudden cardiac death. The mechanisms responsible for this beneficial effect are not understood clearly, since beta-blockers, in doses used in most clinical trials, are only weakly effective against stable ventricular arrhythmias. Arrhythmias during myocardial ischemia may differ from arrhythmias in other clinical settings in that they depend importantly upon autonomic neural factors, including the balance between levels of sympathetic cardiac stimulation and parasympathetic cardiac inhibition. Beta-blockers reduce sympathetic cardiac stimulation, and they may influence this balance favorably in another important way: a well documented, but not generally appreciated property of beta-blocking drugs is that they also increase levels of vagal cardiac inhibition. I propose that beta-blockade prevents arrhythmic deaths in post-infarction patients in part by increasing levels of vagal cardiac inhibition.
β-肾上腺素能阻断药物主要通过预防心脏性猝死来延长心肌梗死后患者的生命。这种有益作用的机制尚不清楚，因为在大多数临床试验中使用的剂量下，β受体阻滞剂对稳定型室性心律失常的疗效甚微。心肌缺血期间的心律失常可能与其他临床情况下的心律失常不同，因为它们在很大程度上依赖于自主神经因素，包括交感神经对心脏的刺激水平与副交感神经对心脏的抑制水平之间的平衡。β受体阻滞剂可减少交感神经对心脏的刺激，并且它们可能以另一种重要方式对这种平衡产生有利影响：β受体阻断药物的一种有充分文献记载但未得到普遍认识的特性是，它们还会增加迷走神经对心脏的抑制水平。我提出，β受体阻断在一定程度上通过增加迷走神经对心脏的抑制水平来预防心肌梗死后患者的心律失常性死亡。
