Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
J Neurol. 2013 Feb;260(2):475-83. doi: 10.1007/s00415-012-6660-x. Epub 2012 Sep 15.
Postprandial hypotension (PPH) is a major clinical problem in patients with autonomic failure such as that observed in multiple system atrophy (MSA). The pathophysiology of PPH remains unclear, although autonomic dysfunction and gastrointestinal vasoactive peptides have been suspected to participate in its pathogenesis. We measured blood pressure and plasma levels of glucose, insulin, noradrenaline, neurotensin, glucagon-like peptide (GLP)-1 and GLP-2 before and after meal ingestion in 24 patients with MSA to reveal the roles of the autonomic nervous system and gastrointestinal vasoactive peptides in PPH. We performed a second meal-ingestion test by administering acarbose to evaluate the effects of acarbose (an α-glucosidase inhibitor) on PPH and vasoactive peptides in 14 patients with MSA and PPH. We also evaluated blood pressure responses to the head-up tilt test and heart rate variability in all the patients. Severities of PPH and orthostatic hypotension were significantly correlated. Patients with PPH had significantly worse orthostatic hypotension and lower heart rate variability than those without PPH. Postprandial GLP-1 secretion was higher in patients with PPH than in those without PPH. No significant differences were observed in the postprandial increases in plasma levels of glucose, insulin, noradrenaline, neurotensin or GLP-2. Acarbose significantly attenuated postprandial hypotension and tended to decrease GLP-2 secretion. Our results indicate that autonomic failure is involved in the pathogenesis of PPH and confirm that acarbose has a preventive effect against PPH in patients with MSA. Decreased postprandial secretion of GLP-2, which increases intestinal blood pooling, may attenuate PPH in patients with MSA.
餐后低血压（PPH）是自主神经衰竭患者的主要临床问题，如多系统萎缩（MSA）中观察到的那样。尽管自主神经功能障碍和胃肠道血管活性肽被怀疑参与其发病机制，但 PPH 的病理生理学仍不清楚。我们在 24 例 MSA 患者中测量了餐前和餐后的血压和血糖、胰岛素、去甲肾上腺素、神经降压素、胰高血糖素样肽（GLP）-1 和 GLP-2 水平，以揭示自主神经系统和胃肠道血管活性肽在 PPH 中的作用。我们在 14 例 MSA 和 PPH 患者中进行了第二次餐后摄入试验，给予阿卡波糖以评估阿卡波糖（α-葡萄糖苷酶抑制剂）对 PPH 和血管活性肽的影响。我们还评估了所有患者的直立倾斜试验和心率变异性的血压反应。PPH 和直立性低血压的严重程度呈显著相关性。有 PPH 的患者比没有 PPH 的患者的直立性低血压更严重，心率变异性更低。PPH 患者餐后 GLP-1 分泌高于无 PPH 患者。餐后血糖、胰岛素、去甲肾上腺素、神经降压素或 GLP-2 水平升高无显著差异。阿卡波糖显著减轻餐后低血压，并倾向于降低 GLP-2 分泌。我们的结果表明自主神经衰竭参与了 PPH 的发病机制，并证实阿卡波糖对 MSA 患者的 PPH 具有预防作用。餐后 GLP-2 分泌减少可能会减轻 MSA 患者的 PPH，因为 GLP-2 会增加肠道血液淤积。
