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. 1997 Sep;41(3):285–290. doi: 10.1136/gut.41.3.285

Atropine inhibits gastric distension and pharyngeal receptor mediated lower oesophageal sphincter relaxation

R Mittal 1, C Chiareli 1, J Liu 1, R Holloway 1, W Dixon 1
PMCID: PMC1891504  PMID: 9378379

Abstract

Background—Atropine decreases the frequency of transient lower oesophageal sphincter relaxation (TLOSR) through an unknown mechanism. Gastric distension and pharyngeal receptor excitation are two possible sources for the afferent stimulus responsible for TLOSR. 
Aims—To determine whether atropine affects gastric distension induced TLOSR and pharyngeal receptor mediated lower oesophageal sphincter (LOS) relaxation. 
Methods—Oesophageal manometry and pH recordings were performed in 10 healthy volunteers on two separate days in the postprandial setting, following either atropine (15 µg/kg intravenous bolus and 4 µg/kg/h as a maintenance dose) or placebo. Pharyngeal receptor mediated LOS relaxation was studied in nine subjects by rapid injection of minute amounts of water (0.05, 0.1, 0.2, 0.3, and 0.4 ml) in the pharynx before and after atropine. Gastric distension mediated TLOSR was studied in eight subjects by insufflating the stomach with 300, 600 and 900 ml of CO2 before and after atropine. 
Results—Atropine reduced the frequency of spontaneous gastro-oesophageal reflux and TLOSR compared with placebo (p<0.05). Pharyngeal stimulation resulted in bolus volume dependent LOS relaxation. Atropine decreased the frequency and amplitude of pharyngeal receptor mediated LOS relaxation at bolus volumes of 0.05, 0.1, and 0.2 ml. Gastric distension resulted in intermittent episodes of TLOSR. The frequency of gastric distension induced TLOSR was significantly decreased by atropine. 
Conclusion—(1) Atropine reduces the frequency of spontaneous reflux and TLOSR in normal subjects; and (2) gastric distension induced TLOSR and pharyngeal receptor mediated LOS relaxation is inhibited by atropine. 



Keywords: lower oesophageal sphincter relaxation; anticholinergic; pharynx; gastric distension

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Figure 1 .

Figure 1

: Effects of pharyngeal stimulus on LOS relaxation. A manometric record of the effect of injection of water in the pharynx (marked by the arrow) on LOS pressure. Note that soon after the injection of water the LOS relaxes for 30 seconds. There is no relaxation of the crural diaphragm as shown by continued inspiratory pressure oscillations in the LOS pressure tracing and crural diaphragmatic electromyographic activity.

Figure 2 .

Figure 2

: Effects of atropine on the frequency of postprandial GOR and TLOSR. Mean (SEM) data on the frequency of TLOSR and GOR in 10 subjects. Data were collected in the postprandial periods.

Figure 3 .

Figure 3

: Effects of atropine on the incidence of pharyngeal stimulus induced LOS relaxation. Mean (SEM) data in nine normal subjects. The LOS response to pharyngeal stimulus was defined as a decrease in LOS pressure of more than 4 mm Hg.

Figure 4 .

Figure 4

: Effects of atropine on the amplitude of LOS pressure drop and percentage LOS relaxation induced by pharyngeal stimulus. The data summarise the absolute LOS pressure fall and percentage LOS relaxation by pharyngeal stimulus before and after injection of atropine in nine subjects (control and atropine, respectively).

Figure 5 .

Figure 5

: Effects of atropine on pharyngeal stimulus induced LOS relaxation: LOS pressure tracing before and after injection of atropine in the same individual. The same bolus volume (0.3 ml) was used for both the pharyngeal stimulations. Note the absence of LOS relaxation following atropine injection. Crural diaphragmatic activity (inspiratory pressure oscillations) was not affected by pharyngeal stimulus and atropine.

Figure 6 .

Figure 6

: Effects of atropine on gastric distension induced TLOSR. Data are mean (SEM) in seven normal subjects. The number of TLOSRs was measured in the 15 minute periods after the ingestion of each volume of CO2.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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