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 37 records · Page 2Linked to original sources
PubMed1999

Different receptors mediating the inhibitory action of exogenous ATP and endogenously released purines on guinea-pig intestinal peristalsis.

1 Adenosine 5'-triphosphate (ATP) is an enteric neurotransmitter which acts at purine receptors on intestinal nerve and muscle. This study set out to shed light on the receptor mechanisms by which exogenous and endogenous ATP influences intestinal peristalsis. 2 Peristalsis in isolated segments of the guinea-pig small intestine was triggered by a perfusion-induced rise of the intraluminal pressure. Motor changes were quantified by alterations of the peristaltic pressure threshold (PPT) at which propulsive muscle contractions were elicited. 3 ATP (>/= 3 microM) increased PPT and abolished peristalsis at concentrations of 100-300 microM. Adenosine 5'-O-2-thiodiphosphate (ADPbetaS, 3-100 microM) was more potent, whereas alpha,beta-methylene ATP (alpha,beta-meATP, 3-100 microM) was less potent, than ATP in depressing peristalsis. 4 8-Phenyltheophylline (10 microM) attenuated the anti-peristaltic effect of 10 and 30 microM ATP but not that of higher ATP concentrations. Apamin (0.5 microM) counteracted the ability of ATP, ADPbetaS and alpha,beta-meATP to enhance PPT. Suramin (300 microM) and pyridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 150 microM) antagonized the inhibitory effect of alpha,beta-meATP on peristalsis but did not alter the effect of ATP and ADPbetaS. 5 PPADS (50-150 microM) reduced PPT by as much as 50%. This stimulant effect on peristalsis was prevented by suramin (300 microM) but left unaltered by apamin (0.5 microM) and NG-nitro-L-arginine methyl ester (300 microM). 6 These data show that exogenous and endogenous ATP inhibits intestinal peristalsis via different apamin-sensitive purinoceptor mechanisms. Exogenous ATP depresses peristalsis mostly via suramin- and PPADS-insensitive P2 receptors, whereas endogenous purines act via P2 receptors sensitive to both suramin and PPADS.

Adenosine Diphosphate↗
PubMed1999

Initiation of peristalsis by circumferential stretch of flat sheets of guinea-pig ileum.

1. Segments of isolated guinea-pig intestine, 12 mm long, were distended slowly by intraluminal fluid infusion or by mechanical stretch as either a tube or flat sheet. In all cases, at a constant threshold length, a sudden, large amplitude contraction of the circular muscle occurred orally, corresponding to the initiation of peristalsis. 2. Circumferential stretch of flat sheet preparations evoked graded contractions of the longitudinal muscle (the 'preparatory phase'), which were maintained during circular muscle contraction. This suggests that the lengthening reported during the emptying phase of peristalsis is due to mechanical interactions. 3. The threshold for peristalsis was lower with more rapid stretches and was also lower in long preparations (25 mm) compared with short preparations (5-10 mm), indicating that ascending excitatory pathways play a significant role in triggering peristalsis. 4. Stretching a preparation beyond the threshold for peristalsis evoked contractions of increasing amplitude; thus peristalsis is graded above its threshold. However, during suprathreshold stretch maintained at a constant length, contractions of the circular muscle quickly declined in amplitude and frequency. 5. Circular muscle cells had a resting membrane potential approximately 6 mV more negative than the threshold for action potentials. During slow circumferential stretch, subthreshold graded excitatory motor input to the circular muscle occurred, prior to the initiation of peristalsis. However, peristalsis was initiated by a discrete large excitatory junction potential (12 +/- 2 mV) which evoked bursts of smooth muscle action potentials and which probably arose from synchronized firing of ascending excitatory neuronal pathways.

Animals↗
PubMed1994

The role of enteric inhibitory motoneurons in peristalsis in the isolated guinea-pig small intestine.

1. Peristalsis is a co-ordinated motor behaviour in which an anally propagated contraction of the circular muscle propels intraluminal contents. The role of excitatory motoneurons in peristalsis is well established; however the role of enteric inhibitory motoneurons is unknown. 2. A combination of a nitric oxide synthase inhibitor and apamin, which blocks relaxation of the circular muscle of guinea-pig small intestine mediated by enteric inhibitory motoneurons, was used to investigate the role of inhibitory motoneurons in peristalsis in isolated segments of guinea-pig small intestine. 3. N omega-nitro-L-arginine methyl ester (L-NAME, 400 microM) and N omega-nitro-L-arginine (L-NOArg, 100 microM) significantly reduced the threshold volume required to trigger emptying of the intestine. This effect was reversed by L-arginine (4 mM) and L-arginine alone increased the threshold volume for initiation of peristalsis. Sodium nitroprusside (0.1-10 microM), which generates nitric oxide, also increased the threshold volume. L-NAME, L-NOArg, L-arginine and sodium nitroprusside did not alter the maximal intraluminal pressure generated during emptying. Contraction of the longitudinal muscle during the initial phase of fluid infusion was significantly increased by L-NAME and L-NOArg and reduced by sodium nitroprusside (1 nM to 10 microM). 4. Apamin (0.5 microM) did not significantly alter the threshold volume necessary to initiate peristalsis or contraction of the longitudinal muscle. However, the maximal pressure generated when the intestine was emptying was significantly increased. Furthermore, short segments of circular muscle contracted apparently randomly, before peristaltic emptying was triggered. 5. A combination of L-NAME and apamin completely disrupted peristalsis. Contractions of the circular muscle did not always start at the oral end. Stationary contractions as well as contractions propagating orally and anally were observed. 6. It is concluded that enteric inhibitory motoneurons are crucial for peristalsis to occur. They are important in setting the threshold at which peristaltic emptying is triggered, via nitric oxide. They are essential for the propagation of the circular muscle contraction, via an apamin-sensitive mechanism of transmission. Contraction of the longitudinal muscle during peristalsis is partly inhibited by a nitric oxide-mediated mechanism.

Animals↗
PubMed1995

Effect of aging on the secondary esophageal peristalsis: presbyesophagus revisited.

In this study we determined the effect of aging on the capability of the human esophagus to generate secondary peristalsis. We studied nine healthy young (35 +/- 2 yr, 25-45 yr) and nine healthy elderly (74 +/- 3 yr, 70-83 yr) volunteers. We stimulated secondary peristalsis by intraesophageal air injection and balloon distension. All young volunteers exhibited secondary esophageal peristalsis. In four elderly volunteers, secondary peristalsis could not be elicited with injection of any of the tested air volumes. Frequency of stimulation of secondary peristalsis and lower esophageal sphincter (LES) relaxation in response to intraesophageal air distension in the elderly was significantly lower than that in the young (P < 0.01). Stimulation of secondary peristalsis by balloon distension was less consistent compared with the air injection. In conclusion, 1) in the elderly, compared with the young, secondary esophageal peristalsis is either absent or is evoked less frequently after esophageal distension, and complete LES relaxation in response to esophageal air distension is less frequent, and 2) in both young and elderly, secondary esophageal peristalsis is induced more frequently after generalized esophageal distension by air than its segmental distension by a balloon.

Adult↗
PubMed2000

Disruption of primary and secondary esophageal peristalsis by afferent stimulation.

Recent studies have shown that afferent signals originating from the pharynx inhibit progression of primary esophageal peristalsis. Our aim was to further elucidate the effect of esophageal and pharyngeal afferent stimulation on primary and secondary esophageal peristalsis. We studied the effect of esophageal air distension and pharyngeal water stimulation on progression of primary and secondary peristalsis in nine healthy volunteers aged 27 +/- 2 yr (4 men, 5 women). At a threshold volume, rapid injection of water into the pharynx, directed posteriorly, resulted in complete halt of the progressing secondary and primary esophageal peristalses in both the proximal and distal esophagus. The threshold volume of injected water for inducing inhibition was similar for secondary (0.6 +/- 0.2 ml) and primary (0.5 +/- 0.1 ml) esophageal peristalsis. Progression of primary peristalsis induced by a dry swallow and secondary peristalsis induced by intraesophageal air distension were completely inhibited by intraesophageal injection of 15 +/- 2 ml of air in 70% and 75% of the trials, respectively. We conclude that afferent signals induced by esophageal air distension and pharyngeal water stimulation inhibit propagation of both primary and secondary esophageal peristalsis, suggesting a shared neural control mechanism for these types of peristalsis.

Adult↗
PubMed2003

Evaluation of peristalsis in multiple segments of the guinea-pig isolated small intestine: optimisation of tissue use by refined in vitro methodology.

Peristalsis is the aboral movement by which the intestine propels its contents. Since pharmacological research requires an experimental model with which drug-induced modifications of peristalsis can be reliably quantified, we set out to develop and validate an in vitro method for studying peristalsis in multiple gut segments. In our arrangement, up to four 10cm segments isolated from the guinea-pig jejunum and ileum can be set up in parallel and their lumens perfused. Peristalsis was elicited by pressure-evoked wall distension, and the peristalsis-induced changes in the intraluminal pressure were evaluated with software that determined the peristaltic pressure threshold, the frequency, maximal acceleration and amplitude of the peristaltic waves, and the residual baseline pressure. Validation experiments showed that the peristalsis parameters at baseline and after modification by morphine (0.01-10microM) did not differ between segments from the jejunum and ileum, or between segments examined in a consecutive manner. In conclusion, our work succeeded in optimising the use of the guinea-pig jejunum and ileum for multiple recordings of peristalsis in vitro, and in refining the recording and evaluation of peristaltic motility. This system promises to be particularly useful in the pharmacological screening and testing of drugs which modify peristalsis.

Animal Use Alternatives↗
PubMed1966

The effects of pressure and pharmacologically active substances on gastric peristalsis in a transmurally stimulated rat soomach-duodenum preparation.

1. A rat stomach-duodenum preparation in which pressures in the body and the antrum and flow through the pylorus could be recorded simultaneously has been used to study the effects of pressure and pharmacologically active substances on the peristalsis induced by transmural stimulation.2. Vagal and transmural stimulation produced vigorous peristalsis and episodic flow. Simultaneous stimulation of the peri-arterial nerves abolished peristalsis and relaxed the pylorus.3. After repeated stimulation the preparation lost tone and peristalsis failed. Peristalsis and tone could then be improved by lowering intragastric pressure. Vigorous peristalsis could be restored in an inactive preparation by eserine and more transiently by 5-HT.4. Drugs which increased smooth muscle tone improved peristalsis and, under the conditions used, they reduced flow. Eserine was more active in this respect than acetylcholine or 5-HT.5. Adrenaline and hyoscine abolished peristalsis and caused the stomach and the pylorus to relax.6. The results suggest that the peristaltic activity of the antrum is more important than the tone of the pylorus itself in controlling gastric emptying.

Acetylcholine↗
PubMed2004

Total fundoplication is superior to partial fundoplication even when esophageal peristalsis is weak.

BACKGROUND: About a decade ago, partial (240 degrees) fundoplication became popular for treating gastroesophageal reflux disease in cases where the patient's primary esophageal peristalsis was weak. A total (360 degrees) fundoplication was reserved for patients with normal peristalsis (tailored approach). The theory was that partial fundoplication was an adequate antireflux measure, and by posing less resistance for the weak esophageal peristalsis to overcome, it would give rise to less dysphagia. Short-term results seemed to confirm these ideas. STUDY DESIGN: This study reports the longterm followup of patients in whom a tailored approach (type of wrap chosen to match esophageal peristalsis) was used, and the results of a nonselective approach, using a total fundoplication regardless of the amplitude of esophageal peristalsis. We analyzed clinical and laboratory findings in 357 patients who had an operation for gastroesophageal reflux disease between October 1992 and November 2002. Group 1 was composed of 235 patients in whom a tailored approach was used between October 1992 and December 1999 (141 patients, partial fundoplication and 94 patients, total fundoplication). Group 2 contained 122 patients in whom a nonselective approach was used (total fundoplication regardless of quality of peristalsis). RESULTS: In group 1, heartburn from reflux (ie, pH monitoring test was abnormal) recurred in 19% of patients after partial fundoplication and in 4% after total fundoplication. In group 2, heartburn recurred in 4% of patients after total fundoplication. The incidence of postoperative dysphagia was similar in the two groups. CONCLUSIONS: These data show that laparoscopic partial fundoplication was less effective than total fundoplication in curing gastroesophageal reflux disease, and compared with a partial (240 degrees) fundoplication, a total (360 degrees) fundoplication was not followed by more dysphagia, even when esophageal peristalsis was weak.

Deglutition Disorders↗
PubMed1999

Stimulant action of pituitary adenylate cyclase-activating peptide on normal and drug-compromised peristalsis in the guinea-pig intestine.

1. Pituitary adenylate cyclase-activating peptide (PACAP) is known to influence the activity of intestinal smooth muscle. This study set out to examine the action of PACAP on normal and drug-inhibited peristalsis and to shed light on its site and mode of action. 2. Peristalsis in isolated segments of the guinea-pig small intestine was elicited by distension through a rise of the intraluminal pressure. Drug-induced motility changes were quantified by alterations of the peristaltic pressure threshold at which aborally moving peristaltic contractions were triggered. 3. PACAP (1-30 nM) stimulated normal peristalsis as deduced from a concentration-related decrease in the peristaltic pressure threshold (maximum decrease by 55%). The peptide's stimulant effect remained intact in segments pre-exposed to apamin (0.5 microM), N-nitro-L-arginine methyl ester (300 microM), naloxone (0.5 microM), atropine (1 microM) plus naloxone (0.5 microM) or hexamethonium (100 microM) plus naloxone (0.5 microM). 4. PACAP (10 nM) restored peristalsis blocked by morphine (10 microM), noradrenaline (1 microM) or N6-cyclopentyladenosine (0.3 microM) and partially reinstated peristalsis blocked by Rp-adenosine-3',5'-cyclic monophosphothioate triethylamine (100 microM) but failed to revive peristalsis blocked by hexamethonium (100 microM) or atropine (1 microM). The peptide's spectrum of properistaltic activity differed from that of naloxone (0.5 microM) and forskolin (0.3 microM). 5. The distension-induced ascending reflex contraction of the circular muscle was facilitated by PACAP (1-30 nM) which itself evoked transient nerve-mediated contractions of intestinal segment preparations. 6. These data show that PACAP stimulates normal peristalsis and counteracts drug-induced peristaltic arrest by a stimulant action on excitatory enteric motor pathways, presumably at the intrinsic sensory neurone level. The action of PACAP seems to involve multiple signalling mechanisms including stimulation of adenylate cyclase.

Animals↗
PubMed2000

Secondary oesophageal peristalsis in gastro-oesophageal reflux disease.

BACKGROUND AND AIMS: To evaluate the status of secondary oesophageal peristalsis in gastro-oesophageal reflux disease (GORD) and the effect of healing of oesophagitis on these abnormalities. METHODS: Twenty-one patients diagnosed with GORD and 10 control subjects in the same age group were studied. Primary peristalsis was elicited by 10 5 mL water boluses and secondary peristalsis by 10 20 mL boluses of air injected 15 cm above the lower oesophageal sphincter. RESULTS: The pattern of primary peristalsis was normal in a significantly lower number of patients compared with control subjects, six patients (28.6%) versus seven controls (70%), (P<0.05). Similarly, the number of subjects with a normal pattern of secondary peristalsis was also lower in the patient group (zero vs three; P<0.05). A normal primary peristaltic response occurred with 71 (33.8%) of the 210 water boluses in the patients and 73 (73%) of the 100 water boluses in the control subjects, respectively (P<0.001). A normal secondary peristaltic response was seen with 15 (7.1%) of 210 air boluses in patients and 32 (32%) of 100 air boluses in the control subjects (P<0.001). The amplitude of secondary peristaltic waves and the duration of contraction (mean+/-SEM) were significantly lower in patients compared with the control subjects (43.5+/-4.7 vs 89.0+/-13.1 and 3.4+/-0.8 vs 3.9+/-0.3, respectively; P=<0.05). In the 13 patients in whom repeat evaluation was performed after healing of oesophagitis, there was no significant change in the number of patients with normal peristaltic response, number of normal responses to air and water boluses, or amplitude, duration and velocity of peristalsis. CONCLUSION: Significant abnormalities of secondary oesophageal peristalsis occur in patients with GORD and these are not reversed by healing of oesophagitis.

Adolescent↗
PubMed2000

Effect of white wine on esophageal peristalsis and acid clearance.

BACKGROUND: In a previous study it was demonstrated that white wine reduces the lower esophageal sphincter pressure and induces gastroesophageal reflux characterized by reflux episodes of long duration. In the present study, it was evaluated whether wine disturbs esophageal peristalsis and acid clearance. METHODS: Twelve healthy volunteers (7F, 23-37 years) received 300 ml white wine (8% vol/vol; WW), an ethanol solution (8% vol/vol; ET) or tap water (WA) together with a standardized meal in a random order. Acid clearance was tested by instillation of 15 ml 0.1 N HCI into the distal esophagus. The number of swallows (dry swallow every 30 sec) were counted until pH rose again above 5. Five wet swallows (5 ml) were applied to test primary peristalsis and five insufflations of 20 ml of air were performed to test secondary peristalsis. Each test was done immediately after and 60 min after ingestion of the beverages. RESULTS: A significantly higher number of swallows were needed to clear the esophagus immediately after ingestion of wine (P < 0.01; median number: WW 12; ET 8; WA 7) due to an increase in the frequency of failed, simultaneous, and low-amplitude contractions. The frequency of triggered secondary contractions was decreased (P < 0.02; WW 70%; ET 100%; WA 100%) and the latency between air injection and onset of secondary peristalsis was prolonged (P < 0.05; WW 9 sec; ET 7 sec; WA 6 sec) immediately after ingestion of white wine. Wet swallow induced primary peristalsis was not influenced by wine. No significant differences in the measured parameters were seen 60 min after ingestion of the three beverages. CONCLUSION: White wine disturbs temporarily esophageal clearance due to a disturbance of triggering secondary peristalsis and due to an increase in ineffective contractions. The ethanol content alone is not responsible for the effects of white wine on esophageal peristalsis and acid clearance.

Adult↗
PubMed2000

Low potential of dobutamine and dopexamine to block intestinal peristalsis as compared with other catecholamines.

OBJECTIVE: Catecholamines are frequently used in critically ill patients to restore stable hemodynamics and to improve organ perfusion. One effect of short-term or long-term administration of catecholamines may be inhibition of propulsive motility in the intestine. We therefore analyzed the effect of dopexamine, dobutamine, and dopamine on ileal peristalsis and compared their action with that of epinephrine and norepinephrine, which have long been known to suppress intestinal peristalsis. DESIGN: In vitro study on excised guinea pig ileum segments. SETTING: Laboratory for experimental studies at the University. SUBJECTS: Isolated guinea pig ileum. INTERVENTIONS: Segments of ileum excised from guinea pigs were mounted in a tissue bath in Krebs-Henseleit solution and bubbled with 95% oxygen/5% CO2. Luminal perfusion with the same solution was performed at a rate of 0.35 mL/min. The bath temperature was kept at 36.5 degrees C. Peristalsis was recorded via changes in the intraluminal pressure. The drugs under investigation (dopamine, epinephrine, norepinephrine, dobutamine, and dopexamine) were added to the tissue bath. MEASUREMENTS AND MAIN RESULTS: Low concentrations of each catecholamine, except epinephrine, caused a decrease in the pressure threshold, which reflects a stimulatory effect on peristalsis. Higher catecholamine concentrations caused a concentration-related increase in the threshold, cumulating in a complete block of peristalsis. The rank order of inhibitory potency was epinephrine > norepinephrine > dopamine > dobutamine approximately dopexamine. Dobutamine and dopexamine were about 500-fold less active than epinephrine in suppressing peristalsis. CONCLUSIONS: This study shows that dobutamine and dopexamine have the least potential to block propulsive motility in the intestine, whereas epinephrine demonstrates the most adverse inhibitory effect. Because at low concentrations dobutamine and dopexamine even stimulate peristalsis, these drugs appear to be superior compared with other catecholamines with regard to their direct effects on intestinal motility.

Adrenergic beta-Agonists↗
PubMed2000

Characteristics of secondary oesophageal peristalsis in operated and non-operated patients with chronic gastro-oesophageal reflux disease.

BACKGROUND AND AIMS: Secondary oesophageal peristalsis contributes to oesophageal volume clearance and may be impaired in a significant proportion of patients with chronic gastro-oesophageal reflux disease (GORD). This study aimed to investigate the triggering of secondary peristalsis in chronic GORD patients compared to those previously operated on with anti-reflux surgery. PATIENTS AND METHODS: Healthy volunteers, chronic GORD patients with proven oesophagitis and patients successfully operated on with anti-reflux surgery (> 3 years ago) were investigated. Secondary peristalsis was elicited by oesophageal distension by a bolus of air (10 ml) injected rapidly into the mid-portion of the oesophagus. The peristaltic characteristics in the distal oesophagus were assessed by use of stationary manometry. RESULTS: The primary peristaltic amplitude in the distal third of the oesophagus was significantly higher (P < 0.002) in the non-operated GORD cases than in those recruited for surgery. Furthermore, a difference in the frequency of failed primary peristalsis was revealed (2.1 versus 8.4%) between the non-operated and operated patients. Secondary peristalsis occurred in 65 +/- 13.2% (mean +/- SE) of the healthy subjects on stimulation, which was a higher figure than in the GORD patients. In patients investigated after successful anti-reflux surgery, a secondary peristaltic wave was elicited in only 26 +/- 7.2% of the attempts, which was significantly lower than the 46 +/- 7.7% seen in non-operated GORD patients (P < 0.05). A direct comparison between motor characteristics of primary and secondary peristalsis revealed that the latter amplitudes were significantly lower both in the non-operated and in the operated cases (P < 0.005). CONCLUSIONS: The triggering of secondary peristalsis seems to be impaired in chronic GORD patients. Investigating similar patients > 3 years after successful anti-reflux surgery revealed an even lower prevalence of secondary peristaltic waves, implying persistence of the abnormality after surgery and consistent with other evidence that GORD is associated with a primary defect in oesophageal motor function.

Adult↗
PubMed2005

Peristalsis in the Guinea pig small intestine in vitro is impaired by acetaminophen but not aspirin and dipyrone.

Inhibition of intestinal peristalsis is a major side effect of opioid analgesics. It is unknown whether non-opioid analgesics, such as acetaminophen, acetylsalicylic acid, and dipyrone, exert any effect on intestinal motility. In the current in vitro study we examined the effect of these analgesics on intestinal peristalsis and analyzed some of their mechanisms of action. In isolated segments of the guinea pig small intestine peristalsis was triggered by a perfusion-induced increase of the intraluminal pressure. The peristaltic pressure threshold (PPT) at which peristaltic waves were elicited was used to quantify drug effects on peristalsis. Vehicle (Tyrode's solution), acetaminophen (0.01-100 microM), acetylsalicylic acid (100-300 microM), and dipyrone (10-100 microM) were added extraserosally to the organ bath. Acetaminophen concentration-dependently increased PPT and abolished peristalsis in four of six segments at the concentration of 10 microM and in all segments tested at 100 microM (EC50=6.0 microM). The increase in PPT resulting from 3 microM acetaminophen was reduced by naloxone and apamin but not changed by L-nitro-arginine methylester (L-NAME), its inactive enantiomer D-NAME, acetylsalicylic acid, methysergide, or tropisetron. Acetylsalicylic acid and dipyrone did not affect peristalsis. The results reveal, for the first time, that acetaminophen concentration-dependently impairs intestinal peristalsis, whereas acetylsalicylic acid and dipyrone lacked such an effect. The inhibition caused by acetaminophen involves transmitters acting via small conductance Ca2+-activated potassium channels, endogenous opioidergic pathways, and presumably inhibition of cyclooxygenase-3.

Acetaminophen↗
PubMed1997

Chest pain and reappearance of esophageal peristalsis in treated achalasia.

BACKGROUND: We wanted to evaluate the clinical significance of the esophageal peristalsis that appears in some achalasia patients after treatment. METHODS: We prospectively investigated the reappearance of esophageal peristalsis in 106 achalasic patients treated with forceful dilatation under endoscopic control (86 metallic dilatations and 20 pneumatic dilatations) and followed up clinically and manometrically for 1 year. Patients were divided in two groups in accordance with the presence (n = 26) or persistent absence (n = 80) of postdilatation esophageal peristalsis. RESULTS: Before treatment, clinical data and manometric findings were comparable in both groups except for esophageal wave amplitude, which was higher in patients with postdilatation peristalsis (36 +/- 5 mmHg versus 24 +/- 2 mmHg, P < 0.05). One year after dilatation manometric findings were similar in the two groups, but esophageal wave amplitude remained higher in the group with postdilatation peristalsis (46 +/- 4 mmHg versus 21 +/- 2 mmHg, P < 0.05). The proportion of patients with persistent dysphagia was similar in the two groups (15% versus 12.5%). However, 10 patients with postdilatation peristalsis (38%) complained of chest pain as opposed to only 5 patients (6%) in the group with aperistalsis (P < 0.01). CONCLUSION: The appearance of esophageal peristalsis after forceful dilatation in achalasic patients is frequently associated with persistent or new chest pain.

Adolescent↗
PubMed2004

[Study on the mechanism of traditional Chinese medicines in promoting gastrointestinal peristalsis].

Traditional Chinese medicine has accumulated rich experience in treating dysfunction of gastrointestinal peristalsis. In recent years, a large number of studies have been made on the mechanism and effects of traditional Chinese medicines on the gastrointestinal peristalsis, and the concept of "gastrointestinal promoting Chinese medicine" has been advocated. These traditional Chinese medicines can be divided into three types: promoting the gastrointestinal peristalsis, inhibiting the gastrointestinal peristalsis, and bi-directional modulating. The in vivo and/or in vitro experiments showed that some of the traditional Chinese medicines for activating blood or regulating qi could promote the stomach peristalsis, and the traditional Chinese medicines for moistening intestines to relieve constipation or invigorating spleen to promote digestion could accelerate the intestinal peristalsis. The mechanism lies in the neuroregulation and gut-peptide regulation. Further research on multi-regulation and of multi-target should be done, for the mechanism of the traditional Chinese medicines in regulating the gastrointestinal peristalsis is far more complicated.

Drugs, Chinese Herbal↗
PubMed1997

Dual excitatory and inhibitory effect of nitric oxide on peristalsis in the guinea pig intestine.

The implications of the enteric neurotransmitter nitric oxide (NO) in intestinal peristalsis were investigated. Propulsive motility in isolated segments of the guinea pig ileum was triggered by intraluminal fluid infusion to distend the intestinal wall, and the pressure threshold for eliciting peristaltic waves was used to quantify facilitation (decrease in threshold) or inhibition (increase in threshold) of peristalsis. The NO donor sodium nitroprusside (0.1-100 microM serosally) caused a prompt facilitation of peristalsis, which in the presence of a threshold concentration of atropine (10 nM) was followed by a concentration-related blockade of peristalsis. Further analysis showed that sodium nitroprusside (10 and 100 microM) first relaxed, then contracted, and finally relaxed the longitudinal muscle of the guinea pig isolated ileum, the contraction being blocked by atropine (1 microM). Inhibition of NO synthase by NG-nitro-L-arginine methylester (100-300 microM) facilitated peristalsis, an effect that was reduced by L-arginine (1 mM) but left unaltered by atropine (10 nM). Blockade of inhibitory neuromuscular transmission by successive exposure of the ileum to apemin (0.5 microM) and NG-nitro-L-arginine methylester (300 microM), in this or reverse order, disrupted the coordinated pattern of peristalsis and caused irregular nonpropulsive contractions of the circular muscle. It is concluded that NO has a dual excitatory and inhibitory effect on intestinal motility. The excitatory effect involves cholinergic motor neurons, whereas the inhibitory effect reflects relaxation of intestinal muscle. Abolition of peristalsis by combined exposure to NG-nitro-L-arginine methylester and apamin attests to an essential role of enteric inhibitory motor neurons in the coordination of propulsive motility in the intestine.

Animals↗
PubMed2000

Regulation of guinea pig intestinal peristalsis by endogenous endothelin acting at ET(B) receptors.

BACKGROUND & AIMS: Endothelins are expressed in many enteric neurons of the gut. Because activation of endothelin ET(A) and ET(B) receptors is known to alter intestinal muscle activity, the effect of ET(A) and ET(B) receptor agonists and antagonists on propulsive peristalsis was examined. METHODS: Repetitive peristalsis in fluid-perfused segments of the guinea pig isolated small intestine was elicited by a rise of the intraluminal pressure and recorded via the pressure changes generated by the peristaltic waves. RESULTS: Endothelin 1 (0.3-10 nmol/L added to the organ bath) stimulated peristalsis as shown by a decrease in the pressure threshold at which peristaltic waves were triggered, whereas the endothelin analog sarafotoxin 6c (0.3-10 nmol/L) inhibited peristalsis as reflected by an increase in the pressure threshold. The ET(A) receptor antagonist BQ-123 (3 micromol/L) converted the properistaltic action of endothelin 1 to an antiperistaltic action, whereas the ET(B) receptor antagonist BQ-788 (3 micromol/L) prevented the antiperistaltic action of sarafotoxin 6c. BQ-788, but not BQ-123, facilitated peristalsis on its own. Additional experiments indicated that the properistaltic action of endothelin 1 is mediated by enteric neurons, whereas the peristaltic motor effects of sarafotoxin 6c and BQ-788 are caused by a direct action on the muscle. CONCLUSIONS: ET(A) receptor activation stimulates, whereas ET(B) receptor activation inhibits, intestinal peristalsis. The ability of BQ-788 to facilitate peristalsis per se points to a physiologic role of ET(B) receptors in peristaltic motor regulation.

Animals↗