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At least 19 recordsLinked to original sources
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↗
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↗
PubMed1989

Recurrent autonomous esophageal peristalsis in patients with chest discomfort.

Routine esophageal manometry revealed a novel pattern of esophageal motility, recurrent autonomous peristalsis, in five patients evaluated for chest discomfort and heartburn. In the absence of swallowing, esophageal peristalsis occurred at frequencies of 4-8 peristaltic sequences per minute for periods of 2-8 min. The recurrent peristaltic sequences developed spontaneously during manometry and were associated with the onset of vague chest discomfort in four patients; one patient reported no symptoms during recurrent peristalsis. Duration and propagation velocity of the recurrent peristaltic contractions differed significantly from primary peristalsis in four patients. Recurrent autonomous esophageal peristalsis is an unusual motor pattern that may be associated with vague chest discomfort. The circuit(s) mediating recurrent autonomous peristalsis are unknown.

Adult↗
PubMed1989

Evidence for an involvement of substance P, but not cholecystokinin-like peptides, in hexamethonium-resistant intestinal peristalsis.

It has previously been found that, in the presence of naloxone, the ganglionic blocking drug hexamethonium fails to completely block peristaltic motility in the isolated ileum of the guinea-pig. This hexamethonium-resistant peristaltic activity is coordinated by enteric nerves since it is abolished by tetrodotoxin. In the present study the neurotransmitter circuitry of this type of peristalsis was studied by means of specific antagonists. Atropine totally suppressed hexamethonium-resistant peristalsis. This type of peristalsis was also strongly inhibited by the tachykinin antagonist, spantide, if a concentration sufficient to antagonize neuronally located substance P receptors was employed. In contrast, the cholecystokinin antagonist, lorglumide, caused only a slight inhibition of hexamethonium-resistant peristalsis. Both substance P and the cholecystokinin-related peptide, ceruletide, potently stimulated the hexamethonium-resistant type of peristaltic activity. These data indicate that, after blockade of nicotinic acetylcholine receptors, tachykinins mediate neuroneuronal coordination of peristalsis whereas acetylcholine acting via muscarinic receptors may be primarily responsible for neuromuscular transmission. Cholecystokinin-like peptides appear to play a modulator rather than a mediator role in hexamethonium-resistant peristalsis.

Animals↗
PubMed1992

Effects of CP-96,345, a novel non-peptide antagonist of NK1 receptor, on the peristalsis in isolated guinea pig ileum.

CP-96,345, a novel non-peptide antagonist of the NK1 receptor, at 10(-8)-10(-6) M decreased the frequency of peristalsis and reduced peristalsis-associated longitudinal muscle contractions in isolated guinea pig ileum. In the presence of 10(-6) M CP-96,345, further addition of 10(-6) M atropine blocked the peristalsis. When 10(-6) M atropine was first applied, more than half of the preparations developed atropine-resistant peristalsis. CP-96,345 at 10(-6) M blocked the atropine-resistant peristalsis. These results are consistent with the view that substance P is involved in the peristalsis in guinea pig ileum.

Animals↗
PubMed1975

Neural organization of esophageal peristalsis: role of vagus nerve.

The purpose of this investigation was 2-fold: first, to determine the velocity of peristalsis in the smooth muscle area of opossum esophagus before and after administration of atropine; second, to evaluate the role of the vagus nerves in the control of the propagative nature of esophageal peristalsis. Intraluminal pressures were measured through a pressure transducer recorder system attached to continuously perfused catheters. The velocity of peristalsis in the lower third of the esophagus progressively decreased from 3.25 plus or minus 0.20 (SE) cm per sec at the 70 to 80% level to 2.17 plus or minus 0.14 (SE) at the 80 to 90%level to 1.83 plus or minus 0.10 (SE) at the 90 to 100% level. After administration of intraperitoneal atropine (100 mug per kg), the velocities were 3.1 plus or minus 0.26 (SE) cm per sec, 2.38 plus or minus 0.22 (SE), and 1.74 plus or minus 0.10 (SE), respectively, at the 70 to 80%, 80 to 90%, and 90 to 100% levels. The changes were not statistically significant. Electrical stimulation of the distal cut end of the vagus nerve induced peristaltic contractions. The velocities of peristalsis after electrical stimulation of the vagus nerve were 3.24 plus or minus 0.72 (SE) cm per sec, 2.81 plus or minus 0.64 (SE), and 1.84 plus or minus 0.34 (SE), respectively, at the 70 to 80%, 80 to 90%, and 90 to 100% levels. Results of this study indicate that the velocity of peristalsis in the smooth muscle area of the opossum esophagus has a caudally decreasing gradient. Bilateral cervical vagotomy and stimulation of the distal cut end initiates peristaltic contraction indicating that the propagative nature of peristalsis in the smooth musurrent, does not alter mucosal cyclic AMP. Dibutyryl cyclic AMP decreased net sodium absorption and increased short circuit current; findings which were qualitatively identical to those produced by taurochenodeoxycholic acid. These studies support the proposal that bile salts stimulate colonic electrolyte secretion by increasing mucosal cyclic AMP.

Animals↗
PubMed1989

Neuronal analysis of pharyngeal peristalsis in the gastropod Navanax in terms of identified motoneurons innervating identified muscle bands. II. Radial and circumferential motor fields.

The neuronal basis of pharyngeal ingestion and peristalsis was studied in the gastropod Navanax inermis. Radially and circumferentially oriented muscles produce expansion and constriction of the pharynx. Motor fields of 11 identified radial motoneurons and 13 identified circumferential motoneurons were determined with respect to circumferential and longitudinal muscle band coordinates by muscle movements, electromyography, antidromic stimulation and axonal anatomy. Activation of these identified motoneurons can account for all the elemental pharyngeal movements observed during feeding. Four motoneurons, each innervating most of radial muscle, can mediate ingestion. Three radial motoneurons with anterior motor fields can mediate anterior expansion during sealing of the pharyngeal lips around prey and during regurgitation. Ten circumferential motoneurons have small arciform motor fields, the distributions of which correspond to the regional specializations in circumferential band organization. Arciform constriction can center eccentric ingested prey within the pharyngeal lumen during peristalsis. Arciform constrictions could combine to form an annular constriction in peristalsis. Small, non-overlapping, circumferential motor fields maximize the number of independent annular units available to produce a fine peristaltic wave. Sphincters have more circumferential motoneurons with smaller motor fields; this innervation permits finer motor control. Radial motoneurons with posterior motor fields can produce expansion caudal to a circumferential constriction during peristalsis. Motor fields of regional radial motoneurons show greater interanimal variability than circumferential motor fields, which is correlated with a less essential role of radial motoneurons in peristalsis. Two circumferential motoneurons with giant posterior pharyngeal motor fields can mediate pharyngeal emptying either in swallowing or in regurgitation.

Action Potentials↗
PubMed1992

Modulation of peristalsis in the guinea-pig isolated small intestine by exogenous and endogenous opioids.

1. A recording method was developed to measure physiological parameters of the preparatory and emptying phases of peristalsis in vitro. This method enabled measurement of: the compliance of the intestinal wall during the preparatory phase (a reflection of the resistance of the wall to distension); longitudinal muscle contraction during the preparatory phase; the threshold volume required to trigger the emptying phase; the maximal ejection pressure and the average power generated during the emptying phase, which reflects the rate at which the intestine performs work. Modulation of these parameters by exogenous and endogenous opioids acting at mu, kappa and delta opioid receptors was investigated. 2. The compliance of the intestinal wall during the preparatory phase was reduced by the mu opioid receptor agonist, [D-Ala2, N-methyl-Phe4, Gly5-ol] enkephalin (DAMGO) but not by the kappa agonist, dynorphin, or the delta agonist, [D-penicillamine2, D-penicillamine5] enkephalin (DPDPE). Reflex contraction of the longitudinal muscle during the preparatory phase was inhibited by DAMGO, dynorphin and DPDPE. The threshold volume required to trigger the emptying phase of peristalsis was increased by DAMGO, dynorphin and DPDPE. 3. The maximal ejection pressure generated during the emptying phase was reduced by dynorphin and DPDPE, but not by DAMGO. The average power generated by the intestine when emptying was not altered by any of the agonists. 4. Electrically stimulated contractions of longitudinal muscle in strips of longitudinal muscle-myenteric plexus were not inhibited by DPDPE. Similarly, DPDPE did not significantly inhibit electrically induced contraction of circular muscle in strips of circular muscle-myenteric plexus.5. Each of the agonist effects on peristaltic parameters was antagonized by the appropriate antagonist:D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) (mu), norbinaltorphimine (nor-BNI) (kappa), naltrindole(delta).6. It is concluded that mu and kappa agonists act primarily on excitatory circular and longitudinal muscle motor neurones. The delta agonist probably acts on enteric neurones presynaptic to excitatory circular and longitudinal muscle motor neurones.7. Antagonists for mu, delta and kappa receptors did not affect any parameters of peristalsis when the intestine emptied against a low resistance. However, when emptying against a high outflow resistance, the average power generated by the intestine was increased by the kappa antagonist, nor-BNI, but not by CTOP or naltrindole.8. It is concluded that endogenous opioids appear to have little role in peristalsis when the intestine is working against a low outflow resistance. However endogenous opioids, acting primarily at kappa receptors,provide a braking mechanism by inhibiting the emptying phase of peristalsis in conditions in which the intestine empties against a higher resistance.

Algorithms↗
PubMed1989

Neomycin prevents indomethacin-induced gastric peristalsis and mucosal injury in the rat.

Inhibition of prostaglandin synthesis together with vagally mediated peristaltic contractions are essential if mucosal injury is to occur in the stomach of indomethacin-treated rats. The neomycin group of antibiotics has been shown to interfere with acetylcholine release. Agents blocking peristalsis have been demonstrated to prevent mucosal injury. We postulated that neomycin might inhibit peristalsis and prevent lesion formation. The effect of oral neomycin and bacitracin on gastric wall tone and peristaltic response to indomethacin were assessed and related to the lesion score. Bacitracin had no effect on either response and severe injury occurred. Neomycin did not block the tonal response to indomethacin but abolished peristalsis and no injury occurred. Induction of peristalsis with insulin in neomycin-indomethacin treated rats restored mucosal injury. It is concluded that neuromuscular blockade by neomycin prevented mucosal lesions by preventing peristalsis and not by impairing the ability of indomethacin to inhibit prostaglandin synthesis.

Animals↗
PubMed1989

Cholinergic control of smooth muscle peristalsis in the cat esophagus.

The aim of this study was to examine in detail the effects of selective cholinergic and other pharmacological antagonists on primary and secondary peristalsis in the smooth muscle of the cat esophagus in order to fully characterize the cholinergic contribution to peristalsis in this species. Primary and secondary peristalsis in the smooth muscle part of the feline esophagus was completely abolished by atropine, 4-dephenylacetoxy-N-methylpiperidine methiodide (4-DAMP) (a selective M2 muscarinic antagonist), hexamethonium, and high doses of nicotine. Pirenzepine (a selective M1 muscarinic antagonist), propranolol, and phentolamine were without effect, as were naloxone, methysergide, and pyrilamine. From these findings we conclude that primary and secondary peristalsis in feline esophageal smooth muscle involves nicotinic ganglionic neurotransmission as well as postganglionic release of acetylcholine that acts directly on muscarinic receptors located on the smooth muscle. Peristalsis in esophageal striated muscle does not involve either synaptic transmission or muscarinic receptors.

Animals↗
PubMedDate not supplied

[Recuperation of ureteral peristalsis in the rat after denervation].

The paper presents the experimental work carried out on the influence of various surgical situations on ureteral peristalsis in the rat. It included 43 rats divided in three groups. Group I (n = 10) acted as control group and had only ureterolysis performed. In group II (n = 10), single section and subsequent anastomosis was performed. Group III (n = 23) included section at two levels, ureter extraction from the animal and subsequent autotransplantation of the ureter. The three groups were re-operated two months later to ratify peristalsis of the intervened ureter. Both in the first and second operations peristalsis, as well as the features and appearance of antiperistaltic waves were quantified. After 60 days, no changes were observed in group I, but groups II and III exhibited normal peristalsis to presence of antiperistaltic waves. Both groups had complications like stenosis, fistulas and hydronephrosis, but also normal functioning, histology and peristalsis.

Animals↗
PubMed1992

Role of nitric oxide in esophageal peristalsis in the opossum.

To explore the involvement of NO in normal peristalsis, the effects of inhibitors of NO synthase, including N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), on esophageal peristaltic contractions induced by diverse stimuli that may involve different neuronal circuits were studied. Studies were performed in opossums. Experimental conditions in vivo included primary peristalsis (P) induced by pharyngeal stroking, short-train (1 second) electrical stimulation of the vagus nerve which caused peristaltic (S) contractions, and long-train (10 second) electrical stimulation of the vagus nerves which caused contractions at the onset of (A contractions) and after (B contractions) the stimulation period. In vitro experiments were performed on strips of esophageal circular muscle using electrical field stimulation which caused contractions at the onset of (on contractions) and after (off contractions) the stimulation period. The administration of L-NAME significantly decreased the latency period and reduced the latency gradient for P contractions, thereby increasing the velocity of peristalsis. Concomitant administration of atropine prolonged the latency period but did not restore the latency gradient. L-NAME abolished B contractions in a dose-dependent fashion. In vitro, L-NAME caused dose-dependent inhibition of off contractions and augmentation of on contractions. These studies support the hypothesis that NO may be involved in (a) both the latency period and the latency gradient, as well as in the contraction amplitude of esophageal peristalsis; and (b) esophageal B and off contractions.

Animals↗
PubMed1979

Oesophageal sensors and their modulatory influence on oesophageal peristalsis in the lobster, Homarus gammarus.

The musculature and innervation of the oesophagus of Homarus gammarus are described as a prerequisite to studies on the mechanisms and control of food ingestion. Of particular interest are two paired sensors (the anterior and posterior oesophageal sensors) which are bilaterally situated at the oesophageal-cardiac sac valve. These are similar to contact chemoreceptors previously described in insects and are classified as such on morphological grounds and with indirect electrophysiological evidence. Oesophageal peristalsis is effected by the coordinated contraction of the Oesophageal musculature. This is controlled by rhythmical bursting neuronal activity, which can be recorded from the nerve trunks in the area. A characteristic burst recorded from the superior oesophageal nerve is used as an indication of oesophageal dilatation during peristalsis for studies on the feedback effects of the oesophageal sensors. Electrical and chemical stimulation of the posterior oesophageal sensors can initiate and increase the frequency of oesophageal peristalsis, while stimulation of the anterior oesophageal sensors can slow and terminate oesophageal peristalsis. The results are discussed and a model presented of the role of the oesophageal sensors in feeding.

Animals↗
PubMed1991

Comparison of primary and secondary esophageal peristalsis in humans: effect of atropine.

To determine whether physiological differences exist between primary (swallow-induced) and secondary (distension-induced) peristalsis in humans, 10 healthy male volunteers underwent esophageal manometry on 2 consecutive days using a perfused intraluminal catheter system that incorporated a latex balloon. Initially the catheter was positioned so that the balloon was centered 16 cm above the lower esophageal sphincter (LES), and intraluminal pressures were recorded 21, 11, 6, and 1 cm above the LES. After a series of wet swallows, dry swallows, and balloon distensions, the catheter was repositioned so that the balloon was 6 cm above the LES and pressures were recorded 1 and 11 cm above the LES. A series of balloon distensions were repeated in this position, and the subject was then given either atropine (10 micrograms/kg iv) or placebo in a double-blind randomized fashion (on consecutive days). The protocol was then repeated in reverse order. Distension-induced responses aboral to the balloon with the balloon located 16 cm above the LES were 1) of lower amplitude, 2) more often nonperistaltic, and 3) less atropine sensitive than swallow-induced contractions at comparable sites. With the balloon located distally (6 cm above LES) contractions induced at the 11-cm site (i.e., orad to the balloon) were much more atropine sensitive than contractions induced at the same site when the balloon was located proximally (i.e., 16 cm above LES). These data suggest that, contrary to previous reports, secondary peristalsis differs significantly from primary peristalsis. Furthermore, atropine differentially effects these two types of peristalsis, suggesting that the neural pathways involved are dissimilar.

Adult↗
PubMed1991

Effect of increased intra-abdominal pressure on peristalsis in feline esophagus.

Our aim in this study was to determine the effect of variations in intrabolus pressure on esophageal peristalsis. In five cats, intrabolus pressure was altered by increasing intragastric pressure to 20-45 mmHg by use of a pressure cuff to compress the abdomen. In each cat, increases in intragastric pressure were associated with comparable increases in pressure of the esophageal bolus while the bolus was in the distal esophagus during esophageal peristalsis. Secondary peristalsis induced by a 5-ml injection of barium into the proximal esophagus was recorded by synchronized videofluoroscopy and esophageal manometry. Graded increases in intrabolus pressure caused an increased prevalence of ineffective, incomplete peristaltic sequences that did not completely clear barium from the esophagus. At intragastric pressures greater than 45 mmHg, 63% of the peristaltic sequences were incomplete. Increases in intrabolus pressure elicited by increased intragastric pressure also caused 1) slowing of the peristaltic wave in the distal esophagus, 2) increased pressure wave duration in the distal esophagus, 3) increased esophageal diameter, and 4) increased duration of lower esophageal sphincter opening. The incidence of retrograde bolus escape was inversely related to the difference between peristaltic wave amplitude and intrabolus pressure. A pressure difference of greater than 20 mmHg prevented retrograde barium escape at all esophageal levels, whereas a difference of less than 20 mmHg was generally associated with retrograde escape of barium in the distal esophagus. We conclude that an increase in intrabolus pressure causes an increase in esophageal distension that is transduced into alterations of esophageal peristalsis by either a myogenic or neural mechanism.

Abdomen↗
PubMed1975

Effect of dry swallows and wet swallows of different volumes on esophageal peristalsis.

The effect of dry swallows and wet swallows of various volumes on esophageal function was studied in normal subjects. An intraesophageal transducer assembly was used to measure the dynamics of esophageal peristalsis. The strength of esophageal contraction (amplitude) following a 1-ml liquid bolus was similar to that following a dry swallow but was significantly less than that following a wet swallow of a larger volume. There was no difference in strength of esophageal squeeze following swallows ranging from 2 to 20 ml. In addition, a wet swallow was associated with slower wave speed, greater duration of the contraction wave, and later time of appearance of the peristaltic wave in the distal esophagus than a dry swallow. Futhermore, the incidence of peristalsis was greater with a wet swallow than a dry swallow. The results of our studies indicate that although the act of swallowing alone in man initiates peristalsis, afferent information contributes to the regulation of primary peristalsis.

Adult↗
PubMed1978

[Pharmacological studies of loperamide, an anti-diarrheal agent. II. Effects on peristalsis of the small intestine and colon in guinea pigs (author's transl)].

Effects of loperamide on peristalsis in the guinea pig intestines were investigated in comparison with those of morphine and atropine. The following results were obtained. The ejection of intraluminal fluid produced by the peristaltic contraction of the isolated ileum was suppressed by loperamide at a concentration of 10(-8) or 2 X 10(-8) g/ml. Peristalsis in the intestinal loop of anesthetized guinea pigs was inhibited by i.v. administration of loperamide at a dose of 0.03 mg/kg. Morphine (0.03 mg/kg i.v.) and atropine (0.05 mg/kg i.v.) also inhibited the peristaltic contraction. The effect of loperamide continued longer than that of morphine. Peristalsis in the colonic loop of anesthetized guinea pigs was inhibited by i.v. administration of loperamide at a dose of 0.01 or 0.03 mg/kg. Morphine (0.1 mg/kg i.v.) and atropine (0.03 mg/kg i.v.) also inhibited the peristaltic contraction of the colonic loop. Loperamide (0.01 or 0.03 mg/kg i.v.) and morphine (0.1 mg/kg i.v.) caused a slight and temporary increase of resting level of intraluminal pressure with inhibition of peristalsis in the colonic loop. These results suggest that loperamide suppresses the peristaltic contraction caused by distension of the intestinal lumen.

Animals↗
PubMed1992

Return of esophageal peristalsis after nifedipine therapy in patients with idiopathic esophageal achalasia.

This study was carried out to demonstrate the possible return of esophageal peristalsis in patients affected by esophageal achalasia chronically treated with sublingual nifedipine and to investigate which parameters are correlated with the return of peristalsis. Thirty-two patients were treated with sublingual nifedipine 10-20 mg taken 30 min before meals. A clinical and manometric evaluation was performed before and after 6 months of therapy. Before treatment, in no patient was peristaltic activity recorded. After 6 months, peristalsis was observed in six patients. In this group, no pretreatment manometric parameter was different from that of the remaining achalasic patients; only the clinical history of dysphagia was significantly shorter (p < 0.001) and the esophageal diameter significantly less (p < 0.001). In conclusion, chronic treatment with sublingual nifedipine can induce a return of esophageal peristalsis in patients with a short clinical history of disease and slightly dilated esophagus.

Administration, Sublingual↗