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  • esophageal motor function  (1)
  • vagal nerve  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 32 (1987), S. 1130-1135 
    ISSN: 1573-2568
    Keywords: lower esophageal sphincter ; muscarinic ; opossum ; vagal nerve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We assessed the characteristics of muscarinic neural transmission in the vagal inhibitory pathway to the lower esophageal sphincter (LES) of anesthetized opossums. LES relaxation was induced by electrical stimulation of the cervical vagus. Measurements were made of LES relaxation before and after intravenous administration of nicotinic (hexamethonium), serotonergic (5-Meo-DMT), nonselective muscarinic (atropine), and selective muscarinic (pirenzepine-M1 and 4-DAMP-M2) antagonists. The latency of LES relaxamethonium, but was not affected by 4-DAMP or 5-Meo-DMT. Given as concurrent intravenous infusions, hexamethonium, 5-Meo-DMT and 4-DAMP added to pirenzepine or atropine did not significantly increase LES relaxation latency above that caused by pirenzepine or atropine alone. None of the antagonists alone had a significant effect on percent LES relaxation. The combination of pirenzepine or 4-DAMP with hexamethonium and 5-Meo-DMT did not affect percent LES relaxation. The combination of atropine with hexamethonium and 5-Meo-DMT reduced LES relaxation to 18%. The combination of pirenzepine and 4-DAMP with hexamethonium and 5-Meo-DMT, however, had no effect on percent LES relaxation. We conclude that muscarinic participation in vagally induced LES relaxation exhibits two functional receptor subtypes: (1) M1 receptors that determine LES relaxation latency and are antagonized by pirenzepine or atropine, and (2) non-M1, non-M2 receptors, (Mx receptors) that contribute to the magnitude of LES relaxation and are antagonized by atropine, but not by pirenzepine or 4-DAMP.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 32 (1987), S. 1331-1336 
    ISSN: 1573-2568
    Keywords: cisapride ; lower esophageal sphincter ; esophageal motor function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this study, we assessed by a double-blinded, cross-over design the effect of intravenous and oral cisapride on esophageal motor activity during the late fed state in normal subjects. For the intravenous study, subjects were given placebo or 10 mg cisapride randomly, while in the oral study, they randomly received placebo or cisapride at 5, 10, or 20 mg. Cisapride given intravenously or orally caused a significant increase in resting LES pressure. The increase in LES pressure after oral administration was significant only after the 20 mg dose. Esophageal-body peristaltic amplitude, determined for all smooth-muscle sites, showed a modest but significant increase of approximately 10 mm Hg after intravenous cisapride, whereas no significant increase occurred after oral cisapride. Propagation time of peristalsis was unaffected by intravenous or oral cisapride. Side effects of treatment were minimal and at no time necessitated cessation of the study. We conclude that in healthy subjects during the late fed period, (1) cisapride at 10 mg intravenously or 20 mg orally increased resting LES pressure and (2) at 10 mg intravenously, but at no oral dose, cisapride increased peristaltic amplitude without affecting propagation time. The potentiating effect of cisapride on LES pressure suggests that cisapride could have an ancillary role in the therapy of gastroesophageal reflux disease.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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