Gastric pacing has received increasing attention recently. However, few studies have systematically assessed the effect of pacing on gastric dysrhythmias. The aims of this study were to investigate the effect of gastric pacing on gastric dysrhythmia and to explore whether the effect of gastric pacing was mediated via cholinergic nerves. Eight hound dogs implanted with three pairs of serosal electrodes were studied. Three study sessions were performed on each dog. The experiment was conducted sequentially as follows: a 30-min myoelectrical recording immediately after a meal, intravenous injection of atropine or saline, and three sequential 20-min myoelectrical recordings with or without gastric pacing during the second 20-min recording. The percentage of regular slow waves (3.5-7.0 cycles/min) was calculated using spectral analysis. The percentage of the regular slow waves was progressively reduced from 96.7 ± 1.7% at baseline to 29.6 ± 9.0 (P < 0.001), 23.1 ± 7.1 (P < 0.001), and 27.3 ± 4.3% (P < 0.001), respectively, during the first, second, and third 20 min after atropine injection. Normalization of the gastric slow wave was achieved with gastric pacing 2.3 ± 1.0 min after the initiation of pacing. The percentage of regular slow waves was significantly increased both during pacing (93.6 ± 2.4 vs. 23.1 ± 7.1%, P < 0.002) and after pacing (70.9 ± 6.8 vs. 27.3 ± 4.3%, P < 0.003) in comparison with the session without pacing. We conclude that 1) atropine induces gastric myoelectric dysrhythmia in the fed state, 2) gastric pacing is able to normalize gastric postprandial dysrhythmia induced by atropine, and 3) the effect of gastric pacing is not mediated by vagal cholinergic mechanism.

gastric myoelectric activity; gastric motility; electrogastrography; cholinergic mechanism; electrical stimulation

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