Secondary Peristalsis In Humans Research Articles

Effects of esophageal acid infusion vs mosapride on distension-induced secondary peristalsis in humans.

Secondary peristalsis contributes to the clearance of the refluxate from the esophagus. Acute administration of 5-hydroxytryptamine 4 (5-HT4 ) receptors agonist, mosapride or esophageal infusion of hydrochloric acid (HCl) facilitates secondary peristalsis. The aim of this study was to determine whether esophageal acid infusion and administration of mosapride had different effects on secondary peristalsis. Secondary peristalsis was performed with esophageal distension with rapid and slow air injections in 16 healthy subjects. We performed two separate sessions with HCl (0.1 N) and 40 mg oral mosapride to compare their influence on secondary peristaltic parameters. The threshold volume of secondary peristalsis was significantly lower with HCl infusion than mosapride (P = 0.01) by slow air injections. The threshold volume to generate secondary peristalsis was significantly lower with HCl infusion than mosapride (P = 0.002) by rapid air injections. More secondary peristalsis was trigged by rapid air injections after HCl infusion than mosapride (P = 0.003). Infusion of HCl or mosapride administration has similar effects on peristaltic wave amplitude and duration of primary and secondary peristalsis. Acute esophageal acid infusion can induce greater mechanosensitivity to distension-induced secondary peristalsis than 5-HT4 receptors agonist mosapride. The data suggest that acid-sensitive afferents are more likely to contribute to sensory modulation of esophageal secondary peristalsis; however, the motility aspects of secondary peristalsis are comparable between acute esophageal acidification and 5-HT4 receptors activation via mosapride.

Influence of GABA-B Agonist Baclofen on Capsaicin-Induced Excitation of Secondary Peristalsis in Humans.

Objectives:Esophageal instillation of capsaicin enhances secondary peristalsis, but the γ-aminobutyric acid receptor type B (GABA-B) agonist baclofen inhibits secondary peristalsis. This study aimed to investigate whether baclofen could influence heartburn perception and secondary peristalsis subsequent to capsaicin infusion in healthy adults.Methods:Secondary peristalsis was performed by slow and rapid mid-esophagus air injections in 15 healthy subjects. Two different sessions including esophageal infusion of capsaicin-containing red pepper sauce (0.84 mg) following pre-treatment with placebo or baclofen were randomly performed to test the effects on heartburn perception and secondary peristalsis.Results:The intensity of heartburn symptom subsequent to capsaicin infusion was significantly greater after pre-treatment of baclofen as compared with the placebo (P=0.03). Baclofen significantly increased the threshold volume of secondary peristalsis to slow air injections subsequent to esophageal capsaicin infusion (P<0.001). Baclofen significantly increased the threshold volume of secondary peristalsis to rapid air injections subsequent to esophageal capsaicin infusion (P<0.01). The frequency of secondary peristalsis subsequent to capsaicin infusion was significantly decreased with baclofen as compared with the placebo (P<0.002). Baclofen had no effect on any of the peristaltic parameters of secondary peristalsis subsequent to capsaicin infusion.Conclusions:The GABA-B agonist baclofen appears to attenuate the esophagus to capsaicin-induced excitation of secondary peristalsis in healthy adults. Our study suggests the inhibitory modulation for GABA-B receptors on capsaicin-sensitive afferents mediating secondary peristalsis in human esophagus.

Sa1654 - Influence of GABAB Agonist Baclofen on Capsaicin Induced Excitation of Esophageal Secondary Peristalsis in Humans

Sa1654 - Influence of GABAB Agonist Baclofen on Capsaicin Induced Excitation of Esophageal Secondary Peristalsis in Humans

Effects of prucalopride on esophageal secondary peristalsis in humans.

Objectives:Prucalopride, a high-affinity 5-hydroxytrypatamine 4 (5-HT4) receptors agonist, has been shown to improve colon motility in adults. Secondary peristalsis helps the clearance of retained food bolus and refluxate from the esophagus, but the effects of prucalopride on esophageal secondary peristalsis are unknown. We aimed to assess the effects of prucalopride on distension-induced secondary peristalsis in healthy adults.Methods:Two separate sessions with prucalopride and placebo were performed in 11 healthy adults to test the effects on secondary peristalsis. Secondary peristalsis was performed with slow and rapid mid-esophageal injections of air after a baseline recording of esophageal motility.Results:Prucalopride significantly decreased the threshold volume to generate secondary peristalsis during slow air injection (9.8±1.4 vs. 14.4±0.9 ml, P=0.005) and rapid air injection (3.9±0.3 vs. 5.2±0.4 ml, P=0.008). Secondary peristalsis was generated more frequently after application of prucalopride (80% (70–100%) vs. 70% (60–73%), P=0.01). Prucalopride increased the wave amplitude of distal esophagus during slow air injection (147.9±28.5 vs. 104.2±16.8 mm Hg, P=0.048) and rapid air injection (128.0±13.3 vs. 105.7±12.3 mm Hg, P=0.016). Primary peristaltic amplitudes were also significantly increased by the application of prucalopride.Conclusions:Acute administration of prucalopride enhances mechanosensitivity of distension-induced secondary peristalsis and promotes esophageal contractility in healthy adults. Whether prucalopride could be a therapeutic option for the treatment of subjects with esophageal hypomotility needs further study.

Sa1324 Effects of Prucalopride on Esophageal Secondary Peristalsis in Humans

Sa1324 Effects of Prucalopride on Esophageal Secondary Peristalsis in Humans

Effects of esophageal capsaicin instillation on acid induced excitation of secondary peristalsis in humans.

Esophageal instillation of capsaicin or hydrochloric acid enhances secondary peristalsis. Our aim was to investigate whether intra-esophageal capsaicin infusion can influence symptom perception and physiological alteration of secondary peristalsis subsequent to acid infusion. Secondary peristalsis was induced by mid-esophagus injections of air in 18 healthy subjects. Two different sessions including esophageal infusion of hydrochloric acid (0.1 N) following pretreatment with saline or capsaicin-containing red pepper sauce were randomly performed at least one week apart. Symptoms of heartburn and secondary peristalsis were determined and compared between each study session. The intensity of heartburn symptom subsequent to acid infusion was significantly reduced after capsaicin infusion as compared with saline infusion (54 ± 3 vs 61 ± 3; P = 0.03). Capsaicin infusion significantly increased the threshold volume of secondary peristalsis to rapid air injections subsequent to esophageal acid infusion (8.0 ± 0.5 mL vs 4.4 ± 0.3 mL; P < 0.0001). The frequency of secondary peristalsis subsequent to acid infusion was significantly decreased after capsaicin infusion as compared to saline infusion (70% [60-82.5%] vs 80% [70-90%]; P = 0.03). Capsaicin infusion significantly decreased the pressure wave amplitude of secondary peristalsis subsequent to acid infusion during rapid air injections (90.6 ± 8.7 mmHg vs 111.1 ± 11.1 mmHg; P = 0.03). Capsaicin appears to desensitize the esophagus to acid induced excitation of secondary peristalsis in humans, which is probably mediated by rapidly adapting mucosal mechanoreceptors. High capsaicin-containing diet might attenuate normal physiological response to abrupt acid reflux by inhibiting secondary peristalsis.

Tu1145 Effects of Esophageal Capsaicin Instillation on Acid Induced Excitation of Secondary Peristalsis in Humans

Tu1145 Effects of Esophageal Capsaicin Instillation on Acid Induced Excitation of Secondary Peristalsis in Humans

Influence of repeated infusion of capsaicin-contained red pepper sauce on esophageal secondary peristalsis in humans.

The transient receptor potential vanilloid 1 has been implicated as a target mediator for heartburn perception and modulation of esophageal secondary peristalsis. Our aim was to determine the effect of repeated esophageal infusion of capsaicin-contained red pepper sauce on heartburn perception and secondary peristalsis in healthy adults. Secondary peristalsis was performed with mid-esophageal injections of air in 15 healthy adults. Two separate protocols including esophageal infusion with saline and capsaicin-contained red pepper sauce and 2 consecutive sessions of capsaicin-contained red pepper sauce were randomly performed. After repeated infusion of capsaicin-contained red pepper sauce, the threshold volume to activate secondary peristalsis was significantly increased during slow (p<0.001) and rapid air injections (p=0.004). Acute infusion of capsaicin-contained red pepper sauce enhanced heartburn perception (p<0.001), but the intensity of heartburn perception was significantly reduced after repeated capsaicin-contained red pepper sauce infusion (p=0.007). Acute infusion of capsaicin-contained red pepper sauce significantly increased pressure wave amplitudes of distal esophagus during slow (p=0.003) and rapid air injections (p=0.01), but repeated infusion of capsaicin-contained red pepper sauce significantly decreased pressure wave amplitude of distal esophagus during slow (p=0.0005) and rapid air injections (p=0.003). Repeated esophageal infusion of capsaicin appears to attenuate heartburn perception and inhibit distension-induced secondary peristalsis in healthy adults. These results suggest capsaicin-sensitive afferents in modulating sensorimotor function of secondary peristalsis in human esophagus.

Mo1875 Effect of Repeated Esophageal Infusion of Capsaicin-Contained Red Pepper Sauce on Secondary Peristalsis in Humans

Mo1875 Effect of Repeated Esophageal Infusion of Capsaicin-Contained Red Pepper Sauce on Secondary Peristalsis in Humans

Comparable effects of capsaicin‐containing red pepper sauce and hydrochloric acid on secondary peristalsis in humans

We aimed to evaluate whether acute esophageal instillation of capsaicin and hydrochloric acid had different effects on distension-induced secondary peristalsis. Secondary peristalsis was induced by slow and rapid air injections into the mid-esophagus after the evaluation of baseline motility in 16 healthy subjects. The effects on secondary peristalsis were determined by esophageal instillation with capsaicin-containing red pepper sauce (pure capsaicin, 0.84 mg) and hydrochloric acid (0.1 N). The administration of capsaicin induced a significant increase in the visual analogue scale score for heartburn as compared with hydrochloric acid (P = 0.002). The threshold volume for generating secondary peristalsis during slow and rapid air distensions did not differ between capsaicin and hydrochloric acid infusions. Hydrochloric acid significantly increased the frequency of secondary peristalsis in response to rapid air distension compared with capsaicin infusion (P = 0.03). Pressure wave amplitude during slow air distension was greater with the infusion of hydrochloric acid than capsaicin infusion (P = 0.001). The pressure wave duration during rapid air distension was longer after capsaicin infusion than hydrochloric acid infusion (P = 0.01). The pressure wave amplitude during rapid air distension was similar between capsaicin and hydrochloric acid infusions. Despite subtle differences in physiological characteristics of secondary peristalsis, acute esophageal instillation of capsaicin and hydrochloric acid produced comparable effects on distension-induced secondary peristalsis. Our data suggest the coexistence of both acid- and capsaicin-sensitive afferents in human esophagus which produce similar physiological alterations in secondary peristalsis.

Influence of Intraluminal Acidification on Esophageal Secondary Peristalsis in Humans

Secondary peristalsis contributes to clearance of retained refluxate or material from the esophagus. The goal of our study was to investigate the effects of hydrochloric acid (HCl) on physiological characteristics of esophageal secondary peristalsis in healthy adults. After recording esophageal motility baseline for primary peristalsis, secondary peristalsis was stimulated with slow and rapid air injections in the mid-esophageal in 16 healthy subjects. Normal saline and HCl (0.1 N) were separately infused into the esophagus to test whether they had effects on secondary peristalsis. After infusion of HCl, the threshold volume to generate secondary peristalsis was significantly decreased during rapid and slow air infusions (both P < 0.05). The frequency of secondary peristalsis was increased after HCl infusion (90 % [72.5-100 %] versus 85 % [72.5-90 %], P = 0.002). Infusion of HCl significantly increased pressure wave amplitude during rapid and slow air infusions (both P < 0.05). Infusion of saline did not affect any parameters of secondary peristalsis. The occurrence of heartburn was generated in 7 of 16 subjects after infusion of HCl with an increase in visual analogue scale score (12.5). Our data show that acute esophageal acid infusion enhances sensitivity of distension-induced secondary peristalsis and enhances secondary peristaltic activity. The study supports the evidence of the presence of acid-sensitive afferents in the modulation of distension-induced secondary peristalsis in humans.

Heterogeneity in Esophageal Motility in Reflux Patients With Different Symptom Presentation: Studies With Combined Impedance and Manometry

peristalsis could be modulated by baclofen and mosapride. Methods: In all 15 healthy subjects (5 female, mean age 22, range 20-26 yr), secondary peristalsis was generated by slow and rapid mid-esophageal injections of air after a baseline recording of esophageal motility. Three separate sessions with 40 mg oral baclofen, 40 mg oral mosapride or placebo were randomly performed to test their effects on esophageal secondary peristalsis with at least a 1-week interval. Results: Baclofen significantly increased the threshold volume for triggering secondary peristalsis during slow air distension (P = 0.003) and rapid air distension (P = 0.002). Baclofen significantly reduced the rate of secondary peristalsis by rapid air distension from 90% to 30% (P = 0.0002). Despite increasing basal LES pressure (P = 0.03), baclofen did not affect any of peristaltic parameters by primary or secondary peristalsis. Mosapride significantly decreased the threshold volume for triggering secondary peristalsis during rapid air distension (P = 0.04). Secondary peristalsis was triggered more frequently in response to rapid air distension after application of mosapride (P = 0.02). Mosapride significantly increased pressure wave amplitudes of secondary peristalsis during slow (P = 0.001) and rapid air distension (P = 0.002). Conclusions: Inhibition of baclofen on the triggering of secondary peristalsis presents during esophageal distension, indicating that sensory part of secondary peristalsis is probably mediated by the GABAB receptors. However, baclofen does not lead to any motility change in secondary peristalsis as induced by either slow or rapid air distension. Mosapride appears to enhance sensitivity to distension-induced secondary peristalsis and facilitates secondary peristaltic contractility, suggesting the involvement of 5-HT4 in the modulation of esophageal secondary peristalsis in humans.

Effects of mosapride on esophageal secondary peristalsis in humans

Secondary peristalsis is important for the clearance of refluxate or retained food bolus from the esophagus. Mosapride is a prokinetic agent that enhances GI motility by stimulating 5-hydroxytrypatamine(4) (5-HT(4) ) receptors, but its effects on secondary peristalsis are yet unclear in humans. We aimed to investigate the effect of a 5-HT(4) agonist mosapride on esophageal distension-induced secondary peristalsis in normal subjects. After a baseline recording esophageal motility, secondary peristalsis was generated by slow and rapid mid-esophageal injections of air in 15 healthy subjects. Two separate sessions with 40mg oral mosapride or placebo were randomly performed to test their effects on esophageal secondary peristalsis. Mosapride decreased the threshold volume for triggering secondary peristalsis during rapid air distension (4.5±0.3 vs 5.3±0.4mL; P=0.04) but not slow air distension (14.3±1.2 vs 13.3±1.3mL; P=0.41). Secondary peristalsis was triggered more frequently in response to rapid air distension after application of mosapride [100% (90-100%) vs 90% (80-100%); P=0.02]. Mosapride significantly increased pressure wave amplitudes of secondary peristalsis during slow (135.4±13.8 vs 105.0±12.9mmHg; P=0.001) and rapid air distensions (124.0±11.6 vs 95.9±14.0mmHg; P=0.002). Mosapride enhances sensitivity to distension-induced secondary peristalsis and facilitates secondary peristaltic contractility. These data provide an evidence for modulation of esophageal secondary peristalsis by the 5-HT(4) agonist mosapride, as well support for its clinical utility.

Effects of capsaicin-containing red pepper sauce suspension on esophageal secondary peristalsis in humans

Capsaicin-sensitive afferents have been implicated in the modulation of gastrointestinal sensorimotor functions. Secondary peristalsis is important for the clearance of retained refluxate or material from the esophagus. The aim of this study was to evaluate the effects of capsaicin-containing red pepper sauce suspension on esophageal secondary peristalsis in healthy adults. After a baseline recording of esophageal motility, secondary peristalsis was generated by slow and rapid mid-esophageal injections of air in 10 healthy subjects. Two separate sessions with saline and capsaicin-containing red pepper sauce were randomly performed to test their effects on esophageal secondary peristalsis. Infusion of capsaicin significantly increased pressure wave amplitude during rapid (P = 0.002) and slow air infusions (P = 0.01). After capsaicin, the threshold volume to generate secondary peristalsis was significantly decreased during rapid (P < 0.05) and slow air infusions (P = 0.02). Infusion of saline did not affect any parameters of secondary peristalsis during rapid or slow air infusion. The administration of capsaicin was accompanied by the occurrence of heartburn in all subjects. The acute administration of capsaicin-containing red pepper sauce suspension enhances sensitivity to distension-induced secondary peristalsis and facilitates secondary peristaltic contractility. These data suggest the involvement of capsaicin-sensitive afferents in the modulation of esophageal distension-induced secondary peristalsis in humans.

T1879 Mechanisms of Esophageal Distension-Induced Secondary Peristalsis in Humans: Studies With Capsaicin and Lidocaine

T1879 Mechanisms of Esophageal Distension-Induced Secondary Peristalsis in Humans: Studies With Capsaicin and Lidocaine

Effects of lidocaine on esophageal secondary peristalsis in humans

Secondary peristalsis is important for the clearance of retained food bolus or refluxate from the esophagus. Lidocaine has been used to evaluate the role of mucosa-mediating pathways of esophageal reflexes in animal model, but its effects on esophageal secondary peristalsis are yet unclear in humans. We aimed to investigate whether esophageal secondary peristalsis can be affected by intraluminal infusion of lidocaine into the esophagus. After a baseline recording esophageal motility, secondary peristalsis was generated by slow and rapid mid-esophageal injections of air in 13 healthy subjects. Two separate sessions with saline and lidocaine were randomly performed to test their effects on esophageal secondary peristalsis by mid-esophageal air distension. Secondary peristalsis can be induced by slow or rapid air infusion. Secondary peristalsis was triggered less frequently in response to rapid air distension after lidocaine infusion (P = 0.001). After lidocaine infusion, the threshold volume to generate secondary peristalsis was significantly increased during rapid (P = 0.001), but not slow air infusions (P = NS). Infusion of lidocaine or saline did not affect pressure wave amplitude or duration during rapid and slow air infusions (P = NS). We have demonstrated selectively inhibitory effect of lidocaine on the triggering of esophageal secondary peristalsis during acute gaseous esophageal distension. The data suggest that part of the activation of secondary peristalsis is probably mediated by lidocaine-sensitive mechanoreceptors; however, the infusion of lidocaine does not lead to any motility change in secondary peristalsis induced by either slow or rapid air infusions.

Mechanisms of Secondary Esophageal Peristalsis

Ever since the introduction of radiographic methods to study esophageal motility almost a century ago, it has been recognized that peristalsis in the human esophagus can be excited either by swallowing or by reflex, without a swallow. The latter phenomenon has been called, for many decades, secondary peristalsis. Secondary peristalsis is widely accepted as a common phenomenon, but it has not received much study. Fleshler et al[1]described the great similarity between primary and secondary peristalsis in humans. They, and others who studied the phenomenon, such as Creamer and Schlegel,[2]used distention as the stimulus to excite secondary, or reflex, peristalsis. The question of whether other kinds of receptors, receptors to acids, or osmotic pressure can also excite secondary peristalsis remains unexplored. Since it is theory at best that secondary peristalsis in humans commonly occurs after an episode of gastroesophageal reflux, it may well be that acid or osmoreceptors are involved in the initiation of the reflex. Still, since the reflux of gastric contents also probably excites mechanoreceptors, we cannot separate the stimuli to investigate them individually with respect to their relative capacities to excite the reflex, at least in the clinical situation.