Key result
During 60° head-up tilt, leg vascular resistance increased by 30% in patients with pure autonomic failure, which was not significantly different from the 72% increase in healthy controls.
Why the study?
Is leg vasoconstriction during orthostatic challenges abolished in patients with postganglionic autonomic failure?
Observational (n=17)
Is leg vasoconstriction during orthostatic challenges abolished in patients with postganglionic autonomic failure?
Patients with postganglionic autonomic failure maintain leg vasoconstriction during orthostatic challenges, indicating that the sympathetic nervous system is not the sole mechanism for this response.
Preserved leg vasoconstriction in autonomic failure during tilt; challenges sympathetic exclusivity and leaves open non-neural mechanisms for prospective study.
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.
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Groothuis et al. (2010) conducted an observational in Autonomic failure (pure autonomic failure and dopamine-β-hydroxylase deficiency) (n=17). 60° head-up tilt vs. Healthy controls was evaluated on Leg vascular resistance during 60° head-up tilt. During 60° head-up tilt, leg vascular resistance increased by 30% in patients with pure autonomic failure, which was not significantly different from the 72% increase in healthy controls.
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