*Department of Behavioral Biology, Johns Hopkins University, Baltimore, MD 21218, U.S.A.
Clin Sci (Lond). 2014 Feb;126(4):289-96. doi: 10.1042/CS20130222.
POTS (postural tachycardia syndrome) is a chronic form of OI (orthostatic intolerance). Neuropathic POTS is characterized by decreased adrenergic vasoconstriction, whereas hyperadrenergic POTS exhibits increased adrenergic vasoconstriction. We hypothesized that midodrine, an α1-adrenergic receptor agonist, would increase CVR (calf vascular resistance), decrease C(v) (calf venous capacitance) and decrease orthostatic tachycardia in neuropathic POTS, but not alter haemodynamics in hyperadrenergic POTS. A total of 20 POTS patients (12 neuropathic and eight hyperadrenergic), ages 12-20 years, participated in this randomized placebo-controlled double-blind cross-over study. Of these subjects, 15 were female. POTS subjects received 2 weeks of treatment with midodrine or placebo, with increased dosing from 2.5 to 10 mg three times daily. Following a 7-day drug-washout period, subjects received the cross-over treatment. HR (heart rate), MAP (mean arterial pressure), Q(calf) (calf blood flow) and CVR were measured supine and during 35° HUT (head-up tilt). C(v) was measured supine. In neuropathic POTS, midodrine decreased supine HR, Q(calf) and C(v), while increasing MAP and CVR compared with placebo. During HUT, in neuropathic POTS, midodrine decreased HR, Q(calf) and C(v), while increasing MAP and CVR. In hyperadrenergic POTS, placebo and midodrine both decreased upright HR and increased supine CVR. Placebo also increased supine C(v), compared with midodrine in hyperadrenergic POTS. Therefore midodrine improved postural tachycardia in neuropathic POTS by increasing CVR and decreasing Q(calf) and C(v), whereas these effects were not seen in hyperadrenergic POTS patients who experienced a placebo effect. This suggests that midodrine is probably an effective treatment for neuropathic POTS, but not for hyperadrenergic POTS.
体位性心动过速综合征（POTS）是一种慢性直立不耐受（OI）形式。神经源性 POTS 的特征是去甲肾上腺素能血管收缩减少，而高肾上腺素能 POTS 表现为去甲肾上腺素能血管收缩增加。我们假设米多君，一种α1-肾上腺素能受体激动剂，将增加小腿血管阻力（CVR），减少小腿静脉容量（Cv），并减少神经源性 POTS 的直立性心动过速，但不会改变高肾上腺素能 POTS 的血液动力学。共有 20 名 POTS 患者（12 名神经源性和 8 名高肾上腺素能），年龄 12-20 岁，参加了这项随机安慰剂对照双盲交叉研究。其中 15 名女性。POTS 患者接受米多君或安慰剂治疗 2 周，剂量从每天 2.5 次增加到 10 毫克。在 7 天的药物洗脱期后，患者接受了交叉治疗。心率（HR）、平均动脉压（MAP）、小腿血流量（Q（小腿））和 CVR 在仰卧位和 35°头高位倾斜（HUT）时测量。Cv 在仰卧位测量。在神经源性 POTS 中，与安慰剂相比，米多君降低了仰卧位 HR、Q（小腿）和 Cv，同时增加了 MAP 和 CVR。在 HUT 期间，在神经源性 POTS 中，米多君降低了 HR、Q（小腿）和 Cv，同时增加了 MAP 和 CVR。在高肾上腺素能 POTS 中，安慰剂和米多君都降低了直立 HR，增加了仰卧位 CVR。与高肾上腺素能 POTS 中的米多君相比，安慰剂还增加了仰卧位 Cv。因此，米多君通过增加 CVR 并降低 Q（小腿）和 Cv 来改善神经源性 POTS 的直立性心动过速，而这些作用在高肾上腺素能 POTS 患者中没有出现，他们经历了安慰剂效应。这表明米多君可能是治疗神经源性 POTS 的有效药物，但对高肾上腺素能 POTS 无效。
