title: H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans.
abstract: The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pylori status, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale U539, Human Nutrition Research Center, and Department of Gastroenterology and Hepatology, University of Nantes, 44035 Nantes, France.
authors.forename: F
authors.initials: F
authors.lastname: Zerbib
authors.forename: V
authors.initials: V
authors.lastname: Bicheler
authors.forename: V
authors.initials: V
authors.lastname: Leray
authors.forename: M
authors.initials: M
authors.lastname: Joubert
authors.forename: S
authors.initials: S
authors.lastname: Bruley des Varannes
authors.forename: J P
authors.initials: JP
authors.lastname: Galmiche
mesh_terms: D000328:Adult; D003187:Compliance; D016207:Cytokines / Q000096:biosynthesis; D004943:Esophagogastric Junction / Q000502:physiology*; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D009126:Muscle Relaxation; D017288:Pain Threshold; D011312:Pressure; D012844:Sincalide / Q000031:analogs & derivatives / Q000494:pharmacology; D013270:Stomach / Q000502:physiology
chemical_list: C090019:8-sulfocholecystokinin octapeptide; D016207:Cytokines; D012844:Sincalide