Bouhaddi M, Vuillier F, Fortrat J O, Cappelle S, Henriet M T, Rumbach L, Regnard J
Physiologie--Explorations Fonctionnelles Rénales and UPRES EA479 IFR133, Centre Hospitalier Universitaire, Besançon F-25030, France.
Auton Neurosci. 2004 Nov 30;116(1-2):30-8. doi: 10.1016/j.autneu.2004.06.009.
In idiopathic Parkinson's disease (PD), autonomic dysfunction is frequent, causing orthostatic hypotension. The respective roles of disease progression and dopaminergic treatment remain unclear. In this study, we investigated the autonomic control of cardiovascular functions and its relation to L-dopa therapy in both newly diagnosed (ND) and long-term-treated (LT) patients. Study subjects were: (1) nine ND patients never having undergone treatment with L-dopa; (2) 18 LT patients who had been receiving L-dopa treatment for a long period. ND patients were investigated before L-dopa treatment and after stabilization of their L-dopa dosage. LT patients were investigated once with their regular treatment and once after a 12-h interruption of L-dopa treatment; (3) nine healthy subjects served as controls. At each test session, blood pressure (BP), heart rate (HR), plasma catecholamines, heart rate variability (HRV), and spontaneous baroreflex sensitivity were assessed in the supine and upright positions. Before receiving L-dopa medication, ND patients had reduced E/I ratios (HR response/deep breathing) and lowered HRV when compared to controls; this was evidence of early effects of the disease on autonomic HR control. Introduction of L-dopa treatment reduced BP, HR, and plasma levels of adrenaline and noradrenaline. Similar changes were found in LT patients when contrasting the short-term treatment interruption and the usual L-dopa dosage. The treatment-linked increase in plasma dopamine also correlated with the decrease in noradrenaline. These results showed that mild impairment of autonomic cardiovascular control occurred early in the course of PD. They also provided evidence that the side effects of L-dopa aggravated the impairment of the autonomic control of BP and HR.
在特发性帕金森病(PD)中,自主神经功能障碍很常见,可导致直立性低血压。疾病进展和多巴胺能治疗各自的作用仍不清楚。在本研究中,我们调查了新诊断(ND)和长期治疗(LT)患者心血管功能的自主神经控制及其与左旋多巴治疗的关系。研究对象包括:(1)9名从未接受过左旋多巴治疗的ND患者;(2)18名长期接受左旋多巴治疗的LT患者。ND患者在左旋多巴治疗前及左旋多巴剂量稳定后进行调查。LT患者在常规治疗时及左旋多巴治疗中断12小时后各进行一次调查;(3)9名健康受试者作为对照。在每次测试期间,在仰卧位和直立位评估血压(BP)、心率(HR)、血浆儿茶酚胺、心率变异性(HRV)和自发性压力反射敏感性。在接受左旋多巴药物治疗前,与对照组相比,ND患者的E/I比值(HR反应/深呼吸)降低,HRV降低;这是疾病对自主神经HR控制早期影响的证据。左旋多巴治疗的引入降低了血压、心率以及肾上腺素和去甲肾上腺素的血浆水平。在对比短期治疗中断和常规左旋多巴剂量时,LT患者也发现了类似变化。与治疗相关的血浆多巴胺增加也与去甲肾上腺素的减少相关。这些结果表明,在PD病程早期就出现了自主神经心血管控制的轻度损害。它们还提供了证据表明左旋多巴的副作用加剧了血压和心率自主控制的损害。