Tachygastria induced by gastric electrical stimulation is mediated via <i>α</i>‐ and <i>β</i>‐adrenergic pathway and inhibits antral motility in dogs

Ouyang, Hui; Xing, Jinhong; Chen, Jiande

doi:10.1111/j.1365-2982.2005.00696.x

Cited by 49 publications

(64 citation statements)

References 36 publications

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“…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). In the present study, examination of spinal neuronal activation by GES indicated that effects of GES on gastric function might primarily involve spinal sympathetic afferent pathways.…”

Section: Afferent Pathwaysmentioning

confidence: 46%

“…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). Thus, these studies provide evidence for a role of the gastric sympathetic efferent pathway in effects of GES on gastric motility.…”

Section: Introductionmentioning

confidence: 69%

“…The reason behind this selection is that this set of parameters was known more effective in activating GD-responsive neurons in the paraventricular nucleus (Tang et al 2006). Parameter D is typically used to alter gastric motility functions (Ouyang et al 2005). In the present study, the four sets of GES parameters mainly induced excitatory responses in most spinal neurons with gastric input.…”

Section: Effects Of Gesmentioning

confidence: 84%

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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

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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.

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Section: Afferent Pathwaysmentioning

confidence: 46%

Section: Introductionmentioning

confidence: 69%

Section: Effects Of Gesmentioning

confidence: 84%

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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

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“…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

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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.

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Antibiotic duration and gastric dysmotility in preterm neonates

Sadder,

Brown,

Roblyer

et al. 2024

J. pediatr. gastroenterol. nutr.

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ObjectivesProlonged antibiotic use after birth is associated with neonatal feeding intolerance and functional gastrointestinal disorders (FGIDs). A gastric dysrhythmia (tachygastria) with frequencies >4–9 cycles per minute, measured by electrogastrography (EGG), is associated with FGIDs. The relationship between prolonged antibiotic use and % time spent in tachygastria is unknown in preterm infants. We aimed to compare weekly changes in % tachygastria between preterm infants receiving long (>48 h) versus short (≤48 h) courses of antibiotics for early onset sepsis evaluation (initiated at <3 days of life).MethodsThis was a longitudinal, prospective cohort study of 88 preterm infants (<34 weeks' gestation) with weekly EGG recordings from the first week of life until 40 weeks' post‐menstrual age, discharge, or death. We calculated % of EGG recording time in tachygastria and determined the mean across weekly sessions. A mixed effects model assessed variance in % tachygastria between the short‐ and long‐antibiotic exposure groups across all weeks.ResultsBaseline characteristics were similar between the two groups. There was no difference in % tachygastria between short and long antibiotic exposure groups across nine postnatal weeks (p = 0.08).ConclusionsEarly, prolonged antibiotic exposure among preterm infants may not lead to significant gastric dysrhythmia. Future studies including larger sample sizes and a “no antibiotic” exposure arm are essential in elucidating this potential relationship.

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

Abstract: 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.

Cited by 49 publications

References 36 publications

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

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

Antibiotic duration and gastric dysmotility in preterm neonates

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