中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (2): 189-194.doi: 10.4103/1673-5374.177707

• 综述:脊髓损伤修复保护与再生 •    下一篇

脊髓损伤患者的心血管功能障碍

  

  • 出版日期:2016-02-15 发布日期:2016-02-15
  • 基金资助:

    美国NIH基金;美国国防部基金

Cardiovascular dysfunction following spinal cord injury

Elizabeth Partida, Eugene Mironets, Shaoping Hou, Veronica J. Tom   

  1. Spinal Cord Research Center, Department of Neurobiology & Anatomy, Drexel University College of Medicine, Philadelphia, PA, USA
  • Online:2016-02-15 Published:2016-02-15
  • Contact: Veronica J. Tom, Ph.D.,veronica.tom@drexelmed.edu.
  • Supported by:

    This work was supported by research grants to VJT from the National Institutes of Health (R01 NS085426) and the Department of Defense (W81XWH-14-1-060).

摘要:

脊髓损伤后常会发生感觉和植物神经功能障碍。特别是,高胸椎或颈椎脊髓损伤断棘上血管舒缩途径,
由于放松管制的交感神经导致血流动力学紊乱。交感神经兴奋性降低,脊髓损伤患者可能会出现低血压,心脏心律失常和低体温。在慢性期,中枢神经元和周围血管变化导致体位性低血压而危及生命自主神经反射异常。自主神经反射异常以发作性,大规模的交感神经放电的导致伴有心动过缓严重的高血压为主要特点。该综合征经常由损伤水平以下不愉快的内脏或感官刺激所导致。研究表明,神经生长因子诱导腰骶初级降钙素基因相关肽+芽生,提高脊髓固有的可塑性,有助脊髓损伤后交感神经兴奋。因此,脊柱内回路重组可能改变交感神经元的输入模式。为了防止自主神经反射异常的发生,需要有效的避免潜在的触发刺激。一旦刺激引起自主神经反射异常,血管扩张剂等药理学试剂注射可以减少动脉血压的尖峰。此外,需要明确脊髓损伤潜在的心血管功能障碍神经病理生理机制,以便更好地开发新的治疗方法,恢复血流动力学性能。

Abstract:

Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury (SCI). Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics
due to deregulated sympathetic outflow. As a result of the reduced sympathetic activity, patients with SCI may experience hypotension, cardiac dysrhythmias, and hypothermia post-injury. In the chronic phase, changes within the CNS and blood vessels lead to orthostatic hypotension and life-threatening autonomic
dysreflexia (AD). AD is characterized by an episodic, massive sympathetic discharge that causes severe hypertension associated with bradycardia. The syndrome is often triggered by unpleasant visceral or sensory stimuli below the injury level. Currently the only treatments are palliative – once a stimulus elicits
AD, pharmacological vasodilators are administered to help reduce the spike in arterial blood pressure. However, a more effective means would be to mitigate AD development by attenuating contributing mechanisms,
such as the reorganization of intraspinal circuits below the level of injury. A better understanding of the neuropathophysiology underlying cardiovascular dysfunction after SCI is essential to better develop novel therapeutic approaches to restore hemodynamic performance.

Key words: blood pressure, heart rate, autonomic dysreflexia, hypertension, bradycardia, spinal cord lesion, sprouting, plasticity, bladder distension, relay, sympathetic activity