Goldstein David S, Pechnik Sandra, Holmes Courtney, Eldadah Basil, Sharabi Yehonatan
the Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md 20892-1620, USA.
Hypertension. 2003 Aug;42(2):136-42. doi: 10.1161/01.HYP.0000081216.11623.C3. Epub 2003 Jun 30.
Supine hypertension occurs commonly in primary chronic autonomic failure. This study explored whether supine hypertension in this setting is associated with orthostatic hypotension (OH), and if so, what mechanisms might underlie this association. Supine and upright blood pressures, hemodynamic responses to the Valsalva maneuver, baroreflex-cardiovagal gain, and plasma norepinephrine (NE) levels were measured in pure autonomic failure (PAF), multiple-system atrophy (MSA) with or without OH, and Parkinson's disease (PD) with or without OH. Controls included age-matched, healthy volunteers and patients with essential hypertension or those referred for dysautonomia. Baroreflex-cardiovagal gain was calculated from the relation between the interbeat interval and systolic pressure during the Valsalva maneuver. PAF, MSA with OH, and PD with OH all featured supine hypertension, which was equivalent in severity to that in essential hypertension, regardless of fludrocortisone treatment. Among patients with PD or MSA, those with OH had higher mean arterial pressure during supine rest (109+/-3 mm Hg) than did those lacking OH (96+/-3 mm Hg, P=0.002). Baroreflex-cardiovagal gain and orthostatic increments in plasma NE levels were markedly decreased in all 3 groups with OH. Among patients with PD or MSA, those with OH had much lower mean baroreflex-cardiovagal gain (0.74+/-0.10 ms/mm Hg) than did those lacking OH (3.13+/-0.72 ms/mm Hg, P=0.0002). In chronic autonomic failure, supine hypertension is linked to both OH and low baroreflex-cardiovagal gain [corrected]. The finding of lower plasma NE levels in patients with than without supine hypertension suggests involvement of pressor mechanisms independent of the sympathetic nervous system.
仰卧位高血压常见于原发性慢性自主神经功能衰竭。本研究探讨了在这种情况下仰卧位高血压是否与体位性低血压(OH)相关,如果相关,这种关联的潜在机制是什么。在纯自主神经功能衰竭(PAF)、伴有或不伴有OH的多系统萎缩(MSA)以及伴有或不伴有OH的帕金森病(PD)患者中测量了仰卧位和直立位血压、对瓦尔萨尔瓦动作的血流动力学反应、压力反射-心迷走神经增益以及血浆去甲肾上腺素(NE)水平。对照组包括年龄匹配的健康志愿者以及原发性高血压患者或因自主神经功能障碍就诊的患者。压力反射-心迷走神经增益通过瓦尔萨尔瓦动作期间心跳间期与收缩压之间的关系计算得出。PAF、伴有OH的MSA以及伴有OH的PD均有仰卧位高血压,无论是否接受氟氢可的松治疗,其严重程度与原发性高血压相当。在PD或MSA患者中,伴有OH的患者仰卧位休息时的平均动脉压(109±3 mmHg)高于不伴有OH的患者(96±3 mmHg,P = 0.002)。在所有伴有OH的三组患者中,压力反射-心迷走神经增益和血浆NE水平的体位性升高均明显降低。在PD或MSA患者中,伴有OH的患者平均压力反射-心迷走神经增益(0.74±0.10 ms/mm Hg)远低于不伴有OH的患者(3.13±0.72 ms/mm Hg,P = 0.0002)。在慢性自主神经功能衰竭中,仰卧位高血压与OH和低压力反射-心迷走神经增益[校正后]均有关联。与无仰卧位高血压的患者相比,有仰卧位高血压的患者血浆NE水平较低,这一发现提示存在独立于交感神经系统的升压机制参与其中。