Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Peristalsis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2002

Distinct patterns of oesophageal shortening during primary peristalsis, secondary peristalsis and transient lower oesophageal sphincter relaxation.

This study characterized oesophageal shortening during secondary peristalsis and transient lower oesophageal sphincter relaxation (TLOSR) in an attempt to determine its contribution to the opening mechanism. Eight healthy subjects (four males, 26 +/- 1 years) had metal clips affixed at 0, +3, and +8 cm relative to the squamocolumnar junction (SCJ), defining two distal oesophageal segments. Axial clip movement was assessed with concurrent videofluoroscopy and manometry during primary peristalsis, secondary peristalsis and TLOSR. Clip-defined oesophageal segment length change was measured at 0.5-s intervals. The magnitude of the most distal segment shortening was least with TLOSR, greatest with primary peristalsis and intermediate with secondary peristalsis. Conversely, maximal overall oesophageal shortening during TLOSR, evidenced by SCJ movement, was similar to that during primary peristalsis. In 3/12 TLOSRs, the moment of LOS opening and gas reflux was optimally imaged; SCJ excursion was 0.3 +/- 0.1 cm prior to LOS opening and 1.4 +/- 0.7 cm immediately after gas reflux. The segmental pattern of oesophageal shortening was distinct during primary peristalsis, secondary peristalsis and TLOSR. During TLOSR, significant elevation of the SCJ occurred only after LOS opening, suggesting that this was a consequence of oesophageal distension induced by gas reflux rather than a component of the opening mechanism.

Adult↗
PubMed1981

The renal pelvis and ureteral peristalsis. II. The pelvic pressure and its relation to the frequency of ureteral peristalsis.

The coordination between the renal pelvis and ureteral peristalsis is an important part of the hydrodynamics of the upper urinary tract. Pelvic pressure and frequency of ureteral peristalsis were registered simultaneously in 28 adult, female dogs. A mathematical analysis of these observation showed a non-linear relation of a "power function" in approximately 85% of the investigations. Hysteresis was demonstrated between the power functions of the increasing and of the subsequent decreasing diuresis in 15 of the examined dogs. It was concluded that the renal pelvis in a monocalyceal system governs the frequency of ureteral peristalsis and that hysteresis represents a viscoelastic action of the smooth muscle tissue.

Animals↗
PubMed1978

Oesophageal peristalsis. A simple system for the recording of oesophageal peristalsis, and the influence of bolus volume on peak peristaltic pressure amplitude.

Peak oesophageal peristaltic pressure amplitude was recorded in 8 healthy subjects at points 5 and 15 cm proximal to the gastro-oesophageal sphincter, by using an in situ tip-transducer simultaneously with a continuous flush (Intraflo) perfused catheter system with external pressure transducer. Dry swallows and wet swallows of 2.5, 5 and 10ml, respectively, were made in random succession. In all cases the pressures recorded by either system correlated well. In all cases the peristaltic pressure amplitude was significantly higher after the wet swallows. The catheter and flow system used in this study is simple and makes recording of peristaltic pressures independent of the shape of the in situ transducer, and its therefore well suited for measuring the amplitude of oesophageal contractions.

Adult↗
PubMed1996

Dissociation of the ascending excitatory reflex from peristalsis in the guinea-pig small intestine.

Localized distension of the intestine evokes an ascending excitatory reflex and a descending inhibitory reflex in the circular muscle layer. The sequential activation of these two reflexes is believed to underlie the motor pattern of peristalsis, which is responsible for the co-ordinated propulsion of intestinal contents. In this study we have shown that the initiation of peristalsis involves mechanisms additional to those mediating the ascending excitatory reflex. A short length of guinea-pig small intestine was mounted in a partitioned organ bath so that the lumen was occluded by the partition, but neuronal continuity was maintained. The anal segment was distended by intraluminal fluid infusion to evoke a peristalsis; in the oral segment, an isotonic transducer was used to record circular muscle contractions due to ascending excitatory reflexes. Stepwise distension of the anal segment with 5 microliters increments at 10 s intervals, or with a large, single-step infusion, elicited both the ascending excitatory reflex and peristalsis, when carried out at 3 min intervals. The threshold volume for the ascending excitatory reflex was smaller than the threshold for peristalsis with either incremental or single-step distensions. The ascending excitatory reflex appeared with a shorter delay than peristalsis. Tetrodotoxin (0.6 microM) or hexamethonium (100 microM) added to the oral compartment abolished the ascending excitatory reflex but not peristalsis. These drugs abolished both the ascending excitatory reflex and peristalsis when added to the anal compartment. When stimuli were delivered at 1 min intervals, peristalsis failed completely after the first trial, but the ascending excitatory reflex persisted, at a slightly reduced amplitude. When the anal segment was distended to just-subthreshold volume, electrical field stimulation (0.25-0.5 ms, 1-5 Hz for 1 s), delivered at 3 min intervals, evoked ascending excitatory responses but not peristalsis. Higher frequency stimulation (10 Hz) consistently evoked both peristalsis and the ascending excitatory responses. When trains of electrical stimulation were repeated at 1 min intervals, peristalsis quickly failed, but the ascending excitatory response persisted, although reduced in amplitude. The initiation of peristalsis can be dissociated from the ascending excitatory reflex by its threshold volume, by the duration of distension or the intensity of electrical stimulation required, and by its susceptibility to fatigue with repeated mechanical or electrical stimuli. This suggests that the ascending excitatory reflex may be part of the mechanism underlying the initiation of peristalsis, but that additional mechanisms must also be involved. Peristalsis should not be regarded as a reflex response but rather as an all-or-nothing motor pattern, triggered by mechanical stimulation, similar to other co-ordinated motor patterns in vertebrates and invertebrates.

Animals↗
PubMed1995

The inhibitory modulation of guinea-pig intestinal peristalsis caused by capsaicin involves calcitonin gene-related peptide and nitric oxide.

The effect of capsaicin-induced stimulation of afferent neurons on peristalsis and the possible neural mediators involved in this action were examined in the guinea-pig isolated ileum. The intraluminal pressure threshold for eliciting peristaltic waves was used to quantify facilitation (decrease in threshold) or inhibition (increase in threshold) of peristalsis. Capsaicin (0.1-1 microM) caused an initial short-lasting stimulation of peristalsis followed by a prolonged inhibition of peristaltic activity. Capsaicin (1 microM) was ineffective when the gut segments had been pretreated with 3.3 microM capsaicin, which is indicative of an afferent neuron-dependent action of the drug. In contrast, the abolition of peristalsis caused by a high concentration of capsaicin (33 microM) was fully reversible on removal and reproducible on readministration of capsaicin, a feature characteristic of a nonspecific depression of smooth muscle excitability. Baseline peristalsis and the excitatory/inhibitory effect of capsaicin (1 microM) on peristalsis remained unaltered by a combination of the tachykinin NK1 receptor antagonist (+)-(2S, 3S)-3-(2-methoxybenzylamino)-2-phenyl piperidine (CP-99,994; 0.3 microM) and the tachykinin NK2 receptor antagonist (L(-)-N-methyl-N[4-acetylamino-4-phenyl-piperidine-2-(3,4- -dichlorophenyl)butyl]-benzamide (SR-48,968; 0.1 microM). Further experiments, performed in the presence of a low concentration of atropine (10 nM) showed that the calcitonin gene-related peptide (CGRP) antagonist human alpha-calcitonin gene-related peptide (8-37) [hCGRP(8-37); 10 microM] attenuated the delayed inhibitory effect of capsaicin on peristalsis, but did not influence baseline peristaltic activity and the capsaicin-induced facilitation of peristalsis. Blockade of nitric oxide (NO) synthesis by NG-nitro-L-arginine methylester (L-NAME, 300 microM) facilitated baseline peristaltic activity and reduced the delayed inhibition of peristalsis caused by capsaicin (1 microM) without affecting the initial peristalsis-stimulating action of capsaicin. The effects of L-NAME were prevented by L-arginine (1 mM). The data of the current study indicate that capsaicin-sensitive afferent neurons do not participate in the neural pathways subserving peristalsis in the guinea-pig small intestine, but modulate peristaltic activity upon stimulation with capsaicin. The initial stimulant action of capsaicin on peristalsis is independent of tachykinins acting via NK1 or NK2 receptors, while the delayed capsaicin-induced depression of peristalsis involves CGRP and NO.

Animals↗
PubMed2005

Evaluation of esophageal peristalsis in patients with esophageal tumors: initial experience with cine MR imaging.

We evaluated esophageal peristalsis in patients with esophageal tumors by cine MR using steady-state free precession (SSFP) sequence and correlated the alteration of the esophageal peristalsis with clinical symptoms and tumor stages. Thirteen patients with pathologically proven esophageal tumors, including 12 esophageal cancers and one submucosal leiomyoma, underwent cine MRI using true fast imaging with steady precession (trueFISP) sequence, which is one SSFP sequence, after contrast-enhanced MR scanning for clinical purposes. A total of 120 serial images were obtained within 60 s through the plane along the long axis of the esophagus while patients chewed gum. The serial trueFISP images were evaluated for the presence, frequency, speed of progression, and passage of peristalsis through the tumor. The data from cine MRI were compared with clinical symptoms and tumor stages. Peristalsis was clearly identified in all patients. Seven patients with complete interruption of peristalsis had dysphagia; one with partially impaired peristalsis could intake solid foods with discomfort; and two with partially impaired peristalsis and three with preserved peristalsis remained asymptomatic. Patients with complete or partial interruption of peristalsis had Stage T3 or T4 esophageal cancer. In conclusion, trueFISP cine MR imaging enables direct visualization of esophageal peristalsis in relation to esophageal tumors. Complete interruption of peristalsis causes dysphagia, whereas partial interruption of and preserved peristalsis usually do not cause digestive problems. Interruption of peristalsis may indicate impaired muscle function caused by invasion of advanced esophageal cancers.

Esophageal Neoplasms↗
PubMed1994

Secondary oesophageal peristalsis in patients with non-obstructive dysphagia.

Secondary peristalsis was investigated in 30 patients with non-obstructive dysphagia and 20 age matched controls. Oesophageal motility was recorded at 3 cm intervals along the oesophageal body. Primary peristalsis was tested with 5 ml water swallows. Secondary peristalsis was stimulated with 10 ml boluses of air and water injected in the mid-oesophagus and by distensions (5 seconds duration) with a 3 cm balloon at the same level. Primary peristalsis was normal in 19 of the 20 control subjects and in nine of the 30 patients with dysphagia; 11 patients had diffuse spasm and 10 had non-specific abnormalities of primary peristalsis. Secondary peristalsis was triggered significantly less frequently by air and water distension in dysphagia patients (median success rate of 10% for the air boluses and 0% for the water boluses) than in control subjects (50% and 30% respectively, p < 0.005), and was abnormal in six of nine patients with normal primary peristalsis, nine of 11 patients with diffuse spasm and eight of 10 patients with non-specific motor abnormalities. The median frequency of balloon induced secondary peristalsis, however, was not significantly different in the two groups (0% controls, 40% non-obstructive dysphagia, p = 0.22). For each stimulus, there were no significant differences in the response rate in the three subgroups of patients. The major pattern of failure of secondary peristalsis in response to the air and water boluses was the complete absence of any oesophageal response. The amplitude of complete secondary peristalsis triggered by the water boluses and the balloon was greater in the patients with dysphagia (p = 0.03) than in normal subjects, while the amplitude of the secondary peristaltic responses triggered by the air boluses was similar in the two groups. Secondary peristaltic velocity was also similar in normal subjects and patients with non-obstructive dysphagia. Patients with non-obstructive dysphagia show a noticeable defect in the triggering of secondary peristalsis which may make an important contribution to the delayed oesophageal bolus transit and dysphagia seen in this condition.

Adult↗
PubMed1994

Stimulation and characteristics of secondary oesophageal peristalsis in normal subjects.

The study evaluates the triggering and characteristics of secondary oesophageal peristalsis in 25 healthy volunteers. Secondary peristalsis was stimulated by rapid intraoesophageal injection of boluses of air and water, and by a five second oesophageal distension with a balloon. Air and water boluses triggered secondary peristalsis that started in the proximal oesophagus regardless of injection site. Response rates were volume dependent with 83% of the 20 ml air boluses triggering secondary peristalsis compared with 2% for the 2 ml water bolus (p < 0.0001). Response rates for air and water were similar for equal bolus volumes and were not influenced by the site of injection. In contrast, balloon distension usually induced a synchronous contraction above the balloon, with secondary peristalsis starting below the balloon after deflation. The peristaltic response rate to balloon distension was also volume dependent and the middle balloon was more effective in triggering secondary peristalsis than either the upper or lower balloons (p < 0.001). Secondary peristaltic amplitude was less than that of primary peristalsis (p < 0.001). Secondary peristaltic velocity with a water bolus was slower (p = 0.001) than that of primary peristalsis. Intravenous atropine significantly reduced secondary peristaltic responses to all stimuli. There was also a significant reduction in pressure wave amplitude for air stimulated secondary peristalsis while those for the water responses were similar. Secondary peristaltic velocity with air and water boluses was not changed by atropine. The reproducibility of testing secondary peristalsis was examined six volunteers and did not show any significant differences on separate test days in response rate and peristaltic amplitude or velocity. It is concluded that in normal subjects, secondary peristalsis can be more reliably triggered by intraoesophageal air or water infusion than balloon distension. Secondary peristaltic amplitude and velocity are stimulus but not site or volume dependent and propagation is partially mediated by cholinergic nerves.

Adult↗
PubMed1995

Integrity and characteristics of secondary oesophageal peristalsis in patients with gastro-oesophageal reflux disease.

Secondary peristalsis contributes to oesophageal acid clearance. The aim of the study was to evaluate the integrity and characteristics of secondary peristalsis in patients with gastro-oesophageal reflux disease. Studies were performed in 22 patients with reflux disease and 20 age matched controls. Oesophageal motility was recorded at 3 cm intervals along the oesophageal body. Primary peristalsis was tested with 5 ml water swallows. Secondary peristalsis was stimulated with 10 ml boluses of air and water injected in the mid-oesophagus and by 5 second distensions with a 3 cm balloon at the same level. It was found that primary peristalsis was normal in 19 of 20 control subjects and in 14 of 22 patients with reflux disease. In patients with reflux disease, intact secondary peristalsis was triggered infrequently by air and water distension (median success rate of 0% for both stimuli) and occurred significantly less frequently than in control subjects (50% and 30% respectively). The frequency of balloon induced secondary peristalsis, however, was similar in the two groups (0% controls, 20% reflux disease). The major pattern of failure of secondary peristalsis was the complete absence of any oesophageal secondary peristaltic response. The amplitudes of the intact secondary peristaltic responses were not significantly different for the two groups. Peristaltic velocity for air and balloon induced secondary peristalsis was also similar in control subjects and patients with reflux disease whereas water induced secondary peristalsis was slower in the reflux patients. In conclusion, patients with reflux disease exhibit a pronounced defect in the triggering of secondary peristalsis.

Adult↗
PubMed2000

Modulation of peristalsis by cannabinoid CB(1) ligands in the isolated guinea-pig ileum.

The effect of cannabinoid drugs on peristalsis in the guinea-pig ileum was studied. Peristalsis was induced by delivering fluid into the oral end of an isolated intestinal segment. Longitudinal muscle reflex contraction, threshold pressure and threshold volume to trigger peristalsis, compliance of the intestinal wall during the preparatory phase (a reflection of the resistance of the wall to distension) and maximal ejection pressure during the emptying phase of peristalsis were measured. The cannabinoid agonists WIN 55,212-2 (0.3 - 300 nM) and CP55,940 (0.3 - 300 nM) significantly decreased longitudinal muscle reflex contraction, compliance and maximal ejection pressure, while increased threshold pressure and volume to elicit peristalsis. These effects were not modified by the opioid antagonist naloxone (1 microM) and by the alpha-adrenoceptor antagonist phentolamine (1 microM). The inhibitory effect of both WIN 55,212-2 and CP55,940 on intestinal peristalsis was antagonized by the cannabinoid CB(1) receptor antagonist SR141716A (0.1 microM), but not by the cannabinoid CB(2) receptor antagonist SR144528 (0.1 microM). In absence of other drugs, the CB(1) receptor antagonists SR141716A (0.01 - 1 microM) and AM281 (0.01 - 1 microM) slightly (approximatively 20%) but significantly increased maximal ejection pressure during the empty phase of peristalsis without modifying longitudinal muscle reflex contraction, threshold pressure, threshold volume to trigger peristalsis and compliance. It is concluded that activation of CB(1) receptors reduces peristalsis efficiency in the isolated guinea-pig, and that the emptying phase of peristalsis could be tonically inhibited by the endogenous cannabinoid system.

Animals↗
PubMed1996

Initiation of esophageal secondary peristalsis by slow fluid infusion in the opossum: effect of hydrochloric acid.

We investigated the mechanisms of slow fluid infusion-induced secondary peristalsis and the effects of hydrochloric acid on this response. In 13 chronically esophagostomized opossum, acidic and neutral barium sulfate were infused into the distal esophagus at a rate of 1.1 ml/min, while recording the esophageal dimension by videofluoroscopy and esophageal intraluminal pressure concurrently. The effects of atropine, tetrodotoxin, capsaicin, and bilateral cervical vagotomy on the response to slow fluid infusion were examined. Acidic barium initiated secondary peristalsis more frequently and at shorter latency with less increase of preperistaltic intraesophageal pressure than neutral barium (P < 0.05). Atropine abolished secondary peristalsis initiated by neutral barium. For acidic barium, atropine decreased the incidence of secondary peristalsis, increased the latency for initiation of secondary peristalsis, and initiated secondary peristalsis more distally (P < 0.05). Tetrodotoxin or vagotomy and capsaicin abolished activation of secondary peristalsis. We concluded that secondary peristalsis can be stimulated in response to slow distension by minute amounts of fluid. This peristalsis is atropine and capsaicin sensitive and vagally mediated. The presence of acid significantly lowers the threshold for stimulation of secondary peristalsis induced by slow fluid distension. This effect seems to be atropine resistant.

Animals↗
PubMed2001

Loss of secondary esophageal peristalsis is not a contributory pathogenetic factor in posterior laryngitis.

Secondary esophageal peristalsis helps prevent the entry of gastric acid into the pharynx by clearing the refluxed gastric contents back into the stomach. Because the loss of this mechanism may contribute to the pathogenesis of reflux-induced laryngeal disorders, our aim was to study the frequency of stimulation and parameters of secondary esophageal peristalsis in patients with posterior laryngitis (PL). We studied 14 patients (45 +/- 5 years) with PL documented by videolaryngoscopy and 11 healthy controls (46 +/- 6 years). The upper esophageal sphincter (UES) pressure was monitored by a sleeve assembly incorporating an injection port 5 cm distal to the sleeve. The esophageal body and lower esophageal sphincter (LES) pressures were measured by an LES sleeve assembly. Primary esophageal peristalsis was induced by 5-mL water swallows. Secondary esophageal peristalsis was induced by abrupt injection of volumes of air, incrementally increased by 5 mL, into the esophagus. Secondary esophageal peristalsis could not be elicited by injection of any volume (up to 60 mL) in 3 PL patients and 2 controls. These 5 subjects had normal primary peristalsis. The threshold volume of air required to stimulate secondary esophageal peristalsis in PL patients (median, 15 mL) was similar to that of controls (median, 10 mL). The parameters of the secondary esophageal peristaltic pressure wave were similar in both groups, and in both groups, they were similar to those of primary peristalsis. The UES response to the injection of the threshold volume that induced secondary esophageal peristalsis in PL patients was contraction in 58% of the trials, partial relaxation in 3%, and no response in 39%. The findings were similar to those in the controls. The LES response to injection of the threshold volume was complete relaxation in both the PL patients and the controls. We conclude that the integrity of secondary esophageal peristalsis is preserved in PL patients.

Adolescent↗
PubMed2000

Central nervous system nitric oxide induces oropharyngeal swallowing and esophageal peristalsis in the cat.

BACKGROUND & AIMS: The functional role of brainstem nitric oxide (NO) in swallowing and esophageal peristalsis remains unknown. We examined the effects of blockade of central nervous system (CNS) NO synthase (NOS) on swallowing and on primary and secondary peristalsis. METHODS: (1) The effect of intravenous (IV) NOS inhibitor N(G)-nitro-L-arginine (L-NNA) on swallowing and swallowing-induced peristalsis was examined. (2) An NOS inhibitor (N(G)-monomethyl-L-arginine [L-NMMA]) was administered into the fourth ventricle intracerebroventricularly (ICV), and its effects on swallowing and primary and secondary peristalsis were examined. RESULTS: (1) IV L-NNA significantly reduced the number of oropharyngeal swallows and the induction of primary peristalsis in the smooth muscle portion of the esophageal body; the change was not significant within the striated muscle portion. (2) L-NMMA given ICV significantly reduced the number of oropharyngeal swallows and the incidence of primary peristalsis in both smooth and striated muscle, but the reduction in amplitude was significant only for the smooth muscle contraction. There was a significant reduction in both the amplitude and incidence of secondary peristalsis, only in the smooth muscle portion. CONCLUSIONS: CNS NO is an important neurotransmitter in the induction of oropharyngeal swallowing and esophageal peristalsis. The neural substrates mediating striated and smooth muscle peristalsis may be both anatomically and neurochemically distinct.

Animals↗
PubMed1999

Effect of cisapride on secondary peristalsis in patients with gastroesophageal reflux disease.

OBJECTIVE: Improvement of esophageal acid clearance appears to be an important effect of cisapride in the treatment of reflux disease. The mechanism underlying this effect is not clear. Esophageal peristalsis is a major component of the acid clearance process. In normal subjects secondary peristalsis is an important mechanism of esophageal acid clearance during sleep, and this response appears to be impaired in patients with reflux esophagitis. The effects of cisapride on secondary peristalsis are not known. The aim of this study was to investigate the effects of cisapride on the triggering and characteristics of secondary peristalsis in patients with reflux esophagitis. METHODS: In 17 patients with reflux esophagitis and impaired secondary peristalsis cisapride, 10 mg q.i.d., or placebo were administered in a randomized double blind, crossover design for 4 days separated by a 4-7 day washout period. On the fourth day of treatment, primary peristalsis and secondary peristalsis in response to 10- and 20-ml air boluses were assessed. RESULTS: Secondary peristaltic success and amplitude were greater with the 20-ml bolus than with the 10-ml bolus. However, cisapride had no effect on either secondary peristaltic success or amplitude. Cisapride also had no effect on primary peristalsis or basal LES pressure. CONCLUSIONS: The improvement in esophageal acid clearance by cisapride is not explainable by improvement in secondary peristalsis.

Adult↗
PubMed1997

Outcome of laparoscopic Nissen fundoplication in patients with disordered preoperative peristalsis.

BACKGROUND: A 360 degrees or Nissen fundoplication remains controversial in patients with disordered peristalsis, some surgeons preferring a partial wrap to minimise postoperative dysphagia. AIM: To evaluate symptoms and manometric outcome in patients with disordered peristalsis after Nissen fundoplication. PATIENTS: In an initial series of 345 patients studied prospectively, 31 patients who had undergone a Nissen fundoplication had disordered peristalsis. Using preoperative manometry, patients were classified as: equivocal primary peristalsis (eight patients); abnormal primary peristalsis (four patients); abnormal maximal contraction pressure (13 patients); abnormal primary peristalsis and maximal contraction pressure (six patients). METHODS: Postoperatively, patients underwent a barium meal, oesophageal manometry and standardised clinical review by a blinded scientific officer. RESULTS: Twenty eight (90%) patients had satisfaction scores of at least 8 out of a maximum of 10 and all would undergo surgery again. Whereas 15 (48%) patients had dysphagia scores greater than 4/10 preoperatively, only two (6%) had these scores at one year. Improved peristalsis was seen in 78% of postoperative manometric studies, and mean preoperative lower oesophageal sphincter pressure increased from 6.6 (range 0-21) mm Hg to 19 (4-50) mm Hg. CONCLUSIONS: These results are similar to the overall group of 345 patients and suggest that disordered peristalsis, and possibly even absent peristalsis, is not a contraindication to Nissen fundoplication as performed in these patients.

Adult↗
PubMed1985

Oesophageal peristalsis in the cat: the role of central innervation assessed by transient vagal blockade.

Studies were performed on five cats to assess the role of extrinsic vagal innervation in the control of peristalsis in the smooth muscle oesophagus. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks previously isolated in skin loops on each side of the neck. Peristalsis throughout the body of the oesophagus was monitored using a continuously perfused multilumen manometry tube. Striated and smooth muscle portions of the esophagus were delineated by abolishing smooth muscle activity with atropine. Secondary peristalsis was assessed by intra-oesophageal balloon distension studies. The threshold volume for balloon-induced secondary peristalsis was lower in the smooth muscle oesophagus. Unilateral vagal blockade reduced the incidence of primary and secondary peristalsis in the striated muscle oesophagus but not in the smooth muscle oesophagus. Bilateral vagal nerve blockade abolished primary swallow-induced peristalsis and secondary peristalsis in both the smooth and striated muscle cat oesophagus. Administration of cholinergic agents or adrenergic blocking agents failed to restore secondary peristalsis in the smooth muscle oesophagus during vagal cooling. We conclude that connections to the central nervous system via the vagal nerve trunks are required for normal secondary as well as primary peristalsis in both the smooth and striated muscle portions of the cat oesophagus.

Animals↗
PubMed1992

Evidence that stretch receptors for peristalsis are located in the mucosal layer of the guinea pig ileum.

Location of stretch receptors triggering the peristalsis was investigated in the isolated guinea pig ileum. Peristalsis was cyclically induced by perfusing the lumen with Krebs solution flowing at a constant rate. Peristalsis was promptly abolished by serosally applied 3 x 10(-7) M tetrodotoxin, 10(-4) M lidocaine, 10(-6) M morphine or 10(-5) M nicotine, confirming the claim that peristalsis was neurally regulated by the myenteric plexus. Intraluminal application of 3 x 10(-7) M tetrodotoxin not only blocked the peristalsis, but also inhibited the contractions of the longitudinal muscle elicited by transmural stimulation or 10(-4) M nicotine by the same extent as those by serosal tetrodotoxin, suggesting that the blockade of peristalsis was due to the tetrodotoxin infiltrating into the muscle layer. In contrast, intraluminal application of 0.1% glutaraldehyde or perfusing the lumen with the low NaCl (20 mM)-containing Krebs solution abolished the peristalsis without critically inhibiting the neurogenic contractions of the longitudinal muscle, indicating that the blockade of peristalsis by these intraluminal treatments was ascribed to the actions on the mucosal layer. These results may imply that stretch receptors are located in the mucosal layer of the guinea pig ileum, and the impairment of the functions of these receptors by the intraluminal treatments leads to the blockade of the peristalsis.

Animals↗
PubMed1986

Acid gastro-oesophageal reflux episodes as related to the quality of preceding peristalsis. A study in normal subjects.

It has earlier been demonstrated after long-term monitoring of pH and peristalsis in the oesophagus that episodes of acid gastro-oesophageal reflux occur in normal volunteers. To determine whether there is a connection between gastro-oesophageal reflux and prior peristalsis, pH and peristalsis were monitored for 12 h in 26 asymptomatic subjects. The recorded peristalsis was divided into brief bursts of peristaltic contractions (less than or equal to 60 sec) and more prolonged continuous activity. Peristaltic periods were limited to prior and subsequent peristalsis by a non-peristaltic course of greater than 30 sec. Continuous peristalsis was defined as a sequence of peristaltic contractions with a mutual distance between individual peristaltic waves of greater than or equal to 30 sec. A total of 81 episodes of reflux were recorded, of which 67 were preceded by peristaltic activity. Brief bursts of peristalsis, unrelated to reflux episodes, were frequently terminated by bolus-transporting peristaltic waves (p less than 0.001). When the last contraction before reflux was considered, an increased frequency of non-propagating peristalsis was found (p less than 0.01). In addition, a closer time relationship was observed between peristalsis and reflux if the last contraction was of the upper segmentary type, as compared with propagating activity (p less than 0.001). In conclusion, reflectory sphincter relaxation producing reflux may possibly be triggered by contractions in the upper part of the oseophagus, not followed by a bolus-transporting peristaltic wave.

Adult↗