Draghici Adina E, Taylor J Andrew
Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, United States; Cardiovascular Research Laboratory, Spaulding Rehabilitation Hospital, Cambridge, MA, United States.
Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, United States; Cardiovascular Research Laboratory, Spaulding Rehabilitation Hospital, Cambridge, MA, United States.
Auton Neurosci. 2018 Jan;209:37-42. doi: 10.1016/j.autneu.2017.08.007. Epub 2017 Aug 18.
The arterial baroreflex is a primary regulator of autonomic outflow to effectively regulate acute changes in blood pressure. After a spinal cord injury (SCI), regulation of autonomic function is disrupted, although the damage of the autonomic pathways may not necessarily be related to the severity of injury (i.e. level and completeness). Nonetheless, it can be assumed that there would be greater loss of sympathetic innervation with higher level of injury and that cardiac parasympathetic control would remain intact regardless of injury level. In those with SCI, impaired baroreflex regulation has implications not only for adequate pressure regulation, but also for long term cardiovascular health. In this review, we discuss the expected impact ofan SCI on baroreflex control and the studies that have investigated baroreflex sensitivity in this population. The data generally indicates that baroreflex sensitivity is lesser in those with chronic injuries. However, these findings are counter to the expected effect of an SCI and hence may indicate that the effect of an SCI on baroreflex control might be secondary to long term deconditioning and/or vascular stiffening of baroreceptive arteries. Furthermore, the alterations in the ability to regulate pressure do not impact the relationship between spontaneous heart rate and blood pressure variabilities. In addition, those with SCI are not adequately able to control blood pressure changes in response to orthostasis, resulting in frank hypotension in a significant proportion of those with high level injuries.
动脉压力反射是自主神经输出的主要调节机制，可有效调节血压的急性变化。脊髓损伤（SCI）后，自主神经功能的调节会受到干扰，尽管自主神经通路的损伤不一定与损伤的严重程度（即损伤平面和完整性）相关。尽管如此，可以推测，损伤平面越高，交感神经支配的丧失就越严重，而无论损伤平面如何，心脏副交感神经控制都将保持完整。在脊髓损伤患者中，压力反射调节受损不仅对血压的适当调节有影响，而且对长期心血管健康也有影响。在这篇综述中，我们讨论了脊髓损伤对压力反射控制的预期影响以及研究该人群压力反射敏感性的研究。数据总体表明，慢性损伤患者的压力反射敏感性较低。然而，这些发现与脊髓损伤的预期效果相反，因此可能表明脊髓损伤对压力反射控制的影响可能继发于长期失用和/或压力感受性动脉的血管硬化。此外，压力调节能力的改变并不影响自发心率与血压变异性之间的关系。此外，脊髓损伤患者不能充分控制因直立位引起的血压变化，导致相当比例的高位损伤患者出现明显的低血压。
