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Type: Journal article
Title: Triggering of transient LES relaxations in ferrets: role of sympathetic pathways and effects of baclofen
Author: Staunton, E.
Smid, S.
Dent, J.
Blackshaw, L.
Citation: American Journal of Physiology: Gastrointestinal and Liver Physiology, 2000; 279(1 42-1):G157-G162
Publisher: Amer Physiological Soc
Issue Date: 2000
ISSN: 0193-1857
Abstract: Activation of gastric vagal mechanoreceptors by distention is thought to be the trigger for transient lower esophageal sphincter relaxations (TLESR), which lead to gastroesophageal reflux. The contribution of higher-threshold gastric splanchnic mechanoreceptors is uninvestigated. GABA(B) receptor agonists, including baclofen, potently reduce triggering of TLESR by low-level gastric distention. We aimed to determine first whether this effect of baclofen is maintained at high-level distention and second the role of splanchnic pathways in triggering TLESR. Micromanometric/pH studies in conscious ferrets showed that intragastric glucose infusion (25 ml) increased triggering of TLESR and reflux. Both were significantly reduced by baclofen (7 micromol/kg ip) (P < 0.05). When 40 ml of air was added to the glucose infusion, more TLESR occurred than with glucose alone (P < 0.01). These were also reduced by baclofen (P < 0.001). TLESR after glucose/air infusion were assessed before and after splanchnectomy (2-4, 9-11, and 23-25 days), which revealed no change. Baclofen inhibits TLESR after both low- and high-level gastric distention. Splanchnic pathways do not contribute to increased triggering of TLESR by high-level gastric distention.
Keywords: Muscle, Smooth
Esophagogastric Junction
Splanchnic Nerves
Gastroesophageal Reflux
Receptors, GABA-B
Muscle Relaxants, Central
Muscle Denervation
DOI: 10.1152/ajpgi.2000.279.1.g157
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