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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/R1392    most recent 00006.2009v1 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 PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Sun, Y. Articles by Chen, J. D. Z. PubMed PubMed Citation Articles by Sun, Y. Articles by Chen, J. D. Z.

Articles

Effects and mechanisms of gastrointestinal electrical stimulation on slow waves: a systematic canine study

¹Veterans Research and Education Foundation, Veterans Affairs Medical Center, Oklahoma City, Oklahoma; ²Division of Gastroenterology, University of Texas Medical Branch at Galveston, Galveston, Texas

Submitted January 6, 2009 ; accepted in final form August 19, 2009

The aims of this study were to determine optimal pacing parameters of electrical stimulation on different gut segments and to investigate effects and possible mechanisms of gastrointestinal electrical stimulation on gut slow waves. Twelve female hound-mix dogs were used in this study. A total of six pairs of electrodes were implanted on the stomach, duodenum, and ascending colon. Bilateral truncal vagotomy was performed in six of the dogs. One experiment was designed to study the effects of the pacing frequency on the entrainment of gut slow waves. Another experiment was designed to study the modulatory effects of the vagal and sympathetic pathways on gastrointestinal pacing. The frequency of slow waves was 4.88 ± 0.23 cpm (range, 4–6 cpm) in the stomach and 19.68 ± 0.31 cpm (range, 18–22 cpm) in the duodenum. There were no consistent or dominant frequencies of the slow waves in the colon. The optimal parameters to entrain slow waves were: frequency of 1.1 intrinsic frequency (IF; 10% higher than IF) and pulse width of 150–450 ms (mean, 320.0 ± 85.4 ms) for the stomach, and 1.1 IF and 10–20 ms for the small intestine. Electrical stimulation was not able to alter colon slow waves. The maximum entrainable frequency was 1.27 IF in the stomach and 1.21 IF in the duodenum. Gastrointestinal pacing was not blocked by vagotomy nor the application of an - or β-adrenergic receptor antagonist; whereas the induction of gastric dysrhythmia with electrical stimulation was completely blocked by the application of the - or β-adrenergic receptor antagonist. Gastrointestinal pacing is achievable in the stomach and small intestine but not the colon, and the maximal entrainable frequency of the gastric and small intestinal slow waves is about 20% higher than the IF. The entrainment of slow waves with gastrointestinal pacing is not modulated by the vagal or sympathetic pathways, suggesting a purely peripheral or muscle effect.

gastrointestinal motility; slow wave dysrhythmia; sympathetic modulation; vagal nerve modulation