[Show abstract][Hide abstract] ABSTRACT: 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.
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to systematically evaluate and compare the effects of synchronized dual-pulse gastric electrical stimulation (SDPS) and conventional gastric electrical stimulation (CGES) on antral contractions, gastric tone, and autonomic functions.
Seven female hound dogs implanted with four pairs of electrodes on gastric serosa were studied in two separate experiments. The first experiment was designed to investigate the effects of SDPS/CGES on gastric tone and heart rate variations. The second experiment was performed to study the effects of SDPS/CGES on antral contractions.
1) SDPS induced gastric antral contractions in the fasting state, whereas CGES at the intrinsic or a tachygastrial frequency had no effects on fasting antral contractions. 2) SDPS enhanced postprandial antral contractions impaired by glucagon; however, CGES at a tachygastrial frequency inhibited postprandial antral contractions. In addition, CGES at the intrinsic frequency of the stomach had no effects on postprandial antral contractions. 3) SDPS or CGES at the intrinsic frequency of the stomach had no effects on gastric tone, but CGES at a tachygastrial frequency reduced gastric tone. 4) SDPS excited vagal activity, but CGES at a tachygastrial frequency inhibited vagal activity.
SDPS improves antral contractions but does not affect gastric tone and thus may have potential for treating gastric motility disorders. CGES at a tachygastrial frequency inhibits gastric tone and contractions and may be applicable for treating obesity. The excitatory or inhibitory effects of SDPS/CGES on gastric motility may be mediated via vagal pathway.
[Show abstract][Hide abstract] ABSTRACT: Aims: The aim of this study was to investigate and compare effective parameters for gastric electrical stimulation (GES) to modulate gastric muscle functions in different species. Methods: Four species: Pigs, dogs, rats, and mice implanted with two pairs of electrodes on the serosal surface of the stomach were studied, respectively. Experiment 1 was designed to entrain/pace gastric slow waves and included a series of 5-min periods with long-pulse GES of different pulse widths and frequencies. Experiment 2 was designed to induce gastric dysrhythmia with long-pulse GES of different frequencies. Gastric slow waves were recorded during the entire experiment. Results: 1) The minimum pulse width for GES to completely entrain the slow waves was similar (100-400 msec) in all four species. 2) With fixed amplitude (4 mA) and pulse width (400 msec), the highest frequency at which slow waves could be paced was similar (about 10-60% higher than the intrinsic slow wave frequency) in all species. 3) With fixed pulse width of 400 msec and amplitude of 6 mA, GES with nine to 18 cycles per min (cpm) was able to induce dysrhythmia in dogs. In addition, there was no significant difference among these frequencies of 9-18 cpm. 4) GES with 400 msec, 6 mA, and 9 cpm was able to induce dysrhythmia in all species. These effective GES parameters in results 1-4 were similar to those used in humans in the literature. Conclusions: There is no significant difference in stimulation parameters when GES is applied to alter gastric slow waves in different animal models. Furthermore, the effective parameters for GES to alter slow waves are similar between the humans and various animal models. These findings suggest that stimulation parameters obtained from animal studies are applicable in humans.
[Show abstract][Hide abstract] ABSTRACT: The aims of this study were to determine optimal pacing parameters of electrical stimulation on different gut segments and to investigate effects and possible mechanisms of gastrointestinal electrical stimulation on gut slow waves. Twelve female hound-mix dogs were used in this study. A total of six pairs of electrodes were implanted on the stomach, duodenum, and ascending colon. Bilateral truncal vagotomy was performed in six of the dogs. One experiment was designed to study the effects of the pacing frequency on the entrainment of gut slow waves. Another experiment was designed to study the modulatory effects of the vagal and sympathetic pathways on gastrointestinal pacing. The frequency of slow waves was 4.88 +/- 0.23 cpm (range, 4-6 cpm) in the stomach and 19.68 +/- 0.31 cpm (range, 18-22 cpm) in the duodenum. There were no consistent or dominant frequencies of the slow waves in the colon. The optimal parameters to entrain slow waves were: frequency of 1.1 intrinsic frequency (IF; 10% higher than IF) and pulse width of 150-450 ms (mean, 320.0 +/- 85.4 ms) for the stomach, and 1.1 IF and 10-20 ms for the small intestine. Electrical stimulation was not able to alter colon slow waves. The maximum entrainable frequency was 1.27 IF in the stomach and 1.21 IF in the duodenum. Gastrointestinal pacing was not blocked by vagotomy nor the application of an alpha- or beta-adrenergic receptor antagonist; whereas the induction of gastric dysrhythmia with electrical stimulation was completely blocked by the application of the alpha- or beta-adrenergic receptor antagonist. Gastrointestinal pacing is achievable in the stomach and small intestine but not the colon, and the maximal entrainable frequency of the gastric and small intestinal slow waves is about 20% higher than the IF. The entrainment of slow waves with gastrointestinal pacing is not modulated by the vagal or sympathetic pathways, suggesting a purely peripheral or muscle effect.
[Show abstract][Hide abstract] ABSTRACT: To investigate the effect of two-channel gastric electrical stimulation (GES) with trains of pulses on gastric emptying and slow waves.
Seven dogs implanted with four pairs of electrodes and equipped with a duodenal cannula were involved in this study. Two experiments were performed. The first experiment included a series of sessions in the fasting state with trains of short or long pulses, each lasted 10 min. A 5-min recording without pacing was made between two sessions. The second experiment was performed in three sessions (control, single-channel GES, and two-channel GES). The stimulus was applied via the 1st pair of electrodes for single-channel GES (GES via one pair of electrodes located at 14 cm above the pylorus), and simultaneously via the 1st and 3rd channels for two-channel GES (GES via two pairs of electrodes located at 6 and 14 cm above the pylorus). Gastric liquid emptying was collected every 15 min via the cannula for 90 min.
GES with trains of pulses at a pulse width of 4 ms or higher was able to entrain gastric slow waves. Two-channel GES was about 50% more efficient than single-channel GES in entraining gastric slow waves. Two-channel but not single-channel GES with trains of pulses was capable of accelerating gastric emptying in healthy dogs. Compared with the control session, two-channel GES significantly increased gastric emptying of liquids at 15 min (79.0% +/- 6.4% vs 61.3% +/- 6.1%, P < 0.01), 30 min (83.2% +/- 6.3 % vs 68.2% +/- 6.9%, P < 0.01), 60 min (86.9% +/- 5.5 % vs 74.1% +/- 5.9%, P < 0.01), and 90 min (91.0% +/- 3.4% vs 76.5% +/- 5.9%, P < 0.01).
Two-channel GES with trains of pulses accelerates gastric emptying in healthy dogs and may have a therapeutic potential for the treatment of gastric motility disorders.
World Journal of Gastroenterology 06/2009; 15(19):2406-11. · 2.55 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Rectal distension (RD) 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+/-1.7 vs. 8.0+/-1.4, P<0.001). Naloxone partially blocked the effect of EA on antral contractions. 2) RD reduced the percentage of normal GSW from 98.8+/-0.8% at baseline to 76.1+/-8.6% (P<0.05) that was increased to 91.8+/-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.
[Show abstract][Hide abstract] ABSTRACT: Although several pathophysiologic abnormalities have been noted in functional dyspepsia (FD), their pathogenesis is poorly understood. We hypothesized that chronic gastric hypersensitivity and gastric motor dysfunction seen in FD patients can be modeled in rats by transient gastric irritation during the neonatal period, a time of known neuronal vulnerability to long-term plasticity.
Ten-day-old male rats received 0.2 mL 0.1% iodoacetamide (IA) in 2% sucrose daily by oral gavages for 6 days; controls received 2% sucrose. Rats in both groups were then followed to adulthood (8-10 weeks) at which point behavioral, visceromotor, and great splanchnic nerve responses to graded gastric balloon distention (GD; 20-80 mm Hg) and gastric motor function were tested.
IA-treated rats exhibited hypersensitivity to GD in a dose-dependent manner, as compared with the control group. The threshold of afferent nerve activation was lower and nerve responses to GD were significantly increased in IA-treated rats. Although IA-treated rats ingested food at a lower rate, gastric emptying was not significantly different between IA and control groups. However, gastric accommodation was significantly reduced in the IA group. No significant gastric pathology was seen in hypersensitive adult rats compared with controls.
These studies demonstrate that gastric irritation in the neonatal period can result in chronic gastric hypersensitivity and gastric motor dysfunction in adults even in the absence of significant detectable gastric pathology. Our results offer insight into the pathogenesis of chronic functional dyspepsia and provide a potential model for further study to this important clinical problem.
[Show abstract][Hide abstract] ABSTRACT: This study was to investigate the effect of gastric electrical stimulation (GES) with short pulses, long pulses, short-pulse trains or long-pulse trains on gastric dysrhythmia and motion-sickness signs induced by vasopressin.
Seven male beagle dogs implanted with four pairs of electrodes on gastric serosa were studied. The study was performed in six sessions in a randomized order. In session 1 or 2, either saline or vasopressin was infused without GES. In session 3, 4, 5 and 6, GES with short pulses, long pulses, trains of short pulses or trains of long pulses was performed before and during vasopressin infusion. Gastric slow waves and motion-sickness signs were recorded in each session.
(1) Vasopressin induced gastric dysrhythmia and motion sickness-like signs (ANOVA, P < 0.001). (2) GES with short pulses or trains of short pulses was capable of preventing vasopressin-induced emetic response (P < 0.001), but did not normalize gastric dysrhythmia. (3) GES with long pulses or trains of long pulses was able to normalize gastric dysrhythmia induced by vasopressin (P < 0.001), but showed no effects on vasopressin-induced motion-sickness signs.
GES with short pulses or trains of short pulses prevents vasopressin-induced emetic response with no improvement in gastric dysrhythmia. GES with long pulses or trains of long pulses normalizes gastric dysrhythmia induced by vasopressin with no effects on signs.
Digestive Diseases and Sciences 03/2008; 53(3):630-5. · 2.26 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Gastric electrical stimulation (GES) is known to improve vomiting with short pulses, normalize dysrhythmia with long pulses, and accelerate gastric emptying with 2 channels. The aim of this study was to assess the effects of a new method GES, namely, 2-channel GES with dual pulses on gastric emptying of solids as well as gastric dysrhythmia and emetic responses.
Seven beagle dogs implanted with 4 pairs of electrodes were studied. A novel method of GES was proposed: 2-channel dual-pulse GES in which each stimulus was composed of a short pulse followed with a long pulse, and stimulation was delivered at 2 different locations. The study was performed to test the effects of this new method of GES on vasopressin-induced delayed gastric emptying of solids, gastric dysrhythmia, and emetic responses.
(1) Vasopressin-induced gastric dysrhythmia and emetic responses, as well as delayed gastric emptying of solids (P < .01). (2) Two-channel, but not 1-channel, dual-pulse GES was able to accelerate vasopressin-induced delayed gastric emptying of solids. (3) Both 1- and 2-channel dual-pulse GES was capable of improving dysrhythmia and emetic responses (P < .01).
The novel method of 2-channel dual-pulse GES is capable of accelerating gastric emptying of solids and improving dysrhythmia and emetic responses induced by vasopressin. This new method of GES may have a potential for gastroparesis.
Surgery 02/2008; 143(1):72-8. · 3.37 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This study was designed to evaluate the effect of vaginal electrical stimulation on rectal tone and compliance and anal sphincter pressure and to explore possible mechanisms involved in the effects of vaginal electrical stimulation on rectal tone in conscious dogs.
Seven dogs inserted with a probe with two ring electrodes were studied. The study included two experiments. The first experiment was composed of two series of sessions rectal tone and compliance; and anal sphincter pressure. Each series included three sessions: vaginal electrical stimulation with long pulses, vaginal electrical stimulation with trains of long pulses, and vaginal electrical stimulation with trains of short pulses. The second experiment was performed in two sessions: vaginal electrical stimulation with long pulses plus guanethidine, and vaginal electrical stimulation with trains of long pulses plus guanethidine. In each session, rectal tone was recorded.
1) Vaginal electrical stimulation with long pulses or trains of long pulses but not trains of short pulses significantly decreased rectal tone and increased anal sphincter pressure. 2) None of the vaginal electrical stimulation methods altered rectal compliance. 3) The inhibitory effect of vaginal electrical stimulation on rectal tone was abolished by guanethidine.
Vaginal electrical stimulation with long pulses or trains of long pulses but not trains of short pulses reduces rectal tone and increases anal sphincter pressure. The inhibitory effect of vaginal electrical stimulation on rectal tone is mediated by the sympathetic pathway. These findings suggest that vaginal electrical stimulation may be a potential therapy for fecal incontinence.
Diseases of the Colon & Rectum 01/2008; 50(12):2104-11. · 3.34 Impact Factor