Cholinergic blockade inhibits gastro-oesophageal reflux and transient lower oesophageal sphincter relaxation through a central mechanism

Citation
Jc. Fang et al., Cholinergic blockade inhibits gastro-oesophageal reflux and transient lower oesophageal sphincter relaxation through a central mechanism, GUT, 44(5), 1999, pp. 603-607
Citations number
17
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
GUT
ISSN journal
00175749 → ACNP
Volume
44
Issue
5
Year of publication
1999
Pages
603 - 607
Database
ISI
SICI code
0017-5749(199905)44:5<603:CBIGRA>2.0.ZU;2-J
Abstract
Background-Atropine, an anticholinergic agent with central and peripheral a ctions, reduces gastro-oesophageal reflux (GOR) in normal subjects and pati ents with gastro-oesophageal reflux disease (GORD) by inhibiting the freque ncy of transient lower oesophageal sphincter relaxation (TLOSR). Aims-To compare the effect of methscopolamine bromide (MSB), a peripherally acting anticholinergic agent, with atropine on the rate and mechanism of G OR in patients with GORD. Methods-Oesophageal motility and pH were recorded for 120 minutes in 10 pat ients with GORD who were studied on three separate occasions. For the first two recording periods, either atropine (15 mu g/kg bolus, 4 mu g/kg/h infu sion) or saline were infused intravenously. MSB (5 mg orally, four times da ily) was given for three days prior to the third recording period. Results-Atropine significantly reduced basal LOS pressure (12.6 (0.17) mm H g to 7.9 (0.17) mm Hg), and the number of TLOSR (8.1 (0.56) to 2.8 (0.55)) and reflux episodes (7.0 (0.63) to 2.0 (0.43)) (p<0.005 for all comparisons ). MSB reduced basal LOS pressure (12.6 (0.17) to 8.7 (0.15) mm Hg, p<0.005 ), but had no effect on the frequency of TLOSR (8.1 (0.56) to 7.5 (0.59)) a nd reflux episodes (7.0 (0.63) to 4.9 (0.60)) (p>0.05). Conclusion-In contrast to atropine, MSE has no effect on the rate of TLOSR or GOR in patients with GORD. Atropine induced inhibition of TLOSR and GOR is most likely mediated through a central cholinergic blockade.