Lown B, Verrier R L, Rabinowitz S H
Am J Cardiol. 1977 May 26;39(6):890-902. doi: 10.1016/s0002-9149(77)80044-1.
Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.
脑刺激可引发多种心律失常，并降低心室易损阈值。在急性心肌缺血的动物中，此类刺激足以引发心室颤动。迷走神经冲动或肾上腺儿茶酚胺并非这种脑-心联系的传导途径。心率或血压的伴随升高并非心脏兴奋性改变的先决条件。交感神经活动增强，无论是由神经作用还是神经体液作用所诱发，都会使心脏易发生心室颤动。通过手术和药物去神经支配或反射性降低交感神经张力可实现保护作用。在急性心肌缺血时，增强的交感神经活动是导致早期异位活动激增并常引发心室颤动的原因。交感神经放电的不对称性也可能促成严重心律失常的发生。迷走神经通过其毒蕈碱样作用，对心脏易损性产生间接影响，这是消除伴随的肾上腺素能影响的结果，而非对心室有任何直接胆碱能作用。此类相互作用存在解剖学、生理学以及分子学基础。现有实验证据表明，多种类型的环境应激可损伤心脏，降低心脏对心室颤动的易损阈值，并在冠状动脉闭塞的动物中引发潜在的恶性室性心律失常。现有证据表明，在人类中，如同在实验动物中一样，给予儿茶酚胺可诱发室性心律失常，而迷走神经活动则产生相反的作用。此外，在某些个体中，多种应激和各种心理状态可引发室性异位活动。
