Neural and psychologic mechanisms and the problem of sudden cardiac death

摘要: Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In animal with acute myocardial ischemia such stimuli suffice to fibrillation. Vagal neural traffic or adrenal catecholamines are not conduits for this brain-heart linkage. Accompanying increases in heart rate blood pressure prerequisites changes cardiac excitability. Increased sympathetic activity, whether induced by neurohumoral action, predisposes Protection be achieved surgical pharmacologic denervation reflex reduction tone. With ischemia, augmented activity accounts early surge ectopic frequently precipitating Asymmetries discharge may also contribute genesis serious arrhythmias. The vagus nerve, through its muscarinic exerts an indirect effect on vulnerability, consequence annulment concomitant adrenergic influence, rather than any direct cholinergic action ventricles. There exist anatomic, physiologic as well molecular bases interactions. Available experimental evidence indicates that environmental stresses diverse types injure heart, threshold vulnerability fibrillation and, coronary occlusion, potentially malignant man, animal, administration induce arrhythmia, whereas vagal opposite effect. Furthermore, certain subjects various psychologic states activity.