No abstract

The aim of this study was to determine the effects and mechanism of synchronized gastric electrical stimulation (SGES) on gastric contractions and gastric emptying. The first experiment was designed to study the effects of SGES on antral contractions in four randomized sessions. Sessions 1 (control) and 2 (atropine) were performed in the fasting state, composed of three 30-min periods (baseline, stimulation, and recovery). Sessions 3 (control) and 4 (SGES performed during 2nd 20-min period) were performed in the fed state, consisting of two 20-min periods; glucagon was injected after the first 20-min recording. The second experiment was designed to study the effect of SGES on gastric emptying and consisted of two sessions (control and SGES). SGES was delivered with train duration of 0.5–0.8s, pulse frequency of 40 Hz, width of 2 ms, and amplitude of 4 mA. We found that 1) SGES induced gastric antral contractions in the fasting state. The motility index was 1.3 ± 0.5 at baseline and 6.1 ± 0.7 ( P = 0.001) during SGES. This excitatory effect was completely blocked by atropine. 2) SGES enhanced postprandial antral contractions impaired by glucagon. 3) SGES significantly accelerated glucagon-induced delayed gastric emptying. Gastric emptying was 25.5 ± 11.3% without SGES and 38.3 ± 10.7% with SGES ( P = 0.006 vs. control). This novel method of SGES induces gastric antral contractions in the fasting state, enhances glucagon-induced antral hypomotility in the fed state, and accelerates glucagon-induced delayed gastric emptying. The effect of SGES on antral contractions is mediated via the cholinergic pathway.

Acute IGS inhibits postprandial antral contractions, and this inhibitory effect is mediated via the sympathetic pathway.

The aim of this study was to assess effects of gastric distension on gastric slow waves using internal and cutaneous electrodes and the correlation between these two measurements. The study was performed in five dogs implanted with one pair of serosal electrodes and a gastric cannula. Gastric slow waves were recorded using both cutaneous and internal electrodes in several sessions with different volumes (150-600 mL) of gastric distension with a barostat balloon. Bethanechol was injected in one of sessions. The results revealed that (i) Gastric distension reduced slow wave frequency in a volume-dependent manner and induced bradyarrhythmia at a volume of 600 mL, but had no effects on the amplitude of gastric slow waves. (ii) The cutaneous electrogastrogram (EGG) was significantly correlated with the internal recording in slow wave frequency (r = 0.88, P < 0.001) and regularity (r = 0.44, P = 0.035). (iii) The EGG amplitude was not increased when the stomach was distended but increased after bethanechol. Gastric distension volume dependently reduces slow wave frequency and induces gastric dysrhythmia at a large volume. The frequency and rhythmicity of the slow wave measured from the EGG are significantly correlated with those recorded from the internal electrodes. Relative increase in EGG amplitude reflects contractility rather than the distension of the stomach.

The aim of this study was to investigate the effects and mechanisms of intestinal electrical stimulation (IES) on gastric tone, antral and pyloric contractions, and gastric emptying in dogs. Female hound dogs were equipped with a duodenal or gastric cannula, and one pair of serosal electrodes was implanted in the small intestine. The study consisted of five different experiments. Liquid gastric emptying was assessed by collection of chyme from the duodenal cannula in a number of sessions with and without IES and with and without N-nitro-L-arginine (L-NNA). Postprandial antral and pyloric contractions were measured with and without IES and in the absence and presence of L-NNA or phentolamine by placement of a manometric catheter into the antrum and pylorus via the duodenal cannula. Gastric tone was assessed by measurement of gastric volume at a constant pressure. Gastric emptying was substantially and significantly delayed by IES or L-NNA compared with the control session. IES-induced delay of gastric emptying became normal with addition of L-NNA. IES reduced gastric tone, which was blocked by L-NNA. IES also inhibited antral contractions (frequency and amplitude), and this inhibitory effect was not blocked by L-NNA but was blocked by phentolamine. IES alone did not affect pyloric tone or resistance, but IES ϩ L-NNA decreased pyloric tone. In conclusion, IES reduces gastric tone via the nitrergic pathway, inhibits antral contractions via the adrenergic pathway, does not affect pyloric tone, and delays liquid gastric emptying. IES-induced delay of gastric emptying is attributed to its inhibitory effects on gastric motility. gastrointestinal motility; gastric pacing ELECTRICAL STIMULATION as a potential modality for treatment of morbid obesity is gaining more and more attention (15, 16), since the conventional behavior modifications and pharmacotherapies have not been effective in the long term (11, 29) and surgical interventions result in a high rate of mortality and morbidity (4,9,21,42,46). Gastric electrical stimulation (GES) has been under clinical investigation for the treatment of morbid obesity, and preliminary data from studies of the effects of GES on food intake and weight loss have been encouraging but inconclusive (15, 16).The proximal small intestine plays an important role in regulating gastric emptying (30), optimizing nutrient absorption (26), and signaling satiety in the central nervous system (20). Because intestinal electrical stimulation (IES) may have multiple effects on gastrointestinal functions, including gastric emptying, small bowel transit, nutrient absorption, and feedback signaling of satiety to the central nervous system, it is a very attractive alternative option for treatment of obesity. In 1977, Kelly and Code (28) showed that distal duodenal pacing caused duodenal-gastric reflux of BaSO 4 in dogs and a 25% reduction of the rate of liquid gastric emptying. However, there has been a lack of follow-up studies of the inhibitory effects of IES on gastrointestinal motility and related m...

GES with appropriate parameters inhibits gastric motility, and the effects are reproducible. The GES method optimized to inhibit gastric motility reduces food intake in healthy dogs and may have a therapeutic potential for treating obesity.

The aim was to investigate the effects of electrical field stimulation (EFS) with long and short pulses on gastric emptying, gastric contractility and vagal activity in dogs. Sixteen dogs were equipped with a duodenal cannula, electrodes and strain gauges (10 dogs) in the stomach. Each dog was fed with Ensure and gastric effluent was collected from the cannula. Electrical stimulation was applied via two electrodes (about 12 cm apart, one in the corpus and the other in the antrum) with long pulses (a frequency of 6 cycles min-1, pulse amplitude of 6 mA and width of 100 ms) in 10 dogs and with short pulses (frequency of 30 Hz and pulse width of 300 micros) in six dogs. The electrocardiogram was also recorded and heart rate variability was derived to assess the vagal activity. It was found that: (i). EFS with long pulses did not alter gastric emptying during stimulation but increased gastric emptying during the 45 min immediately after stimulation; (ii). EFS with long pulses increased gastric contractility in both proximal and distal antrum during and after the stimulation; (iii). EFS with long pulses resulted in an increase in vagal tone during the 45 min immediately after stimulation. However, there is no difference during the 45 min period of stimulation; (iv). EFS with short pulses had no effect on gastric emptying. We concluded that long pulse gastric electrical field stimulation with one electrode in the corpus and the other electrode in the antrum has postponed effects on gastric emptying of liquid, gastric contractility and vagal activity.

Rectal distension affects upper GI myoelectrical activity and motility. The aim of this experiment was to investigate the effect of rectal distension on gastric tone, accommodation, and the underlying mechanism. Seven healthy dogs were surgically prepared and studied. Gastric tone and accommodation were assessed with a barostat. In Experiment 1, the effect of rectal distension on gastric tone and accommodation was evaluated; in Experiment 2, rectal distensions with various volumes were randomly applied and its effects on gastric tone were evaluated; and in Experiment 3, the role of the cholinergic pathway in distension-induced gastric relaxation was assessed. The results showed the following. (1) Rectal distension exerted an inhibitory effect on gastric tone, and this response was distension volume-dependent. (2) Postprandial gastric volume was similar in the control (468.6 +/- 24.7 ml) and the distension study (463.2 +/- 17.5 ml). However, rectal distension increased the preprandial gastric volume, and subsequently decreased the extent of gastric accommodation (139.3 +/- 34.7 ml), which was significantly lower than that of the control (383.2 +/- 26.3 ml; P < 0.001). (3) An intravenous bolus of atropine increased the astric volume from the baseline of 89.4 +/- 12.6 ml to 161.5 +/- 9.8 ml (P < 0.01), and subsequent rectal distension further increased this volume, but the overall change was comparable between the control (297.6 +/- 18.7 ml) and the atropine study (312.1 +/- 21.9 ml; P > 0.05). In conclusion, rectal distension inhibits gastric tone in a volume-dependent manner and impairs gastric accommodation. Atropine dose not block the effect of rectal distension on proximal gastric tone, suggesting that the observed effect may not be mediated by cholinergic pathway.