Verrier R L, Lown B
Acta Med Scand Suppl. 1982;660:57-68. doi: 10.1111/j.0954-6820.1982.tb00361.x.
Earlier research in the field of sudden cardiac death is reviewed. Such studies have largely oriented towards the provocation of myocardial injury and asystole in normal animals. However, such investigations constitute an inadequate model to describe the clinical appearance of sudden death, where underlying coronary disease is often present and the precipitating event is usually ventricular fibrillation rather than asystole. This report describes a series of studies designed to investigate the processes underlying cardiac vulnerability and the influence upon it of various psychological stresses. It is concluded that the primary mediator of ventricular vulnerability is the sympathetic nervous system. The efferent vagus appears to exert some protective influence against arrhythmias due to adrenergic stimulation. An appropriate clinical strategy for the treatment of malignant arrhythmias would therefore involve attempts to decrease cardiac sympathetic drive whilst at the same time enhancing vagal tone. Treatments are described which aim to bring this situation about by the use of clonidine, morphine sulphate, l-tryptophan and tyrosine. The use of neurochemical agents in this context appears promising.
本文回顾了早期在心脏性猝死领域的研究。此类研究主要致力于在正常动物中诱发心肌损伤和心搏停止。然而，此类研究不足以描述猝死的临床表现，因为猝死往往存在潜在的冠状动脉疾病，且促发事件通常是室颤而非心搏停止。本报告描述了一系列旨在研究心脏易损性的潜在机制以及各种心理应激对其影响的研究。研究得出结论，心室易损性的主要介导因素是交感神经系统。传出迷走神经似乎对肾上腺素能刺激引起的心律失常具有一定的保护作用。因此，治疗恶性心律失常的合适临床策略应包括尝试降低心脏交感神经驱动，同时增强迷走神经张力。文中描述了通过使用可乐定、硫酸吗啡、L-色氨酸和酪氨酸来实现这一目标的治疗方法。在这种情况下使用神经化学药物似乎前景广阔。
