Macefield Vaughan G
School of Medicine, University of Western Sydney Sydney, NSW, Australia.
Front Physiol. 2012 May 23;3:153. doi: 10.3389/fphys.2012.00153. eCollection 2012.
Because the cardiovascular system and respiration are so intimately coupled, disturbances in respiratory control often lead to disturbances in cardiovascular control. Obstructive Sleep Apnea (OSA), Chronic Obstructive Pulmonary Disease (COPD), and Bronchiectasis (BE) are all associated with a greatly elevated muscle vasoconstrictor drive (muscle sympathetic nerve activity, MSNA). Indeed, the increase in MSNA is comparable to that seen in congestive heart failure (CHF), in which the increase in MSNA compensates for the reduced cardiac output and thereby assists in maintaining blood pressure. However, in OSA - but not COPD or BE - the increase in MSNA can lead to hypertension. Here, the features of the sympathoexcitation in OSA, COPD, and BE are reviewed in terms of the firing properties of post-ganglionic muscle vasoconstrictor neurons. Compared to healthy subjects with low levels of resting MSNA, single-unit recordings revealed that the augmented MSNA seen in OSA, BE, COPD, and CHF were each associated with an increase in firing probability and mean firing rates of individual neurons. However, unlike patients with heart failure, all patients with respiratory disease exhibited an increase in multiple within-burst firing which, it is argued, reflects an increase in central sympathetic drive. Similar patterns to those seen in OSA, COPD, and BE were seen in healthy subjects during an acute increase in muscle vasoconstrictor drive. These observations emphasize the differences by which the sympathetic nervous system grades its output in health and disease, with an increase in firing probability of active neurons and recruitment of additional neurons being the dominant mechanisms.
由于心血管系统与呼吸密切相关，呼吸控制的紊乱常常导致心血管控制的紊乱。阻塞性睡眠呼吸暂停（OSA）、慢性阻塞性肺疾病（COPD）和支气管扩张症（BE）均与肌肉血管收缩驱动力（肌肉交感神经活动，MSNA）大幅升高有关。事实上，MSNA的增加与充血性心力衰竭（CHF）中所见的情况相当，在CHF中，MSNA的增加可补偿心输出量的减少，从而有助于维持血压。然而，在OSA中——而非COPD或BE中——MSNA的增加可导致高血压。在此，根据节后肌肉血管收缩神经元的放电特性，对OSA、COPD和BE中交感神经兴奋的特征进行综述。与静息MSNA水平较低的健康受试者相比，单单位记录显示，在OSA、BE、COPD和CHF中观察到的增强的MSNA均与单个神经元的放电概率和平均放电率增加有关。然而，与心力衰竭患者不同，所有呼吸系统疾病患者均表现出爆发内多次放电增加，有人认为这反映了中枢交感神经驱动力的增加。在肌肉血管收缩驱动力急性增加期间，健康受试者也出现了与OSA、COPD和BE中所见相似的模式。这些观察结果强调了交感神经系统在健康和疾病状态下调节其输出的差异，其中活跃神经元放电概率的增加和额外神经元的募集是主要机制。
