Popa Constantin, Popa Florian, Grigorean Valentin Titus, Onose Gelu, Sandu Aurelia Mihaela, Popescu Mihai, Burnei Gheorghe, Strambu Victor, Sinescu Crina
Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
J Med Life. 2010 Jul-Sep;3(3):275-85.
The aim of this article is to analyze the vascular dysfunctions occurring after spinal cord injury (SCI). Vascular dysfunctions are common complications of SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. Neuroanatomy and physiology of autonomic nervous system, sympathetic and parasympathetic, is reviewed. SCI implies disruption of descendent pathways from central centers to spinal sympathetic neurons, originating in intermediolateral nuclei of T1-L2 cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant vascular dysfunction. Spinal shock occurs during the acute phase following SCI and it is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe arterial hypotension and bradycardia. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Arterial hypotension with orthostatic hypotension occurs in both acute and chronic phases. The etiology is multifactorial. We described a few factors influencing the orthostatic hypotension occurrence in SCI: sympathetic nervous system dysfunction, low plasma catecholamine levels, rennin-angiotensin-aldosterone activity, peripheral alpha-adrenoceptor hyperresponsiveness, impaired function of baroreceptors, hyponatremia and low plasmatic volume, cardiovascular deconditioning, morphologic changes in sympathetic neurons, plasticity within spinal circuits, and motor deficit leading to loss of skeletal muscle pumping activity. Additional associated cardiovascular concerns in SCI, such as deep vein thrombosis and long-term risk for coronary heart disease and systemic atherosclerosis are also described. Proper prophylaxis, including non-pharmacologic and pharmacological strategies, diminishes the occurrence of the vascular dysfunction following SCI. Each vascular disturbance requires a specific treatment.
本文旨在分析脊髓损伤（SCI）后发生的血管功能障碍。血管功能障碍是SCI的常见并发症。心血管紊乱是SCI急性和慢性阶段发病和死亡的主要原因。本文回顾了自主神经系统（交感神经和副交感神经）的神经解剖学和生理学。SCI意味着从中枢到脊髓交感神经元的下行通路中断，这些交感神经元起源于T1-L2脊髓节段的中间外侧核。脊髓以上对交感神经系统控制的丧失导致损伤水平以下的整体交感神经活动降低，以及通过完整迷走神经的无对抗副交感神经流出。SCI伴有明显的血管功能障碍。脊髓休克发生在SCI后的急性期，是损伤水平以下功能和反射的短暂暂停。神经源性休克是脊髓休克的一部分，包括严重的动脉低血压和心动过缓。自主神经反射异常出现在慢性期，即脊髓休克消退后，是一种危及生命的综合征，发生在内脏交感神经流出（T5-T6）以上的SCI患者中，表现为大量反射性交感神经放电失衡。急性和慢性期均会出现伴有体位性低血压的动脉低血压。其病因是多因素的。我们描述了一些影响SCI患者体位性低血压发生的因素：交感神经系统功能障碍、血浆儿茶酚胺水平低、肾素-血管紧张素-醛固酮活性、外周α-肾上腺素能受体反应性过高、压力感受器功能受损、低钠血症和低血容量、心血管失健、交感神经元的形态学改变、脊髓回路的可塑性以及导致骨骼肌泵血活动丧失的运动功能障碍。本文还描述了SCI中其他相关的心血管问题，如深静脉血栓形成以及冠心病和全身性动脉粥样硬化的长期风险。适当的预防措施，包括非药物和药物策略，可减少SCI后血管功能障碍的发生。每种血管紊乱都需要特定的治疗。
