Schmid A, Huonker M, Stahl F, Barturen J M, König D, Heim M, Lehmann M, Keul J
Center for Internal Medicine, Department of Preventive and Rehabilitative Sports Medicine, University of Freiburg, Germany.
J Auton Nerv Syst. 1998 Jan 19;68(1-2):96-100. doi: 10.1016/s0165-1838(97)00127-6.
Spinal cord lesion leads to an interruption of pathways from brain to the peripheral sympathetic nervous system, which results in pathological changes in sympathetic innervation. Free epinephrine (E), norepinephrine (NE) and dopamine (DA) were measured in 30 tetraplegics (TETRA), 15 high-lesion paraplegics (T1 and T4, HPARA), 15 paraplegics with injuries between T5 and T10 (MPARA), 15 low-lesion paraplegics (below T10, LPARA) and 16 non-handicapped control persons (C) at rest, at 60 and 100% of maximal oxygen consumption during graded wheelchair ergometry (WCE). The TETRA showed significant lower E and NE levels at rest and only slight increases during physical exercise. The E and NE concentrations of the paraplegics with a lesion below T5 were significantly higher than those of the high-lesion paraplegics, as well as those of the control persons at every point in the study. All paraplegics and the control persons showed, at submaximal and maximal exercise, a significant increase in NE. Only a slight increase in E in HAPRA was shown. No differences were found at rest and during exercise in E and NE levels in the MPARA and LPARA. No significant differences were found in the dopamine concentration at rest or during exercise for any of the groups. In summary, different levels of lesion and the resulting interruption to sympathetic pathways in the spinal cord are decisive factors in the degree of impairment of sympathetic innervation in SCI persons. Tetraplegics show less preganglionic resting activity because of interruption of impulses from central centers and no considerable stimulation of the sympathetic nervous system during maximal exercise. Individuals with high paraplegia have a partial impairment of catecholamine release, especially of epinephrine, at rest and during exercise. Paraplegics with a lesion level below T5 showed an augmented basal and exercise-induced upper spinal thoracic sympathetic activity in comparison to control persons.
脊髓损伤会导致大脑与外周交感神经系统之间的通路中断,从而引起交感神经支配的病理变化。在30例四肢瘫痪患者(TETRA)、15例高位损伤截瘫患者(T1和T4,HPARA)、15例T5至T10之间损伤的截瘫患者(MPARA)、15例低位损伤截瘫患者(T10以下,LPARA)以及16名非残疾对照者(C)处于静息状态、在分级轮椅运动试验(WCE)中耗氧量达到最大耗氧量的60%和100%时,测定了游离肾上腺素(E)、去甲肾上腺素(NE)和多巴胺(DA)。四肢瘫痪患者在静息时E和NE水平显著较低,在体育锻炼期间仅有轻微升高。损伤低于T5的截瘫患者的E和NE浓度在研究的每个时间点均显著高于高位损伤截瘫患者以及对照者。所有截瘫患者和对照者在次最大和最大运动时,NE均显著增加。高位截瘫患者仅显示E有轻微增加。中低位截瘫患者在静息和运动时E和NE水平未发现差异。任何组在静息或运动时多巴胺浓度均未发现显著差异。总之,不同的损伤水平以及脊髓交感神经通路的相应中断是脊髓损伤患者交感神经支配受损程度的决定性因素。四肢瘫痪患者由于中枢冲动中断,节前静息活动较少,在最大运动时交感神经系统无明显刺激。高位截瘫患者在静息和运动时儿茶酚胺释放存在部分受损,尤其是肾上腺素。与对照者相比,损伤水平低于T5的截瘫患者显示出基础和运动诱导的上胸段脊髓交感神经活动增强。