Kaye David, Esler Murray
Wynn Department of Metabolic Cardiology, Baker Heart Research Institute, PO Box 6492 St. Kilda Road Central, Melbourne, Vic 8008, Australia.
Cardiovasc Res. 2005 May 1;66(2):256-64. doi: 10.1016/j.cardiores.2005.02.012.
The documentation of preferential activation of the cardiac sympathetic outflow in patients with heart failure swept aside an entrenched notion that there was a functional sympathetic denervation of the failing heart and provided a theoretical basis for the clinical evaluation of beta-adrenergic blocker therapy in this condition. The demonstration that heightened sympathetic nervous system activity is central to the pathogenesis and progression of congestive heart failure (CHF) has now led to the rational use of beta-adrenoceptor blockade in CHF. More recently, it has also emerged that the aging heart exhibits some of the characteristic changes in autonomic control which are seen in CHF. Accordingly, alterations in cardiac sympathetic nerve function are now thought to contribute also to the pathophysiology of the aging heart. Furthermore, there is evidence that in humans, sympathoexcitatory rostral projections of brainstem noradrenergic neurons to the forebrain are important in the sympathetic nervous activation of both heart failure and aging. Given these similarities, in this review we compare and contrast the neurobiology of the sympathetic nervous system in the failing heart and the healthy, aging heart, and consider whether the sympathetic activation accompanying aging may, perhaps, underlie and contribute to the neural pathophysiology of heart failure. Our conclusion is, on balance, that this proposition is not supported by the available evidence.
心力衰竭患者心脏交感神经传出支优先激活的相关记录推翻了一个根深蒂固的观念，即衰竭心脏存在功能性交感神经去神经支配，并为这种情况下β-肾上腺素能阻滞剂治疗的临床评估提供了理论基础。交感神经系统活动增强是充血性心力衰竭（CHF）发病机制和病情进展的核心这一观点的证实，现已促使人们合理使用β-肾上腺素能受体阻滞剂治疗CHF。最近还发现，衰老心脏表现出一些在CHF中可见的自主神经控制特征性变化。因此，现在认为心脏交感神经功能改变也参与了衰老心脏的病理生理学过程。此外，有证据表明，在人类中，脑干去甲肾上腺素能神经元向前脑的交感兴奋投射在心力衰竭和衰老的交感神经激活中都很重要。鉴于这些相似之处，在本综述中，我们比较并对比了衰竭心脏和健康衰老心脏中交感神经系统的神经生物学，并探讨衰老伴随的交感神经激活是否可能是心力衰竭神经病理生理学的基础并促成其发展。我们的结论是，总体而言，现有证据不支持这一观点。
