HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/2/G284    most recent 00250.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Kang, Y. M. Articles by Bielefeldt, K. Search for Related Content PubMed PubMed Citation Articles by Kang, Y. M. Articles by Bielefeldt, K.

NEUROREGULATION AND MOTILITY

Experimentally induced ulcers and gastric sensory-motor function in rats

¹Department of Pharmacology, University of Iowa, Iowa City, Iowa; and ²Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

Submitted 4 June 2004 ; accepted in final form 22 September 2004

Prior studies have demonstrated that inflammation can sensitize visceral afferent neurons, contributing to the development of hyperalgesia. We hypothesized that both afferent and efferent pathways are affected, resulting in changes in motor and sensory function. Kissing ulcers (KU) were induced in the distal stomach by injecting 60% acetic acid for 45 s into a clamped area of the stomach. In controls, saline was injected into the stomach. A balloon catheter was surgically placed into the stomach, and electromyographic responses to gastric distension were recorded from the acromiotrapezius muscle at various times after ulcer induction. The accommodation reflex was assessed by slowly infusing saline into the distally occluded stomach. Gastric pressure changes in response to vagal stimulation were measured in anesthetized rats. Contractile function of circular muscle strips was examined in vitro using force-displacement transducers. KU caused gastric hypersensitivity that persisted for at least 14 days. Fluid distension of the stomach led to a rapid pressure increase in KU but not in control animals, consistent with an impaired accommodation reflex. Gastric ulcers enhanced the contractile response to vagal stimulation, whereas the effect of cholinergic stimulation on smooth muscle in vitro was not changed. These data suggest that inflammation directly alters gastric sensory and motor function. Increased activation of afferents will trigger vagovagal reflexes, thereby further changing motility and indirectly activating sensory neurons. Thus afferent and efferent pathways both contribute to the development of dyspeptic symptoms.

visceral hyperalgesia; sensitization; gastric motility

This article has been cited by other articles:

				M. Verma-Gandhu, E. F Verdu, P. Bercik, P. A Blennerhassett, N. Al-Mutawaly, J.-E. Ghia, and S. M Collins Visceral pain perception is determined by the duration of colitis and associated neuropeptide expression in the mouse Gut, March 1, 2007; 56(3): 358 - 364. [Abstract] [Full Text] [PDF]

				J. M. Hauer, B. S. Wical, and L. Charnas Gabapentin Successfully Manages Chronic Unexplained Irritability in Children With Severe Neurologic Impairment Pediatrics, February 1, 2007; 119(2): e519 - e522. [Abstract] [Full Text] [PDF]

				E. P. M. Vianna, J. Weinstock, D. Elliott, R. Summers, and D. Tranel Increased feelings with increased body signals Soc Cogn Affect Neurosci, June 1, 2006; 1(1): 37 - 48. [Abstract] [Full Text] [PDF]