Rosen S G, Cryer P E
Am J Med. 1982 May;72(5):847-50. doi: 10.1016/0002-9343(82)90559-9.
A patient with disabling postural tachycardia without postural hypotension had symptoms that included palpitations, weakness, abdominal and leg pain, light-headedness, headache and diaphoresis that occurred only in the upright position. She was shown to have an enhanced sympathetic neural response to standing (exaggerated plasma nor epinephrine response), and her cardiovascular responsiveness to released catecholamines was clearly intact. However, she was unable to maintain normal sodium balance and had a measurably reduced plasma volume while consuming normal amounts (120 mmol daily) of dietary sodium. Sodium loading (240 mmol ingested daily plus administration of fluorohydrocortisone, 0.1 mg daily) largely corrected the hemodynamic abnormalities, prevented postural symptoms and caused the compensatory sympathetic response to revert to normal.
一名患有无体位性低血压的致残性体位性心动过速的患者，其症状包括心悸、虚弱、腹部和腿部疼痛、头晕、头痛和多汗，这些症状仅在直立位时出现。研究表明，她对站立的交感神经反应增强（血浆去甲肾上腺素反应过度），并且她对释放的儿茶酚胺的心血管反应性明显完好。然而，她无法维持正常的钠平衡，在摄入正常量（每日120 mmol）的膳食钠时，血浆容量明显减少。钠负荷（每日摄入240 mmol并每日给予0.1 mg氟氢可的松）在很大程度上纠正了血流动力学异常，预防了体位性症状，并使代偿性交感神经反应恢复正常。
