Effects of vasopressin and long pulse–low frequency gastric electrical stimulation on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs

The aim of this study was to investigate the effect of vasopressin and long pulse-low frequency gastric electrical stimulation (GES) on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs. The study was performed in eight healthy female dogs implanted with four pairs of gastric serosal electrodes and two pairs of small bowel serosal electrodes, and a duodenal fistula for the assessment of gastric emptying. Each dog was studied in three sessions on three separate days in a randomized order with recordings of gastric and small bowel slow waves. Each study session consisted of 30-min baseline, 30-min stimulation and 30-min recovery period. In sessions 1 and 2, infusion of either saline or vasopressin (0.75 U kg(-1) in 30 mL saline instilled in 30 min) was given during the second 30-min period. The protocol of session 3 was the same as session 2 except long pulse-low frequency GES was performed during the second 30-min period. It was found that: (i) Vasopressin significantly delayed gastric emptying 30 and 45 min after meal and GES did not improve the vasopressin induced delayed gastric emptying; (ii) Vasopressin induced gastric dysrhythmias and GES significantly improved vasopressin induced gastric dysrhythmia; (iii) Vasopressin also induced intestinal slow wave abnormalities but GES had no effect on vasopressin induced small bowel dysrhythmia; (iv) Vasopressin induced symptoms and behaviours suggestive of nausea that were not improved by GES. We conclude that: (i) Vasopressin delays gastric emptying and induces gastric and small bowel dysrhythmias and symptoms in the fed state, and (ii) long pulse-low frequency GES normalizes vasopressin induced gastric dysrhythmia with no improvement in gastric emptying or symptoms.     

Tachygastria induced by gastric electrical stimulation is mediated via α- and β-adrenergic pathway and inhibits antral motility in dogs

BACKGROUND: It is known that tachygastria is associated with gastric hypomotility and retrograde gastric electrical stimulation (RGES) delays gastric emptying and is proposed for treating obesity. The aim was to investigate the effects and mechanisms of RGES on postprandial antral contraction in dogs. METHODS: Seven dogs were implanted with a gastric cannula and three pairs of gastric serosal electrodes. Antral contractions and gastric myoelectrical activity were recorded immediately after a solid meal, with or without RGES, or with GES on the corpus, or with RGES under administration of propranolol. The stimulus was composed of long pulses with a tachygastrial frequency. RESULTS: (i) GES at the tachygastrial frequency impaired gastric myoelectrical activity and induced tachygastria (anovaP<0.05). (ii) GES at the tachygastrial frequency suppressed antral contractions (anovaP<0.01) and the effect was stronger with retrograde stimulation than forward stimulation (P<0.05). (iii) GES-induced tachygastria was correlated with antral hypomotility (r=-0.60, P=0.01). (iv) Propranolol and phentolamine abolished GES-induced tachygastria and antral hypomotility. CONCLUSIONS: Long-pulse RGES at a tachygastrial frequency suppresses postprandial antral contractions, which is attributed to an induction of tachygastria via the alpha- and beta-adrenergic pathway.     

Intestinal electrical stimulation improves delayed gastric emptying and vomiting induced by duodenal distension in dogs.

The aim of this study was to investigate the effects of short-pulse intestinal electrical stimulation (IES) on duodenal distention-induced delayed gastric emptying and vomiting in dogs and its possible mechanisms. The study was performed in 12 dogs with jejunal electrodes and a duodenal cannula in three separate experiments to investigate the effects of IES on duodenal distension (DD)-induced delayed gastric emptying and discomfort signs, vagal efferent activity, and jejunal tone. We found that: (i) IES significantly accelerated gastric emptying of liquid delayed by distension (18.05 +/- 4.06%vs. 7.18 +/- 1.99%, P = 0.036 at 60 min). (ii) IES significantly reduced vomiting and discomfort/pain induced by distension. The average signs score was 15.33 +/- 1.37 during distension which decreased to 6.50 +/- 0.91 (P = 0.0002) with IES. (iii) IES did not change vagal afferent activity, which was assessed by the spectral analysis of the heart rate variability. (iv) IES decreased jejunal tone. In conclusion, IES with parameters commonly used in gastric electrical stimulation for nausea and vomiting associated with gastroparesis improves DD-induced delayed gastric emptying and prevents DD-induced vomiting and discomfort signs. Further studies are warranted to investigate the therapeutic potential of IES for gastrointestinal symptoms associated with disturbances in motility and sensory function in small intestine.     

Gastric electrical stimulation reduces visceral sensitivity to gastric distention in healthy canines

The aim of this study was to investigate the effects and mechanisms of gastric electrical stimulation (GES) on proximal stomach distention-induced visceral sensitivity. Isobaric gastric distention was performed using a barostat system in 8 normal and 6 vagotomized dogs and animal behaviors were noted and graded. The normal dogs were studied in 4 sessions: control (no GES), short pulse GES, long pulse GES, and dual-pulse GES, and the vagotomized dogs were studied in three sessions: control (no GES), long pulse GES and guanethidine. It was found that: 1) proximal stomach distention-induced behavioral changes were mediated by vagal and sympathetic pathways. The total behavior score (TBS) was 40.6 ± 7.4 in the controls, 15.3 ± 8.9 in vagotomized dogs (P=0.006 vs. control) and 8.8 ± 0.9 in the vagotomized dogs with guanethidine (P=0.04 vs. vagotomy). The behavioral changes were mediated via the vagal pathway at distention pressures below 20 mmHg, but mediated via both the vagal and sympathetic pathways at distention pressures equal to and above 20 mmHg. 2) GES with long pulses or dual pulses but not short pulses reduced the distention-induced behavioral score (P=0.003, P=0.006 and P=0.7, respectively) and the effects of GES of long pulses might be mediated via the vagal and sympathetic pathways. In conclusion, gastric distention-induced visceral sensitivity is mediated via the vagal pathway at low distention pressures but via both vagal and sympathetic pathways at high distention pressures. GES with long but not short pulses reduces distention-induced visceral sensitivity.     

Effects of clonidine and tricyclic antidepressants on gastric smooth muscle contractility

To determine if and how clonidine and tricyclic antidepressants affect gastric contractility. Guinea pig fundic and antral circular muscle strips were studied in vitro. The effects of clonidine or amitriptyline added in graded concentrations on contractions to electric field stimulation (EFS), acetylcholine (ACh), and SP in the presence of N(epsilon)-nitro-l-arginine methyl ester (l-NAME) were studied. EFS produced frequency dependent contractions of fundic and antral muscle that were abolished by atropine or tetrodotoxin (TTX). ACh contractions were abolished by atropine but not TTX. Clonidine reduced contractile response to EFS but had no effect on ACh contractions. The threshold concentration of clonidine to inhibit EFS contractions was lower in the fundus than in the antrum. Amitriptyline reduced contractions to both EFS and ACh but not to SP. The threshold concentration of amitriptyline to inhibit EFS contractions was lower in the antrum than in the fundus. Both clonidine and amitriptyline affect gastric contractility. At threshold concentrations, clonidine affects fundic contractility whereas amitriptyline affects antral contractility. Clonidine affects gastric contractility in response to EFS but not to ACh, suggesting alpha-2 receptors on cholinergic nerves that reduce ACh release. Amitriptyline inhibits gastric contractility to EFS and ACh suggesting an inhibitory muscle effect.     

Effects of cyclooxygenase-2 inhibitor on glucagon-induced delayed gastric emptying and gastric dysrhythmia in dogs

The objective of this study was to investigate the effects of cyclooxygenase-2 (COX-2) inhibitor (celecoxib) on delayed gastric emptying and gastric dysrhythmia induced by glucagon. The study was performed in six healthy female dogs implanted with four pairs of gastric serosal electrodes, and a duodenal fistula for the assessment of gastric emptying. Each dog was studied in three randomized sessions: control, glucagon and COX-2 inhibitor (celecoxib). Gastric emptying was assessed every 15 min via a duodenal cannula by calculating the amount of collected phenol red which mixed with the test meal and gastric slow waves were recorded at the same time. We found that: (i) glucagon significantly and substantially decreased gastric emptying of liquids (P < 0.001, anova), increased blood glucose (BG) levels, and induced gastric dysrhythmias. The delayed gastric emptying was correlated with the BG level (R = -0.77, P < 0.001) and (ii) celecoxib improved glucagon-induced delayed gastric emptying at 30, 45, 60 and 75 min after feeding. Celecoxib did not blocked dysrhythmic action of glucagon (P > 0.05, anova). In conclusion, glucagon induces delayed gastric emptying partially via COX-2-derived prostaglandins. However, COX-2-derived prostaglandins are not involved in glucagon-evoked gastric dysrhythmia. Selective COX-2 inhibitors may provide a possible therapeutic option for diabetic gastroparesis.     

Effects and mechanisms of vaginal electrical stimulation on gastric tone in dogs

Abstract  Electrical stimulation of one part of the gut may have beneficial or adverse effects on another region. We hypothesized that electrical stimulation of a visceral organ in one system might have an effect on another visceral organ system. That is, disorders of one system may be treated by interventions of another system and this may lead to a more convenient or less invasive therapies in some cases. The aim of this study was to evaluate the effects and mechanisms of vaginal electrical stimulation (VES) with different parameters on gastric tone and gastric slow waves in conscious dogs. Seven dogs were studied in two experiments. Experiment 1 was to study effects of VES on gastric tone and slow waves. Experiment 2 was performed in two sessions (long pulse VES plus guanethidine and VES with trains of long pulse plus guanethidine) to study involvements of possible sympathetic mechanisms. The results of our experiments were: (i) VES increased the gastric volume in a dose-dependent manner with the increase of stimulation frequency, amplitude or pulse width; (ii) VES had no effects on gastric slow waves; (iii) the inhibitory effect of VES with long pulses or trains of long pulses on gastric tone was abolished by guanethidine; and (iv) few or mild symptoms were noted with stimulation. VES decreases proximal gastric tone in an energy-dependent manner without affecting gastric slow waves. The inhibitory effect of VES is mediated by a sympathetic pathway. Hypertensive gastric tone might be treated using electrical stimulation of the vagina which is minimally invasive.     

Effects and mechanisms of long-pulse gastric electrical stimulation on canine gastric tone and accommodation

Gastric electrical stimulation (GES) has been applied to treat gastroparesis and morbid obesity. The aims of this study were to evaluate the sites of stimulation and the mechanisms of GES on gastric tone and accommodation. Gastric tone and accommodation were evaluated with a barostat in surgically prepared dogs. GES was applied at seven different locations, and gastric tone was assessed at each site. The effect of truncal vagotomy on gastric tone and accommodation and the role of the nitrergic pathway were also evaluated. We have found: 1) GES induced varying degrees of gastric relaxation at all tested locations in normal dogs; 2) Gastric volume was also significantly increased with GES in vagotomized dogs and the change tended to be lower than that of normal animals; 3) Gastric accommodation was reduced during GES in both the normal and vagotomized dogs and the reduction tended to be more in the vagotomized animals; 4) The GES-induced increase in gastric volume was partially abolished by intravenous nitric oxide synthase inhibitor. GES at various sites of the stomach exerts inhibitory effect on gastric tone; the most effective sites are in the antrum along the lesser or greater curvature; the inhibitory effect of GES on gastric tone is partially mediated by the vagal and nitrergic pathway.     

CRF microinjected into the dorsal vagal complex inhibits TRH analog- and kainic acid-stimulated gastric contractility in rats

The effect of CRF microinjected into the dorsal vagal complex (DVC) on centrally-stimulated gastric contractility was investigated in fasted, urethane-anesthetized rats. Miniature strain gauge force transducers were acutely implanted on the corpus of the stomach and contractility was analyzed by computer. Microinjection of the stable thyrotropin-releasing hormone (TRH) analog, RX 77368, (26 pmol) into the DVC induced a 12.2-fold stimulation of gastric contractility within 30 min. Corticotropin-releasing factor (CRF) (63-210 pmol) microinjected into the DVC concomitantly with RX 77368 (26 pmol) induced a dose-related inhibition of stimulated gastric contractility. Neither CRF alone (210 pmol) nor vehicle modified basal gastric contractility. Microinjection of kainic acid (141 pmol) into the raphe pallidus nucleus induced a 3.6-fold stimulation of gastric contractility after 45 min. This stimulation was suppressed by bilateral microinjection of CRF (105 pmol/site) into the DVC. These results demonstrate that CRF acts in the DVC to inhibit centrally-stimulated gastric contractility and suggest that TRH and CRF may interact in the DVC to regulate gastric motor function.     

Responses of vagal efferent fibres to stimulation of gastric mechano- and chemoreceptors in the anaesthetized ferret

The involvement of gastric tension receptors and mucosal chemoreceptors in vagal reflexes was assessed directly by recording single efferent fibres from the cervical vagus nerve in the urethane anaesthetised ferret. 32/39 fibres responded to distension of the gastric corpus, mainly with excitation of firing, 24/39 fibres responded to antral distension, with a higher proportion showing a reduction in firing. Fifty-seven percent of fibres showed a convergent input from corpus and antrum. The magnitude of these responses was large (usually greater than 50%) and of short latency (less than 1 s). Responses to chemical perfusions in the antrum were seen in 14/31 efferent fibres, most of which showed excitation. Latency of response was variable (5-120 s) and may have been influenced by diffusion through the antral mucous barrier. These data indicate a complex arrangement of vagal reflexes involved in pre-pyloric regulation of gastric emptying by mechanical and chemical stimuli in the lumen.     

Efficiency and efficacy of multi-channel gastric electrical stimulation

Gastric electrical stimulation (GES) using single channel has been under investigation for its therapeutic potential for gastroparesis. The aim of this study was to study the efficacy and efficiency of multi-channel GES in accelerating gastric emptying in dogs. The study was performed in eight dogs, and gastric emptying of liquid was assessed in three randomized sessions of control, one-channel GES and four-channel GES. It was found that (i) GES of both one-channel and four-channel was able to completely entrain the slow waves in the entire stomach. However, the stimulation energy required by four-channel GES was only 1% of that required by one-channel GES. (ii) Four-channel, but not one-channel, GES significantly and substantially accelerated gastric emptying. An increase of 121.0 and 93.9% was noted with four-channel GES at 30 and 60 min after the meal, respectively. It was concluded that four-channel GES is substantially more efficient and effective than conventional single-channel GES in improving gastric emptying. It is worthy to explore its therapeutic potential for gastroparesis in clinical settings.     

Glutaminergic vagal afferents may mediate both retching and gastric adaptive relaxation in dogs.

We previously reported that intra-4th-ventricular (i.4th.v.) administration of a non-NMDA receptor antagonist, NBQX, abolished vagally induced retching. This study was undertaken to ascertain whether or not the neuronal response in the solitary tract nucleus (NTS) to vagal stimulation and the vago-vagal gastric reflexes induced by non-emetic stimulation are also abolished by NBQX with a similar latency as in the case of retching. Ketamine and thiopental- or chloralose-anesthetized dogs were decerebrated, and the dorsal surface of the medulla was exposed. This study consisted of two series of experiments. In the first series, extracellular neuronal responses in the NTS to pulse-train vagal stimulation were recorded. Effects of NBQX on the neural response and vagally induced fictive retching were observed. In the second series, effects of glutamate receptor antagonists on gastric corpus responses to esophageal or gastric antral distension were observed. Retching was abolished 5-15 min after an i.4th.v. application of NBQX. and the neuronal responses disappeared within 14 min after application in nine of 10 NTS neurons. On the other hand, corpus contractility was inhibited by esophageal distension, and inhibited and/or enhanced by antral distension. While the inhibitory responses disappeared within 17 min after NBQX, the enhanced response remained even after NBQX and vagotomy, but was abolished by i.v. administration of hexamethonium. These results suggest that adaptive relaxation in the corpus, as well as retching, may be mediated by glutaminergic vagal afferents and non-NMDA receptors in the NTS.     

Bombesin microinjected into the dorsal vagal complex inhibits TRH-stimulated gastric contractility in rats

The effects of centrally injected bombesin on central and peripheral stimulated gastric contractility were investigated in fasted urethane-anesthetized rats. Miniature strain gauge force transducers were acutely implanted on the corpus of the stomach and gastric contractility was analyzed by computer. Intracisternal injection of the stable thyrotropin-releasing hormone (TRH)-analog RX 77368 (77 pmol) induced a stimulation of gastric contractility for 40 min. Intracisternal injection of bombesin (62-620 pmol) followed 30 min later by that of RX 77368 resulted in a dose-related inhibition of the TRH-analog-induced gastric contractility. Intracisternal injection of bombesin (620 pmol) did not modify gastric contractility stimulated by intravenous carbachol. Stimulation of gastric contractility induced by TRH-analog microinjected into the dorsal vagal complex (DVC) was dose-related suppressed by concomitant injections of bombesin (6.2-620 pmol). Neither bombesin alone (6.2 pmol) nor vehicle modified basal gastric contractility. These results demonstrate that bombesin acts within the brain to inhibit vagally stimulated gastric contractility and that the DVC is a sensitive site for bombesin inhibitory action. These findings suggest a possible interaction between TRH and bombesin in the central vagal regulation of gastric contractility.     

Hyperglycemia impairs antro-pyloric coordination and delays gastric emptying in conscious rats

Delayed gastric emptying has been shown in diabetes. Although it has been proposed that hyperglycemia, and not only autonomic neuropathy, contributes to the pathogenesis of delayed gastric emptying, the inhibitory mechanism of hyperglycemia on gastric emptying remains unclear. We studied the effects of hyperglycemia per se on gastric emptying and postprandial gastric motility in conscious rats. Liquid and solid gastric emptying were compared between saline-infused rats and D-glucose-infused rats. Two strain gauge transducers were implanted on the antrum and pylorus and the postprandial antro-pyloric coordination was compared between euglycemia and hyperglycemia. D-glucose infusion for 30 min increased blood glucose level from 5.4 +/- 0.5 to 13.0 +/- 1.3 mM and significantly delayed gastric emptying. Forty minutes after the feeding, contractions with low frequency (<3 cycles min(-1)) and high amplitude (>15 g) of the antrum were observed. This period reflects the emptying process of the gastric content and the coordination between the antrum and pylorus was frequently observed. D-glucose infusion significantly reduced feeding-induced antral contractions and abolished the number of episodes of antro-pyloric coordination. Sham feeding-induced gastric contractions were also significantly reduced by hyperglycemia. Postprandial antro-pyloric coordination was not observed in vagotomized rats, suggesting a mediation of vagus nerve. It is concluded that hyperglycemia impairs antral contractions and antro-pyloric coordination in rats. The inhibitory effect of hyperglycemia on gastric emptying is mediated, at least in part, via impaired vagal activity.     

Gastric Neuromodulation With Enterra System for Nausea and Vomiting in Patients With Gastroparesis

Objective: Gastric electrical stimulation (GES) has been introduced for treating gastric motility disorders, such as gastroparesis, and obesity. A special method of GES using high frequency‐short pulses, called Enterra® Therapy, has been clinically applied to treat nausea and vomiting in patients with gastroparesis. However, its mechanisms are not well understood. Materials and Methods: General methodologies of GES published in the literature are systematically reviewed and their main effects and application are presented. The major part of this review is focused on Enterra Therapy since this is the only method that has been used clinically. A number of different GES methods have been proposed. Results: GES with long pulses or dual pulses, but not short pulses, are able to alter (enhance or inhibit) such parameters of gastric motility as gastric slow waves and gastric emptying. Synchronized GES has been reported to improve antral contractions. GES with high frequency‐short pulses, or Enterra Therapy, is known to improve nausea and vomiting in patients with gastroparesis and has a response rate of 50–70%. Improved gastric accommodation, direct enteric nervous system effects, enhanced vagal activity, and activation of central neurons are believed to be the underlying mechanisms involved in the antiemetic effect of this therapy. Conclusions: GES with high frequency‐short pulses effectively reduces nausea and vomiting in patients with gastroparesis. This antiemetic effect could be mediated via enteric, autonomic, and/or central neural mechanisms. Further systematic and controlled studies are needed to improve the efficacy of Enterra Therapy and to understand its mechanisms of action.     

Motilin, erythromycin, and the gastric migrating motor complex: site of action

Motilin is a putative hormone which induces a premature migrating motor complex when administered exogenously, but the target organ for this hormonal effect is undetermined. Our aim was to determine whether motilin and the motilin agonist, erythromycin, induce a premature migrating motor complex via an effect directly on the stomach. Six dogs underwent splenectomy and ligation of all branches of the splenic artery except the left gastroepiploic and short gastric arteries to the proximal stomach. An intra-arterial catheter was placed in the proximal splenic artery for close intra-arterial injection of motilin and erythromycin directly to the gastric corpus/proximal antrum. After recovery, the minimum effective dose required to induce a premature migrating motor complex was determined for motilin and for erythromycin given close intra-arterially or intravenously (systemically) by monitoring upper gut myoelectric activity. Minimum effective doses of motilin and erythromycin were the same whether given intra-arterially or intravenously. The latency interval or the time to onset of a premature Phase III was less than 2 minutes for intra-arterial or intravenous administration (P > 0.05). The characteristics of induced-Phase HI activity (appearance, duration, velocity) did not differ from spontaneous Phase HI activity (P > 0.05). Although plasma motilin concentrations increased after threshold doses of both motilin and erythromycin, increases in plasma motilin occurred later after erythromycin (lOmin) than after exogenous motilin (3 min). Our findings suggest that motilin initiation of the migrating motor complex does not occur by independent stimulation of putative receptors in the gastric corpus or proximal antrum.     

Inhibitory neural pathway regulating gastric emptying in rats

The relaxation of the pylorus is one of the most important factors for promoting gastric emptying. However, the role of inhibitory neurotransmitters in the regulation of pyloric relaxation and gastric emptying remains unclear. In this study, we investigated the effects of NO biosynthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), and calcium dependent potassium channel blocker, apamin, on vagal stimulation-induced pyloric relaxation and gastric emptying in rats. Sodium nitroprusside (SNP), adenosine 5'-triphosphate (ATP), vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP) caused pyloric relaxations in a dose dependent manner in vivo. Apamin (120 microg/kg) significantly reduced ATP and PACAP-induced pyloric relaxations without affecting SNP- or VIP-induced relaxations. Vagal stimulation (10 V, 1 ms, 1-20 Hz)-induced pyloric relaxation was significantly inhibited by L-NAME (10 mg/kg). The combined administration of L-NAME and apamin almost completely abolished vagal stimulation-induced pyloric relaxation. L-NAME and apamin significantly increased spontaneous contractions in the antrum, pylorus and duodenum. Increased motility index by L-NAME and apamin was significantly higher in the pylorus and duodenum, compared to that of antrum. L-NAME and apamin significantly delayed liquid gastric emptying. These results suggest that besides NO, probably ATP and PACAP, act as inhibitory neurotransmitters in the rat pylorus and regulate gastric emptying.     

9The TANTALUSTM System for obesity: effect on gastric emptying of solids

Background: Gastric electrical stimulation (GES) is currently investigated for the treatment of obesity. The TANTALUS System delivers gastric contractility modulation (GCM) signals in synchrony with gastric slow waves, resulting in significant augmentation of gastric contractions during food intake. We hypothesized that such modulation of contractile activity may affect gastric emptying and plasma ghrelin levels. Aim: To test the effect of GCM of the gastric antrum on gastric emptying of solids and ghrelin levels. Methods: 12 obese subjects were implanted with 2 pairs of antral electrodes and an implantable pulse generator (IPG, TANTALUS ^TM) Gastric emptying test (GE) for solids was performed twice, on separate days, in each subject, starting few weeks after implantation: 1) control, before the start of stimulation, and 2) with stimulation, after device was turned on. Blood samples for ghrelin, were taken at baseline, and at 15, 30, 60 and 120 min after the test meal. Results as mean + SD, analysis by t‐test and p < 0.05. Results: 11 females, 1 male, age: 39.1 ± 8.9 years, BMI: 41.6 ± 3.4, 3 subjects with type 2 diabetes. One diabetic patient did not complete GE test because of technical issues. GCM significantly accelerated gastric emptying: retention at 2 hours 18.7 ± 12.2% vs. 31.9 ± 16.4%, stimulation vs. control respectively, p = 0.008. T ^1/2 78.3 ± 23.5 vs. 95 ± 31.7 min, stimulation vs. control respectively, p = 0.04. Mean results for gastric emptying were within normal at both baseline and stimulation. Meal ingestion induced only minimal, insignificant reduction in ghrelin levels. There was no significant difference in AUC of ghrelin between control and stimulation. Conclusions: After GCM stimulation, there is significant acceleration of gastric emptying of solids in obese patients, without affect on ghrelin levels. The obese subjects did not exhibit the significant, meal‐induced reduction in ghrelin.      

Gastric distension alters frequency and regularity but not amplitude of the gastric slow wave

Abstract 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.     

Effect of electrical stimulation on gastric electrical activity,motility and emptying

Abstract The aim was to measure the effect of gastric electrical stimulation on the frequency of canine antral pacesetter potentials (PPs), the strength of antral contractions, and the rate of gastric emptying while fasting, after feeding and with pentagastrin stimulation. Four conscious dogs with a stimulating electrode placed 10 cm proximal to the pylorus and recording electrodes and strain gauges placed 7, 5 and 3 cm proximal to the pylorus underwent myoelectric and strain gauge recordings while fasting, after feeding (250 ml 5% dextrose labelled with polyethylene glycol), and during pentagastrin infusion (0.5 μg kg^?1 min^?1) on four separate days. On each day, electrical stimulation was done using one of four stimulation frequencies (0, 6, 30 and 1200 stimuli per minute ***[s.p.m.]). Stimulation at 6 and 30 s.p.m. increased the fasting and fed PP frequency, whereas 1200 s.p.m. stimulation did not. Feeding decreased the maximum driven frequency, and pentagastrin increased it. Neither the motility index nor the gastric emptying rate were consistently changed by stimulation at any frequency. In conclusion, canine proximal antral stimulation at 6 and 30 s.p.m. sped PP frequency during fasting and after feeding, but stimulation over a wide range of frequencies had little effect on gastric contractions and emptying.