Key result
Gastric distension abolished the fall in systolic blood pressure induced by intraduodenal glucose (-3 vs -14 mmHg; P=0.01) and attenuated the rise in SMA blood flow in healthy older subjects.
Why the study?
Does gastric distension attenuate the fall in blood pressure and rise in superior mesenteric artery blood flow induced by intraduodenal glucose in healthy older subjects?
RCT (n=8)
random order
Does gastric distension attenuate the fall in blood pressure and rise in superior mesenteric artery blood flow induced by intraduodenal glucose in healthy older subjects?
Absolute Event Rate: -3% vs -14%
p-value: p=0.01
Gastric distension has the capacity to abolish the fall in blood pressure and attenuate the rise in superior mesenteric artery blood flow induced by intraduodenal glucose in healthy older subjects.
Gastric distension may blunt postprandial hypotension in older adults; extends mechanistic evidence on splanchnic flow regulation.
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.
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Vanis et al. (2010) conducted an RCT in Healthy older subjects (n=8). Gastric distension with intraduodenal glucose vs. Intraduodenal glucose alone, saline alone, and saline with distension was evaluated on Maximum change in systolic blood pressure (p=0.01). Gastric distension abolished the fall in systolic blood pressure induced by intraduodenal glucose (-3 vs -14 mmHg; P=0.01) and attenuated the rise in SMA blood flow in healthy older subjects.
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