Univ. of Adelaide Discipline of Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, Australia.
Am J Physiol Regul Integr Comp Physiol. 2012 Feb 15;302(4):R391-9. doi: 10.1152/ajpregu.00464.2011. Epub 2011 Nov 30.
The postprandial reduction in blood pressure (BP) is triggered by the interaction of nutrients with the small intestine and associated with an increase in splanchnic blood flow. Gastric distension may attenuate the postprandial fall in BP. The aim of this study was to determine the effects of differences in intragastric volume, including distension at a low (100 ml) volume, on BP and superior mesenteric artery (SMA) blood flow responses to intraduodenal glucose in healthy older subjects. BP and heart rate (HR; automated device), SMA blood flow (Doppler ultrasound), mesenteric vascular resistance (MVR), and plasma norepinephrine of nine male subjects (65-75 yr old) were measured after an overnight fast on 4 separate days in random order. On each day, subjects were intubated with a nasoduodenal catheter, incorporating a duodenal infusion port, and orally with a second catheter, incorporating a barostat bag, positioned in the fundus. Each subject received a 60-min (t = 0-60 min) intraduodenal glucose infusion (3 kcal/min) and gastric distension at a volume of 1) 0 ml (V0), 2) 100 ml (V100), 3) 300 ml (V300), or 4) 500 ml (V500). Systolic BP fell (P < 0.05) during V0, but not during V100, V300, or V500. In contrast, HR (P < 0.01) and SMA blood flow (P < 0.001) increased and MVR decreased (P < 0.05) comparably on all 4 days. Plasma norepinephrine rose (P < 0.01) in response to intraduodenal glucose, with no difference between the four treatments. There was a relationship between the areas under the curve for the change in systolic BP from baseline with intragastric volume (r = 0.60, P < 0.001). In conclusion, low-volume (≤100 ml) gastric distension has the capacity to abolish the fall in BP induced by intraduodenal glucose in healthy older subjects without affecting SMA blood flow or MVR. These observations support the concept that nonnutrient gastric distension prior to a meal has potential therapeutic applications in the management of postprandial hypotension.
餐后血压(BP)降低是由营养物质与小肠相互作用触发的,与内脏血流增加有关。胃扩张可能会减弱餐后血压下降。本研究旨在确定胃内体积差异(包括低体积 100ml 扩张)对健康老年人十二指肠内葡萄糖引起的血压和肠系膜上动脉(SMA)血流反应的影响。9 名男性受试者(65-75 岁)在 4 天内以随机顺序进行了 4 次试验,在禁食过夜后,使用自动设备测量血压和心率(HR)、SMA 血流(多普勒超声)、肠系膜血管阻力(MVR)和血浆去甲肾上腺素。在每一次试验中,受试者都通过鼻十二指肠导管(内置十二指肠输注端口)和口腔内的另一个导管(内置测压囊)进行插管,导管位于胃底。每位受试者接受 60 分钟(t=0-60 分钟)的十二指肠内葡萄糖输注(3kcal/min)和胃扩张,体积分别为 1)0ml(V0)、2)100ml(V100)、3)300ml(V300)或 4)500ml(V500)。在 V0 期间,收缩压下降(P<0.05),但在 V100、V300 或 V500 期间没有下降。相反,HR(P<0.01)和 SMA 血流(P<0.001)在所有 4 天都有类似的增加,MVR 降低(P<0.05)。十二指肠内葡萄糖引起的血浆去甲肾上腺素升高(P<0.01),4 种处理之间无差异。收缩压从基线变化的曲线下面积与胃内体积之间存在关系(r=0.60,P<0.001)。结论:低容量(≤100ml)胃扩张有能力消除健康老年人十二指肠内葡萄糖引起的血压下降,而不影响 SMA 血流或 MVR。这些观察结果支持这样一种概念,即在餐前进行非营养性胃扩张具有治疗餐后低血压的潜在应用。