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在自主神经衰竭患者中,头高位倾斜期间腿部血管收缩并未消除。

Leg vasoconstriction during head-up tilt in patients with autonomic failure is not abolished.

机构信息

Department of Physiology, Radboud Univ. Nijmegen Medical Centre, PO Box 9101, Nijmegen 6500 HB, The Netherlands.

出版信息

J Appl Physiol (1985). 2011 Feb;110(2):416-22. doi: 10.1152/japplphysiol.01098.2010. Epub 2010 Dec 2.

Abstract

Maintaining blood pressure during orthostatic challenges is primarily achieved by baroreceptor-mediated activation of the sympathetic nervous system, which can be divided into preganglionic and postganglionic parts. Despite their preganglionic autonomic failure, spinal cord-injured individuals demonstrate a preserved peripheral vasoconstriction during orthostatic challenges. Whether this also applies to patients with postganglionic autonomic failure is unknown. Therefore, we assessed leg vasoconstriction during 60° head-up tilt in five patients with pure autonomic failure (PAF) and two patients with autonomic failure due to dopamine-β-hydroxylase (DBH) deficiency. Ten healthy subjects served as controls. Leg blood flow was measured using duplex ultrasound in the right superficial femoral artery. Leg vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. DBH-deficient patients were tested off and on the norepinephrine pro-drug l-threo-dihydroxyphenylserine (l-DOPS). During 60° head-up tilt, leg vascular resistance increased significantly in PAF patients [0.40 ± 0.38 (+30%) mmHg·ml(-1)·min(-1)]. The increase in leg vascular resistance was not significantly different from controls [0.88 ± 1.04 (+72%) mmHg·ml(-1)·min(-1)]. In DBH-deficient patients, leg vascular resistance increased by 0.49 ± 0.01 (+153%) and 1.52 ± 1.47 (+234%) mmHg·ml(-1)·min(-1) off and on l-DOPS, respectively. Despite the increase in leg vascular resistance, orthostatic hypotension was present in PAF and DBH-deficient patients. Our results demonstrate that leg vasoconstriction during orthostatic challenges in patients with PAF or DBH deficiency is not abolished. This indicates that the sympathetic nervous system is not the sole or pivotal mechanism inducing leg vasoconstriction during orthostatic challenges. Additional vasoconstrictor mechanisms may compensate for the loss in sympathetic nervous system control.

摘要

在直立挑战期间维持血压主要通过压力感受器介导的交感神经系统激活来实现,交感神经系统可分为节前和节后部分。尽管脊髓损伤患者存在节前自主神经功能衰竭,但在直立挑战期间仍表现出外周血管收缩的保留。这种情况是否也适用于节后自主神经功能衰竭的患者尚不清楚。因此,我们评估了 5 例纯自主神经衰竭(PAF)患者和 2 例因多巴胺-β-羟化酶(DBH)缺乏引起的自主神经衰竭患者在 60°头高位倾斜期间的腿部血管收缩,并将其与 10 名健康受试者作为对照。使用右股浅动脉的双功能超声测量腿部血流。腿部血管阻力通过动脉-静脉压力梯度除以血流来计算。DBH 缺乏患者在停用和使用去甲肾上腺素前体 l-苏氨酸-二羟基苯丙氨酸(l-DOPS)时进行测试。在 60°头高位倾斜期间,PAF 患者的腿部血管阻力显著增加[0.40±0.38(+30%)mmHg·ml(-1)·min(-1)]。腿部血管阻力的增加与对照组无显著差异[0.88±1.04(+72%)mmHg·ml(-1)·min(-1)]。在 DBH 缺乏患者中,停用和使用 l-DOPS 时,腿部血管阻力分别增加了 0.49±0.01(+153%)和 1.52±1.47(+234%)mmHg·ml(-1)·min(-1)。尽管腿部血管阻力增加,但 PAF 和 DBH 缺乏患者仍存在直立性低血压。我们的结果表明,PAF 或 DBH 缺乏患者在直立挑战期间腿部血管收缩并未被消除。这表明,交感神经系统不是在直立挑战期间引起腿部血管收缩的唯一或关键机制。其他血管收缩机制可能补偿了交感神经系统控制的丧失。

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