Effects of gastric distension on blood pressure and superior mesenteric artery blood flow responses to intraduodenal glucose in healthy older subjects

Author:

Vanis Lora12,Gentilcore Diana12,Hausken Trygve34,Pilichiewicz Amelia N.1,Lange Kylie12,Rayner Christopher K.12,Feinle-Bisset Christine12,Meyer James H.1,Horowitz Michael12,Jones Karen L.12

Affiliation:

1. University of Adelaide, Discipline of Medicine, Royal Adelaide Hospital,

2. National Health and Medical Research Council Centre of Clinical Research Excellence in Nutritional Physiology, Interventions, and Outcomes, Adelaide, South Australia, Australia; and

3. Institute of Medicine, University of Bergen and

4. National Centre for Ultrasound in Gastroenterology, Haukeland University Hospital, Bergen, Norway

Abstract

Postprandial hypotension occurs frequently and is associated with increased morbidity. Gastric distension may attenuate the postprandial fall in blood pressure (BP). Using a barostat, we sought to determine the effects of gastric distension on BP, heart rate (HR), and superior mesenteric artery (SMA) blood flow responses to intraduodenal glucose in eight (6 men, 2 women) healthy older (65–75 yr old) subjects. BP and HR were measured using an automated device and SMA blood flow was measured using Doppler ultrasound on 4 days in random order. SMA blood flow was calculated using the radius of the SMA and time-averaged mean velocity. Subjects were intubated with a nasoduodenal catheter incorporating a duodenal infusion port. On 2 of the 4 days, they were intubated orally with a second catheter, incorporating a barostat bag, positioned in the fundus and set at 8 mmHg above minimal distending pressure. Each subject received a 60-min (0–60 min) intraduodenal infusion of glucose (3 kcal/min) or saline (0.9%); therefore, the four study conditions were as follows: intraduodenal glucose + barostat (glucose + distension), intraduodenal saline + barostat (saline + distension), intraduodenal glucose (glucose), and intraduodenal saline (saline). Systolic and diastolic BP fell during glucose compared with saline ( P = 0.05 and P = 0.003, respectively) and glucose + distension ( P = 0.01 and P = 0.05, respectively) and increased during saline + distension compared with saline ( P = 0.04 and P = 0.006, respectively). The maximum changes in systolic BP were −14 ± 5, +11 ± 2, −3 ± 4, and +15 ± 3 mmHg for glucose, saline, glucose + distension, and saline + distension, respectively. There was an increase in HR during glucose and glucose + distension (maximum rise = 14 ± 2 and 14 ± 3 beats/min, respectively), but not during saline or saline + distension. SMA blood flow increased during glucose and glucose + distension (2,388 ± 365 and 1,673 ± 187 ml/min, respectively), but not during saline, and tended to decrease during saline + distension (821 ± 115 and 864 ± 116 ml/min, respectively). In conclusion, gastric distension has the capacity to abolish the fall in BP and attenuate the rise in SMA blood flow induced by intraduodenal glucose in healthy older subjects.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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