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Effects of two anticholinergic drugs, trospium chloride and biperiden, on motility and evoked potentials of the oesophagus
Author(s) -
Pehl,
Wendl,
Kaess,
Pfeiffer
Publication year - 1998
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.1998.00398.x
Subject(s) - anticholinergic , medicine , saline , anesthesia , atropine , anticholinergic agents , neuromuscular transmission , parasympatholytic , pharmacology , muscarinic acetylcholine receptor , receptor
Background: Anticholinergic drugs are known to impair the motor function of the oesophagus but their effects on the oesophageal afferent pathways are unknown. Aim: To determine the effects of a peripherally‐acting (trospium chloride) and a centrally‐acting (biperiden) anticholinergic drug on the motility and the evoked potentials of the oesophagus. Methods: Nine healthy volunteers were randomized to receive 1.2 mg trospium chloride (TC), 5 mg biperiden (BIP) or saline i.v. Primary peristalsis was elicited by swallowing a 5 mL water bolus and secondary peristalsis by insufflation of 20 mL air, 10 times each. Oesophageal potentials were evoked by electrical stimulation in the distal and proximal oesophagus (30 stimulations at 0.4 Hz, two runs). Results: Both anticholinergic drugs reduced by a similiar amount the contraction amplitudes (TC 17 mmHg, BIP 25 mmHg, saline 67 mmHg; P < 0.01) and the rate of secondary contractions (TC 60%, BIP 70%, saline 95%; P < 0.01). In contrast, only biperiden prolonged the latencies of the evoked potentials (N1 peak, distal oesophagus: BIP 191 ms, TC 102 ms, saline 101 ms; P < 0.01; P1 peak: BIP 322 ms, TC 161 ms, saline 144 ms; P < 0.01). Conclusions: Both anticholinergic drugs depress oesophageal motility, but only the centrally‐acting anticholinergic drug biperiden modifies the oesophageal evoked potentials, suggesting a central cholinergic transmission of the oesophageal afferent pathways.