Normalization of atropine-induced postprandial dysrhythmias with gastric pacing

Abstract

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.

Systematic review: applications and future of gastric electrical stimulation

“…Entrainment of gastric slow waves or pacing has been reported in a number of studies with GES of long pulses with a pulse width in the order of a few hundred milliseconds. 26,[28][29][30][31][32] Typically, GES was performed at a frequency slightly higher than the measured intrinsic frequency of gastric slow waves. When entrainment or pacing occurs, the natural slow waves are phase-locked with stimuli.…”

“…37,38 While the exact mechanisms involved in the normalization of gastric dysrhythmia with long pulse/low frequency GES are unclear, it is known that it does not involve the vagal or cholinergic pathway. 32,36 A recent study reported the entrainment of slow waves in the absence of interstitial cells of Cajal (ICC) in mice, suggesting that pacing can be achieved without ICC. 39 Similar findings were also reported in in vitro studies in ICC knocked out mice.…”

Gastric Arrhythmia and Nausea of Motion Sickness Induced in Healthy Japanese Subjects Viewing an Optokinetic Rotating Drum

“…Numerous studies have indicated that gastric dysrhythmia is detected during nausea [1][2][3][5][6][7][8]. It is not only found in several clinical circumstances, but is also induced by chemical agents such as epinephrine [21]; glucagons [22]; metenkephalin, or PGE 2 [23]; atropine sulfate; neostigmine [11,24,25]; morphine; histamine [25]; insulin; secretin; CCK-pancreozymin; pentagastrin [26]; and serotonin (5-HT 3 ) [27]. However, nausea is not necessarily caused by administering these chemical agents.…”

Cross-talk along gastrointestinal tract during electrical stimulation: effects and mechanisms of gastric/colonic stimulation on rectal tone in dogs

“…GES has been investigated as a therapeutic option in the management of refractory gastroparesis (1,12,15,18,20) and morbid obesity (6 -8). A number of reports is available in the literature on GES with long pulses, demonstrating beneficial effects of this approach on gastric motor and sensory functions (3,9,16,18,20,22,28). However, little is known on the effects of GES on other organs of the gut.…”

“…On the basis of stimulation pulse width, GES can be classified into three categories: long pulses (on the order of milliseconds), short pulses (in the order of microseconds), and pulse trains. Although some of the results are still controversial, the majority of these studies seems to indicate that GES with long pulses at a low frequency (close to or slightly higher than intrinsic gastric slow-wave frequency) is able to normalize gastric dysrhythmias, entrain gastric slow waves, and accelerate gastric emptying (3,10,16,18,20,22). GES with short pulses at a high frequency (4 times or much higher than intrinsic gastric slow waves) is able to significantly reduce symptoms of nausea and vomiting but is minimally effective on gastric motility (1,5,9,11,12).…”