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. 2000 Jul;47(1):30–36. doi: 10.1136/gut.47.1.30

Effect of atropine on proximal gastric motor and sensory function in normal subjects

I Lidums 1, G Hebbard 1, R Holloway 1
PMCID: PMC1727959  PMID: 10861261

Abstract

BACKGROUND AND AIMS—Distension of the proximal stomach is a major stimulus for triggering transient lower oesophageal sphincter (LOS) relaxations. We have shown recently that atropine inhibits triggering of transient LOS relaxations in both normal subjects and patients with gastro-oesophageal reflux disease. Atropine could potentially act centrally by inhibiting the central integrating mechanism in the brain stem, or act peripherally by altering the response of the stomach to distension. The aim of this study was to investigate the effect of atropine on fasting gastric compliance and postprandial gastric tone using an electronic barostat.
METHODS—Fasting and postprandial proximal gastric motor and sensory functions were assessed in 10 normal healthy volunteers. Oesophageal manometry and pH were simultaneously measured. On separate days, atropine (15 µg/kg bolus, 4 µg/kg/h intravenous infusion) or saline was given and maintained for the duration of the recording period.
RESULTS—In the fasting period, atropine significantly reduced minimum distending pressure (5.5 (0.4) v 4.4 (0.4) mm Hg; p<0.005) and increased proximal gastric compliance (81.3 (5.3) v 102.1 (8.7) ml/ mm Hg; p<0.05). In response to a meal, maximal gastric relaxation was similar on both study days. However, during atropine infusion, there was no recovery of proximal gastric tone in the two hour postprandial observation period. Postprandial fullness scores were higher during atropine infusion and correlated with changes in intrabag volume. Atropine significantly reduced the rate of postprandial transient LOS relaxations: first hour, 7.0 (5.3-10.0) v 3.0 (1.0-4.0) (p<0.02); second hour, 5.0 (3.3-5.8) per hour v 1.0 (0-3.0) per hour (p<0.05).
CONCLUSIONS—In humans, fasting and postprandial proximal gastric motor function is under cholinergic control. Atropine induced inhibition of transient LOS relaxations is unlikely to be caused by its effect on the proximal stomach, but rather by a central action on the integrating mechanisms in the brain stem.


Keywords: barostat; compliance; gastric fundus; atropine

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Figure 1  .

Figure 1  

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Diagrammatic illustration of the combined manometric and barostat assembly (left) and a cross sectional view of the assembly (right).

Figure 2  .

Figure 2  

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Effect of atropine or saline on heart rate for the duration of the infusion period . Data are expressed as mean (SEM).

Figure 3  .

Figure 3  

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Effect of atropine on the pressure-volume relationship of the proximal stomach during pressure controlled (A) and volume controlled (B) distension. Data are expressed as mean (SEM). *p<0.05 v saline. MDP, minimum distending pressure.

Figure 4  .

Figure 4  

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Effect of atropine on postprandial changes in proximal gastric volume. Data are expressed as mean (SEM). *p<0.05 v saline.

Figure 5  .

Figure 5  

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Effect of atropine on postprandial fullness (A) and hunger (B) scores. Data are expressed as mean (SEM). *p<0.05 v saline.

Figure 6  .

Figure 6  

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Effect of atropine on the number of transient lower oesophageal sphincter relaxations (TLOSRs). Data are expressed as median (interquartile range). *p<0.05 v saline.

Figure 7  .

Figure 7  

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Effect of atropine on the number of postprandial reflux episodes. Data are expressed as median (interquartile range). *p<0.05 v saline.

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