Implantable Gastric Stimulation Inhibits Gastric Motility via Sympathetic Pathway in Dogs

Zhu, Hongbing; Chen, Jiande D.Z.

doi:10.1381/0960892052993549

Cited by 38 publications

(34 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All recordings were displayed on a computer monitor. Motor activity of the stomach was assessed by using the mean area under the curve (AUC) per second, which was computed with the Polygram Function Testing Software (Medtronic) (52). The data presented in this study were obtained from channel 3, which had the highest quality recording.…”

Section: Recording and Analysis Of Antral Motilitymentioning

confidence: 99%

Electroacupuncture improves impaired gastric motility and slow waves induced by rectal distension in dogs

Chen¹,

Song²,

Yin³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

112

View full text Add to dashboard Cite

puncture improves impaired gastric motility and slow waves induced by rectal distension in dogs. Am J Physiol Gastrointest Liver Physiol 295: G614 -G620, 2008. First published July 24, 2008 doi:10.1152/ajpgi.90322.2008 is known to induce upper gastrointestinal (GI) symptoms. The aim of this study was to investigate the effects and underlying mechanisms of RD on gastric slow waves (GSW) and motor activity and furthermore to investigate the effects and mechanisms of electroacupuncture (EA) on GSW and motor activity. Eight female hound dogs chronically implanted with gastric serosal electrodes and a gastric fistula were studied in six separate sessions. Antral motility, GSW, heart rate variability, and rectal pressure were evaluated for the above purposes. 1) RD at a volume of 120 ml suppressed antral motility significantly. Guanethidine blocked the inhibitory effect of RD. EA at ST36 was able to restore the suppressed antral contractions induced by RD (16.6 Ϯ 1.7 vs. 8.0 Ϯ 1.4, P Ͻ 0.001). Naloxone partially blocked the effect of EA on antral contractions. 2) RD reduced the percentage of normal GSW from 98.8 Ϯ 0.8% at baseline to 76.1 Ϯ 8.6% (P Ͻ 0.05) that was increased to 91.8 Ϯ 3.0% with EA. The effects of EA on the GSW were nullified by the presence of naloxone. 3) EA did not show any significant effect on rectal pressure, suggesting that the ameliorating effects of EA on RD-induced impaired gastric motility were not due to a decrease in rectal pressure. 4) EA increased the vagal activity suppressed by RD. In conclusion, RD inhibits postprandial gastric motility and impairs GSW in dogs, and the inhibitory effects are mediated via the adrenergic pathways. EA at ST36 is able to restore the RD-induced impaired GSW and motor activities, possibly by enhancing vagal activity, and is partially mediated via the opioid pathway. EA may have therapeutic potential for functional gastrointestinal disorders. adrenergic pathway; gastric slow waves; naloxone CHRONIC, IDIOPATHIC, slow-transit constipation and constipationdominant irritable bowel syndrome (IBS) are commonly observed in clinical practice. These patients frequently complain of upper abdominal symptoms such as bloating, upper abdominal discomfort or pain, and vomiting. The symptoms overlap with lower abdominal symptoms and are resistant to dietary and pharmacological treatments because of the constipation issues; they are related to the presence of impaired gastrointestinal myoelectrical activity and reduced upper gastrointestinal motor activity (1,4,13,31,33,37). This phenomenon has led to the hypothesis that rectal distension (RD) with fecal stasis in the colorectal region directly causes reflexive inhibition of proximal gastrointestinal motility (5,7,9,22,32,50).A number of investigations have indicated that RD induces upper gastrointestinal symptoms, inhibits gastric tone and accommodation, and delays gastric emptying (3, 14, 20 -21, 24, 34 -35, 50). However, little information about the effects of RD on gastric contractions is available, although gastric co...

show abstract

Section: Recording and Analysis Of Antral Motilitymentioning

confidence: 99%

Electroacupuncture improves impaired gastric motility and slow waves induced by rectal distension in dogs

Chen¹,

Song²,

Yin³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

112

View full text Add to dashboard Cite

show abstract

“…However, some investigators noted a role of sympathetic pathways in the effects of GES on gastrointestinal functions. The intravenous administration of guanethidine, an adrenergic blockade, prevents the inhibitory effect of GES on antral motility and rectal tone, indicating that GES effects are mediated via sympathetic adrenergic nerve activation (Zhu and Chen 2005;Liu et al 2005). Long-pulse retrograde GES at a tachygastrial frequency suppresses postprandial antral contractions via alpha-and beta-adrenergic pathways (Ouyang et al 2005).…”

Section: Afferent Pathwaysmentioning

confidence: 99%

“…For example, GES significantly inhibits postprandial antral contractions. Guanethidine, an adrenergic blocker, can prevent this effect of GES, suggesting involvement of sympathetic pathways (Zhu and Chen 2005). Intravenous injections of propranolol or phentolamine is reported to abolish long-pulse GES-induced tachygastria and antral hypomotility via the alphaand beta-adrenergic sympathetic pathways (Ouyang et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Modulatory effects and afferent pathways of gastric electrical stimulation on rat thoracic spinal neurons receiving input from the stomach

Qin

Chen

Zhang

et al. 2007

Neuroscience Research

View full text Add to dashboard Cite

Gastric electrical stimulation (GES) has been suggested as a potential therapy for patients with obesity or gastric motility disorders. The aim of this study was to investigate the spinal mechanism of GES effects on gastric functions. Extracellular potentials of single spinal (T9-T10) neurons were recorded in pentobarbital anesthetized, paralyzed, ventilated male rats (n=19). Gastric distension (GD) was produced by air inflation of a balloon. One pair of platinum electrodes (1.0-1.5 cm apart) was sutured onto the serosal surface of the lesser curvature of the stomach. GES with four sets of parameters was applied for one minute: GES-A (6 mA, 0.3 ms, 40 Hz, 2s on, 3s off), GES-B (6 mA, 0.3 ms, 14 Hz, 0.1s on, 5s off), GES-C (6 mA, 3 ms, 40 Hz, 2s on, 3s off), GES-D (6 mA, 200 ms, 12 pulses/min). 62/158 (39%) spinal neurons responded to GD (20, 40, 60 mmHg, 20s. Most GD-responsive neurons (n=43) had excitatory responses; the remainder had inhibitory (n=12) or biphasic responses (n=7). GES-A, -B, -C and -D affected activity of 12/33 (36%), 4/31 (13%), 22/29 (76%) and 13/30 (43%) GD-responsive neurons, respectively. Bilateral cervical vagotomy did not significantly alter mean excitatory neuronal responses to GD (n=5) or GES (n=6). Resiniferatoxin (2.0 μg/kg, i.v.), an ultrapotent agonist of vanilloid receptor-1, abolished excitatory responses to GD and GES in 4/4 neurons recorded in vagotomized rats. The results suggested that GES mainly had an excitatory effect on T9-T10 spinal neurons with gastric inputs; neuronal responses to GES were strengthened with stimulation at an increased pulse width and/or number of pulses. The modulatory effect of GES involved thoracic spinal (sympathetic) afferent fibers containing vanilloid receptor-1.

show abstract

“…The assessment of vagal activity with an advanced spectral analysis of heart rate variability indicates that effects of GES with certain parameters are relevant to increased vagal activity and accelerated gastric emptying in dogs and rats (Liu et al 2004;Ouyang et al 2003). Furthermore, intravenous administration of an adrenergic blocker prevents the inhibitory effect of GES on antral motility and/or rectal tone, indicating an involvement of the sympathetic adrenergic nerve fibers (Zhu and Chen 2005;Liu et al 2005;Ouyang et al 2005). The present study showed that vagotomy did not significantly affect the effects of GES on spinal neuronal activity but intravenous RTX abolished responses to GES in rats with vagotomy.…”

Section: Afferent Pathwaysmentioning

confidence: 99%

“…In rats, GES can activate vagal afferent fibers innervating the stomach (Peles et al 2003) and modulate activity of neurons in the nucleus tractus solitarii receiving gastric vagal afferents (Qin et al 2005). A few recent studies further suggest that effects of GES with varying parameters on gastric motility involve the sympathetic alpha-and beta-adrenergic sympathetic efferent pathways system (Zhu and Chen 2005;Ouyang et al 2005). The spinal sympathetic afferent pathways and the intraspinal neuronal activity relevant to GES effects also have been characterized recently in rats (Qin et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Characterization of T9–T10 spinal neurons with duodenal input and modulation by gastric electrical stimulation in rats

et al. 2007

View full text Add to dashboard Cite

Gastric electrical stimulation (GES) has been suggested as a therapy for patients with gastric motility disorders or morbid obesity. However, it is unclear whether GES also affects intestinal sensory and motor functions. Furthermore, little is known about intraspinal visceroreceptive transmission and processing for duodenal afferent information. The aims of this study were to characterize responses of thoracic spinal neurons to duodenal distension, to determine the afferent pathway, and to examine the effects of GES on activity of these neurons. Extracellular potentials of single T9-T10 spinal neurons were recorded in pentobarbital anesthetized, paralyzed, ventilated male rats (n=19). Graded duodenal distension (DD, 0.2-0.6 ml, 20 s) was produced by water inflation of a latex balloon surgically placed into the duodenum. One pair of platinum electrodes (1.0-1.5 cm apart) was sutured onto the serosal surface of the lesser curvature of the stomach. GES with four sets of parameters was applied for one minute: GES-A (6 mA, 0.3 ms, 40 Hz, 2s on, 3s off), GES-B (6 mA, 0.3 ms, 14 Hz, 0.1s on, 5s off), GES-C (6 mA, 3 ms, 40 Hz, 2s on, 3s off), GES-D (6 mA, 200 ms, 12 pulses/min). Results showed that 33/117 (28%) spinal neurons responded to noxious DD (0.4 ml, 20s). Of these, 7 (6%) neurons had low-threshold responses to DD (≤0.2 ml) and 26 (22%) had high-threshold responses to DD (≥0.4 ml). DD-responsive spinal neurons were encountered more frequently in deeper (depth: 0.3-1.2 mm) than in superficial laminae (depth: <0.3 mm) of the dorsal horn (24/67 vs 9/50, P<0.05). DD excited all 9 superficial neurons. In contrast, 20 deeper neurons were excited and 4 neurons were inhibited by DD. Activity of DD-responsive neurons was affected more frequently with GES-C (13/15, 87%) than GES-A (6/16, 38%), -B (3/15, 20%), -D (5/14, 36%), (P<0.01). Bilateral cervical vagotomy did not significantly alter the effects of DD and GES on 5/5 neurons. Resiniferatoxin (2.0 μg/kg, i.v.), an ultrapotent agonist of transient receptor potential vanilloid receptor-1 (TRPV1), abolished DD responses and GES effects on all neurons examined in vagotomized rats. Additionally, 29/33 (88%) DD-responsive neurons received inputs from somatic receptive fields on the back, flank, and medial/lateral abdominal areas. It was concluded that GES mainly exerted an excitatory effect on T9-T10 spinal neurons with duodenal input transmitted by sympathetic afferent fibers expressing TRPV1; spinal neuronal responses to GES were strengthened with an increased pulse width and/or frequency of stimulation; T9-T10 spinal neurons processed input from the duodenum and might mediate effects of GES on duodenal sensation and motility.

show abstract

Implantable Gastric Stimulation Inhibits Gastric Motility via Sympathetic Pathway in Dogs

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

Cited by 38 publications

References 28 publications

Electroacupuncture improves impaired gastric motility and slow waves induced by rectal distension in dogs

Electroacupuncture improves impaired gastric motility and slow waves induced by rectal distension in dogs

Modulatory effects and afferent pathways of gastric electrical stimulation on rat thoracic spinal neurons receiving input from the stomach

Characterization of T9–T10 spinal neurons with duodenal input and modulation by gastric electrical stimulation in rats

Contact Info

Product

Resources

About