Hakusui S, Sugiyama Y, Iwase S, Hasegawa Y, Koike Y, Mano T, Takahashi A
Department of Neurology, Nagoya University School of Medicine, Japan.
Neurology. 1991 May;41(5):712-5. doi: 10.1212/wnl.41.5.712.
To clarify the mechanism of postprandial hypotension (PPH), we made microneurographic analyses of patients with PPH and 10 healthy controls by recording multi-unit vasoconstrictive impulses of muscle sympathetic nerve activity (MSNA) directly from the tibial nerve fascicles during a glucose tolerance test. Oral intake of 75 grams glucose in 225 ml of water produced significant and prolonged hypotension in all patients and an increase in MSNA in all healthy subjects. Insulin and glucose responses were not significantly correlated with arterial blood pressure reduction. PPH was prevented by an infusion of vasopressin (0.3 U/min) given before glucose intake. These results suggest that PPH is caused by the lack of sympathetic compensation for the systemic hypotensive stress of splanchnic blood pooling that occurs after food ingestion, and that prior treatment with vasopressin reduces the portal venous flow by constricting the splanchnic vessels in patients with PPH.
为阐明餐后低血压（PPH）的机制，我们对PPH患者和10名健康对照者进行了微神经图分析，在葡萄糖耐量试验期间直接从胫神经束记录肌肉交感神经活动（MSNA）的多单位血管收缩冲动。口服225毫升水中含75克葡萄糖会使所有患者出现显著且持续时间较长的低血压，而所有健康受试者的MSNA增加。胰岛素和葡萄糖反应与动脉血压降低无显著相关性。在摄入葡萄糖前输注血管加压素（0.3 U/分钟）可预防PPH。这些结果表明，PPH是由于食物摄入后内脏血液淤积引起的全身低血压应激缺乏交感神经代偿所致，并且预先用血管加压素治疗可通过收缩PPH患者的内脏血管来减少门静脉血流。
