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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

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↗

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↗

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↗

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↗

PubMed1976

Inhibition of peristalsis in guinea-pig isolated ileum and colon by drugs that block prostaglandin synthesis.

1 Methods of analysing peristaltic activity have been evaluated by the use of recordings of longitudinal and circular muscle activity and of propulsion in whole segments of guinea-pig ileum and colon. 2 Some prostaglandin synthesis inhibitors, and antagonists of prostaglandin action were tested for their suitability for studying the role of prostaglandins in peristalsis. Aspirin was suitable; at 10-200 mug/ml it had little effect on responses of longitudinal muscle strips of the guinea-pig ileum to acetylcholine (ACh), histamine, nicotine or prostaglandin E2. Indomethacin (1-4 mug/ml) reduced responses to nicotine and prostaglandin E2. The prostaglandin antagonists polyphloretin phosphate and SC-19220 reduced contractions of ileal longitudinal muscle caused by nerve excitation with either nicotine or transmural stimulation. 3 Aspirin (20-100 mug/ml) or indomethacin (1-4 mug/ml) applied serosally greatly inhibited all aspects of peristalsis in guinea-pig ileum and colon. Inhibition of peristalsis of the ileum by aspirin was antagonized by prostaglandin E2 and that by indomethacin was removed by prostaglandin F2alpha or ACh. Inhibition of colonic peristalsis by aspirin was antagonized by prostaglandin E2 but rarely by ACh, and that by indomethacin by prostaglandin E1 or E2. Mucosal application of aspirin had little effect on either ileum or colon but indomethacin caused some inhibition. 4 These results support the supposition that prostaglandins contribute to peristaltic activity.

Animals↗

PubMed1975

Studies on the mechanism of the action of morphine on the peristalsis of guinea pig ileum in situ.

The influence of some drugs on the effect of morphine on the threshold pressure required to elicit peristalsis in the guinea pig ileum in situ was studied, in order to test the hypothesis that this effect of morphine is mediated by catecholamine release. Tachyphylaxis to this effect of morphine was confirmed. Pretreatemnt with two 8 mg/kg doses of reserpine, 24 and 48 hrs before the experiment, significantly reduced the effect of morphine on the pressure threshold. The i.v. administration of 10 mg/kg dl-Dopa re-established the effect of morphine in reserpinized animals to the level of the untreated controls. Pretreatment with guanethidine (15 mg/kg) decreased and even prevented this effect of morphine. Phentolamine pretreatment (10 mg/kg) also significantly inhibited the effect of morphine. Neither DCI nor propranolol influenced this morphine effect. Pretreatment with reserpine, guanethidine or phentolamine reduced the basic pressure threshold needed to elicit peristalsis. The possibility that the decrease of local circulation induced by hypotenison would reduce the local concentration of morphine was rejected because the same doses of guanethidine or phentolamine did not modify the effect of hexamethonium given i.v. in this preparation. All these results support the idea that the effect of morphine on intestinal peristalsis is mediated by a catecholamine acting on alpha-receptors, e.g. norepinephrine.

Animals↗

PubMed1975

The effect of metoclopramide on inhibition induced by purine nucleotides, noradrenaline, and theophylline ethylenediamine on intestinal muscle and on peristalsis in vitro.

Metoclopramide (N-(diethylaminoethyl)-2-methoxy-4-amino-5-chlorobenzamide) (Mcp) at concentrations of 0.1 and 1.0 muM partially and significantly reduced the relaxations induced by adenosine 5'-triphosphate (ATP), adenosine diphosphate (ADP), and adenosine, was without effect on theophylline ethylenediamine whilst significantly potentiating noradrenaline on the atropine-pretreated (0.1 muM) taenia coli, rabbit ileum, and rat duodenum. Mcp (1.0 muM) decreased the inhibitory effects of ATP, ADP, and adenosine on peristalsis induced in the isolated guinea-pig ileum by a constant increase in intraluminal pressure, did not affect inhibition due to theophylline ethylenediamine, whilst it potentiated inhibition of peristalsis due to noradrenaline. It is proposed that this effect of Mcp may be a specific antagonistic action on receptors sensitive to the putative purinergic transmitter, ATP and ADP, and may be partly responsible for its observed facilitatatory action on peristalsis.

Adenosine↗

PubMed1976

Effects of cholinergic stimulation on human esophageal peristalsis.

The effects of cholinergic stimulation on esophageal peristalsis were studied in normal subjects. An intraesophageal transducer assembly was used to measure the dynamics of esophageal peristalsis before and after edrophonium chloride, 80 mug/kg intravenously. Following endrophonium, there was a marked increase in amplitude of esophageal persistalsis associated with a significant reduction in velocity of esophageal peristalsis and a significant increase in width and time of appearance of the contraction wave following a swallow. Graded doses of endrophonium all resulted in significant increases in peristaltic amplitude with the maximal response occurring at doses of 80 and 160 mug/kg. Similar results were obtained with a more direct-acting cholinergic agent, bethanechol, 80 mug/kg subcutaneously. The relevance of these results as an indication of the importance of cholinergic innervation in regulating esophageal motility are discussed.

Adult↗

PubMed1975

Alteration of esophageal peristalsis by pentagastrin in patients with diffuse esophageal spasm.

Although it has been shown that gastrin and gastric alkalinization affect the lower esophageal sphincter, in vivo studies have not demonstrated a measurable effect of pentagastrin on esophageal peristalsis. In 9 patients with diffuse esophageal spam and in 10 control subjects esophageal peristalsis was recorded before and after pentagastrin infections. Subcutaneous pentagastrin increased peak amplitude significantly more in patients, 31.2 +/- 8.1 mm Hg (mean +/- S.E.M.), than in controls, 12.1 +/- 5.1 mm Hg (P less than 0.02). Max. duration of contraction waves in patients showed a rise of 11.3 +/- 2.7 sec as compared to controls, 1.9 +/- 0.9 sec (P less than 0.01). The effect of pentagastrin on esophageal peristalsis in patients with diffuse esophageal spasm may be explained as denervation supersensitivity.

Carbachol↗

PubMed1992

Myogenic mechanism for peristalsis in opossum smooth muscle esophagus.

We studied the propagation of phasic contractions initiated by tetraethylammonium (TEA, 1-10 mM), high K+ concentration (10-30 mM), and bethanechol (10(-6) to 10(-2) M) in a whole organ in vitro preparation of the opossum smooth muscle esophagus. TEA initiated phasic contractions that began at all sites along the smooth muscle esophagus and propagated in both directions with a velocity similar to that of primary peristalsis. Blockade of neural transmission by tetrodotoxin (TTX, 10(-7) M) did not prevent contraction propagation. Although a majority of contractions initiated by TEA did not propagate the full length of the esophageal specimen, with the addition of TTX most contractions initiated by TEA did propagate the full specimen length in either direction. High K+ concentration and bethanechol elicited propagated contractions similar to those initiated by TEA. We conclude that 1) a myogenic mechanism exists for propagation of contractions along the smooth muscle esophagus and 2) intramural inhibitory nerves modulate the extent of myogenic propagation in the ascending as well as descending direction. We suggest that esophageal peristalsis may occur by myogenic propagation of contractions that are normally initiated in the proximal smooth muscle esophagus by excitatory nerves. Intramural inhibitory nerves may inhibit retrograde propagation as well as mediate descending inhibition in advance of the peristaltic wave.

Animals↗

PubMed1975

[Roentgen kymographic investigations of gastric peristalsis after intravenous injection of caerulein].

Caerulein is a decapeptide which combines the effects of gastrin and cholecystokinin-pancreozymin. It was injected intravenously in doses of 10 to 40 nanoponds caerulein per kilopond bodyweight in 37 patients and roentgen kymography of the stomach carried out before and after the injection. In 89% of the 36 cases which could be evaluated, it increased antral peristalsis. Amplitude and frequency were increased and the periodicity decreased correspondingly. The effect was more marked than that of pentogastrin, presumably because caerulein dose not affect duodenal acidity. The changes in motility therefore correspond with those produced by serotonin and cholecystokinin-pancreoxymin. Control examinations carried out under identical conditions, but without caerulein, showed no change in antral peristalsis.

Ceruletide↗

PubMed1977

Control of ureteral peristalsis during changes in intravesical pressure.

Studies of the ureteral response to changes in intravesical pressure (IP) have been conducted by surgically altering the neural and hydrodynamic integrity of canine ureters. Ureteral function was assessed by acute and chronic recordings of ongoing electrical activity. Intact control ureters responded (acute to 56 per cent; chronic to 83 per cent) to elevated IP with immediate increases and to decreases in IP with slowing or cessation of activity. Acute ureteral ligation mimicked the effects of increased IP, except the responses were much slower. Ureterotomy and the resultant extravasation of urine did not alter the ureteral response. Disruption of renal nerves, whether by selective sectioning or by nephrectomy, was associated with exaggerated ureteral frequency responses which were delayed in onset. Ureters lacking neural connections with the bladder responded with bursts of multiple spikes and increases in the force of peristalsis. These observations are discussed in terms of the myogenic and neurogenic control of ureteral peristalsis.

Animals↗

PubMed1978

The role of prostaglandines in peristalsis of the human colon.

Prostaglandines (PG) of the E and F series cause peristaltic activity in isolated longitudinal muscle strips of the human colon. As this phasic motor reaction can be varied by acetyl choline and adrenaline it was supposed, that prostaglandines contribute to peristalsis. The role of PG E and F in the human colon was studied by inhibiting the prostaglandine synthesis and by antagonizing the prostaglandine-effects. Indomethacin proved to be a suitable inhibitor. HR 546 was found a powerful antagonist. The effect of Pentagastrin and Cholecystokinin (CCK) on peristaltic activity were suppressed by Indomethacin and HR 546. The inhibition of peristalsis by Indomethacin and HR 546 was removed by high doses of PG E and F. On the basis of these results the role of PG for the motility of the gut is discussed.

Cholecystokinin↗

PubMed1978

Transport efficiency of ureteral peristalsis correlated to pacemaker activity of renal pelvis.

The transport efficiency of ureteral peristalsis under the control of the pacemaker was examined during renal pelvic perfusion in dogs. Simultaneous recordings of the perfusion rate, renal pelvic pressure, ureteral electromyogram, and bolus volume were made during each period of perfusion at a constant rate. For a graphic representation of transport efficiency of each peristaltic contraction, changes in balance level between the perfusion rate and the bolus volume were registered by a presettable binary counter. A quantitative evaluation of transport efficiency was also made of each group of peristaltic contractions that was classified by its characteristic distribution of the interperistaltic internal. The pacemaker activity of the renal pelvis and its control of ureteral peristalsis were identified in this preparation. Most of the peristaltic contractions excreted the same volume of fluid that had entered the pelviureteral system during the preceding period of nonperistalsis within the range of studied perfusion rates. The transport efficiency defined as interperistaltic interval x perfusion rate/bolus volume showed a small variation around the value 1 for peristaltic contractions in each group.

Animals↗

PubMed1978

The effect of PGE1 on peristalsis and on perivascular nerve inhibition of peristaltic activity in guinea-pig isolated ileum.

The effect of PGE1 on peristalsis of guinea-pig isolated ileum was examined using a modified Trendelenburg method to evoke and record peristaltic activity. PGE1 (14 nM, 0.11 microM and 0.56 microM) increased peristaltic activity of both longitudinal and circular muscle, mainly by increasing the amplitude of contraction. Preparations of ileum subjected to a 'minimal' peristaltic stimulus were more sensitive to the effects of PGE1 than were preparations subjected to a 'just-maximal' peristaltic stimulus. The inhibition of peristaltic activity caused by perivascular nerve stimulation was antagonized by 0.56 microM PGE1 but slightly increased by 14 nM PGE1.

Animals↗