Esophageal Balloon Distension Research Articles

8 The effect of food on electrical and mechanical activity of the canine antrum

Background: Gastric electrical and mechanical activities are modulated by food, however, the pattern of food‐induced changes and the mechanisms governing them are not well defined.Aim: To characterize food–induced changes in gastric antral activity and to explore underlying mechanisms for such changes.Methods: Experiment 1‐ intended to test the effect of food on gastric signals. Two bipolar electrodes were implanted in the antrum of 7 mongrel dogs for simultaneous recording of slow wave rate, in events /min (SWR), and contractions assessed by electrical impedance (AI) in ohms. A strain‐gauge transducer was implanted in 3 dogs to correlate changes in AI with contractions. The meal consisted of a preload of 100 g of dry food followed in 10 min, by 900 g of the same food, to lengthen meal duration. SWR and AI were determined during 4 periods of 5 min/each (baseline, end of preload, satiety, 10 min after satiety). Experiment was repeated 5 times/dog. Experiment 2‐acute study, under anesthesia with 3 tests: 1) esophageal balloon distension 2) fundic balloon distension at volumes of 50–400 ml, using a balloon of 800 ml, and 3) nitroglycerin infusion, 0.5 (g kg­1 min­1 for 10 min. results as Mean ± SD.Results: Experiment 1‐ frequency of antral contractions by strain‐gauge correlated well with frequency of contractions as measured by AI, R = 0.76. SWRs at baseline, preload, satiety and post satiety were: 5.0 ± 0.3, 4.9 ± 0.4, 3.8 ± 0.65, and 4.4 ± 0.47 respectively. SW amplitudes (ohms) at the same periods were: 5.3 ± 1.4, 8.5 ± 2.1, 12.2 ± 4.3 and 12.0 ± 5.3 respectively; p < 0.05 for satiety and post satiety vs. baseline for both measurements. Both changes peaked around the time of satiety. Mean time interval between satiety and slowest SWR was 80 ± 40 sec. Amplitude of contractions remained elevated for 212 ± 110 min after the meal. Experiment 2‐ fundic distension caused a transient decrease in SWR at lower volumes, but the decrease was sustained at the 400 ml volume, 3.9 ± 0.2 vs. 3 ± 0.8, baseline vs. distension, respectively, p = 0.002. NTG significantly reduced SWR: 4.0 ± 0.7 vs. 3.5 + 0.8, baseline vs. infusion, p = 0.007. Esophageal distension did not affect SWR.Conclusions: Food ingestion causes a significant decrease in SWR and significant enhancement of antral contractions that peak at satiety. This suggests a possible causal relationship that can be potentially useful when considering gastric electrical stimulation for modulation of satiety signals. Both gastric distension and nitrergic pathways affect SWR.

Corrigenda

Neurogastroenterology & MotilityVolume 18, Issue 5 p. 403-403 Free Access Corrigenda First published: 18 April 2006 https://doi.org/10.1111/j.1365-2982.2006.00798.xAboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Neurogastroenterology & Motility 2006; 18, 292–9. Characterization of cortical potentials evoked by oesophageal balloon distention and acid perfusion in patients with functional heartburn M. Yang, Z-S. Li, X-R. Xu, D-C. Fang, D-W. Zou, G-M. Xu, Z-S. Sun & Z-X. Tu Figures 1a and 1b in the above mentioned paper1 contained some errors. The correct figures are printed below. Figure 1Open in figure viewerPowerPoint Morphology of the cortical evoked potentials (CEPs) obtained from a healthy subject and a functional heartburn (FH) patient before saline/acid perfusion. Baseline CEP morphology in response to balloon distention in the healthy subject (1A) and FH patient (1B). CEPs consisted of a triphasic morphology with two negative (N1 and N2) and one positive (P1) components. The study was repeated, and two responses were superimposed to demonstrate the reproducibility of each component. Neurogastroenterology & Motility 2005; 17, 602–33. Abstracts for the 14th Annual Scientific Meeting, September 22–25, 2005, Santa Monica, California American Motility Society The authors of the following Abstracts2 were presented incorrectly. The correct authorship is given below: 76 Pharmacokinetic profile of lubiprostone, a selective GI chloride channel activator, after a single oral dose in multiple animal species R. Ueno, G. P. Perentesis, K. J. Engelke, Y. Kawai 77 Effects of lubiprostone, a novel GI chloride channel activator, on isolated smooth muscle R. Ueno, K. J. Engelke, H. Osama 88 Effect of a chloride channel activator, lubiprostone, on gastrointestinal transit, gastric sensory and motor functions in humans M. Camilleri, A.E. Bharucha, R. Ueno, G.M. Thomforde, K. Baxter, S. McKinzie, and A.R. Zinsmeister References 1 Yang M, Li Z-S, Xu X-R, Fang D-C, Zou D-W, Xu G-M, Sun Z-S, Tu Z-X. Characterization of cortical potentials evoked by oesophageal balloon distention and acid perfusion in patients with functional heartburn. Neurogastroenterol Motility 2006; 18, 292– 9. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar 2 American Motility Society. Abstracts for the 14th Annual Scientific Meeting, September 22–25, 2005, Santa Monica, California. Neurogastroenterol` Motility 2005; 17, 602– 33. Web of Science®Google Scholar Volume18, Issue5May 2006Pages 403-403 FiguresReferencesRelatedInformation

Characterization of cortical potentials evoked by oesophageal balloon distention and acid perfusion in patients with functional heartburn

Oesophageal visceral hypersensitivity is thought to be important in generating symptoms in functional heartburn (FH). However, the neurophysiological mechanisms involved are poorly understood. The aim of this study was to compare the characteristics of oesophageal cortical evoked potentials (CEPs) induced by balloon distension and acid perfusion in FH and controls. We studied 21 FH patients and 12 healthy volunteers. Oesophageal mechanical stimulation was performed using the specially constructed mechanical pump. CEPs were recorded using the 10-20 international system of electroencephalogram recording. Oesophageal distention elicited recognizable, reproducible and muti-peak CEPs. CEP latencies for N1, P1 and N2 components were significantly shorter (P = 0.016, P = 0.003 and P = 0.031, respectively) in FH than in controls before perfusion. Acid perfusion significantly decreased the latencies of N1, P1 and N2 (P = 0.022, P = 0.007 and P = 0.041, respectively) and significantly increased the amplitude of P1-N2 components (P = 0.020) in FH patients, but not in controls. In conclusion, cortical evoked potential responses evoked by oesophageal distention and acid perfusion were greater in FH than in controls, suggesting that dysfunction of visceral neural pathways and/or alterations in cortical processing may produce and mediate oesophageal hypersensitivity in FH. These findings provide the evidence that central sensitization contributes to the development and maintenance of oesophageal hypersensitivity.

Esophageal-gastric relaxation reflex in rat: dual control of peripheral nitrergic and cholinergic transmission

It has long been known that the esophageal distension produced by swallowing elicits a powerful proximal gastric relaxation. Gastroinhibitory control by the esophagus involves neural pathways from esophageal distension-sensitive neurons in the nucleus tractus solitarius centralis (cNTS) with connections to virtually all levels of the dorsal motor nucleus of the vagus (DMV). We have shown recently that cNTS responses are excitatory and primarily involve tyrosine hydroxylase-immunoreactive cells, whereas the DMV response involves both an alpha1 excitatory and an alpha2 inhibitory response. In the present study, using an esophageal balloon distension to evoke gastric relaxation (esophageal-gastric reflex, EGR), we investigated the peripheral pharmacological basis responsible for this reflex. Systemic administration of atropine methyl nitrate reduced the amplitude of the gastric relaxation to 52.0+/-4.4% of the original EGR, whereas NG-nitro-L-arginine methyl ester (L-NAME) reduced it to 26.3+/-7.2% of the original EGR. Concomitant administration of atropine methyl nitrate and L-NAME reduced the amplitude of the gastric relaxation to 4.0+/-2.5% of control. This reduction in the amplitude of induced EGR is quite comparable (4.3+/-2.6%) to that seen when the animal was pretreated with the nicotinic ganglionic blocker hexamethonium. In the presence of bethanechol, the amplitude of the esophageal distension-induced gastric relaxation was increased to 177.0+/-10.0% of control; administration of L-NAME reduced this amplitude to 19.9+/-9.5%. Our data provide a clear demonstration that the gastroinhibitory control by the esophagus is mediated via a dual vagal innervation consisting of inhibitory nitrergic and excitatory cholinergic transmission.

The Effect of Esophageal and Gastric Distension on the Crural Diaphragm

The mechanism of prevention of gastric reflux into the esophagus is not exactly known. The lower esophagus has a barrier function provided by the lower esophageal sphincter. We investigated the hypothesis that the crural diaphragm shares in the barrier function not only mechanically but also actively through a crural-esophageal-gastric reflex action. The study was performed during repair of abdominal ventral and incisional hernias in 20 subjects (11 men, 9 women; age 38.6+/-4.8 years). The electromyographic response of the crural diaphragm to individual balloon distension of esophagus and stomach was recorded by means of a needle electrode inserted into the crural diaphragm and connected to an electromyographic apparatus. The recordings were repeated after separate crural, esophageal, and gastric anesthetization. The crural diaphragm exhibited basal motor unit action potentials, which decreased on esophageal distension (P<0.001) after a mean latency of 17.3+/-2.8 SD ms. The crural diaphragm response to esophageal distension did not occur after the crural diaphragm or esophagus was anesthetized. Gastric distension effected an increase of crural diaphragm electromyographic activity with a mean latency of 18.4+/-4.6 ms; this effect could not be achieved after the crural diaphragm or stomach was anesthetized. The crural diaphragm has a resting tone that relaxes after esophageal distension and contracts after gastric distension. This sphincter-like action of the crural diaphragm appears to be a reflex and is mediated through the esophagocrural inhibitory and gastrocrural excitatory reflexes. The crural diaphragm seems to share actively in the gastroesophageal competence mechanism.

Brain Response to Visceral Aversive Conditioning: A Functional Magnetic Resonance Imaging Study

Brain-imaging studies to date have confounded visceral pain perception with anticipation. We used functional magnetic resonance imaging of the human brain to study the neuroanatomic network involved in aversive conditioning of visceral pain and, thus, anticipation. Eight healthy volunteers (5 male) participated in the study. We used a classic conditioning paradigm in which 3 neutral stimuli (differently colored circles) that acted as conditioned stimuli were paired with painful esophageal distention, air puff to the wrist, or nothing, which acted as unconditioned stimuli. Neural activity was measured during learning, anticipation (pairing only 50% of conditioned stimuli with their unconditioned stimuli), and extinction (unpaired conditioned stimuli) phases. For magnetic resonance imaging, axial slices depicting blood oxygen level-dependent contrast were acquired with a 1.5-T system. Neural responses during the learning phase included areas commonly associated with visceral pain (anterior cingulate cortex, insula, and primary and secondary somatosensory cortices) and innocuous somatosensory perception (primary and secondary somatosensory cortices and insula). During the anticipation and extinction phases of aversive stimulation, brain activity resembled that seen during actual painful esophageal stimulation. In contrast, anticipation and extinction of the innocuous somatic stimulus failed to show that effect. We have shown that actual and anticipated visceral pain elicit similar cortical responses. These results have implications for the design and interpretation of brain-imaging studies of visceral pain. They not only contribute to our understanding of the processing of visceral pain, but also have clinical implications for the management of chronic pain states.

Functional Chest Pain

Functional chest pain is a common, yet poorly understood entity. The focus of this review is to explore the evolving research and clinical approaches with a particular emphasis on the sensory or afferent neuronal dysfunction of the esophagus as a key player in the manifestation of this pain syndrome. Although once regarded as a psychologic or esophageal motility disorder, recent advances have shown that many of these patients have visceral hyperalgesia. Whether visceral hypersensitivity is a central or peripheral perturbation of the gut-brain axis remains debatable. Response to empirical therapy with high-dose proton pump inhibitors, upper endoscopy, or prolonged recording of esophageal pH may identify gastroesophageal reflux disease as a source of chest pain. Esophageal balloon distension study can serve as a useful test for identifying hypersensitivity. Newer techniques, including functional magnetic resonance imaging, magnetoencephalogram, and cortical evoked potentials, are being investigated. High doses of proton pump inhibitors and low doses of tricyclic antidepressants or trazadone remain the mainstay of therapy, although several new approaches including theophylline have been shown to be beneficial.

Effect of Lower Esophageal Sphincter Distension and Acidification on Esophageal Pressure and Electromyographic Activity: The Identification of the “Sphinctero-Esophageal Excitatory Reflex”

The mechanism of esophageal acid clearance through augmenting esophageal peristalsis in response to gastroesophageal reflux (GER) is not exactly known. We investigated the hypothesis that lower esophageal sphincter (LES) dilatation rather than the refluxed acid affected reflex increase in the esophageal peristaltic activity aiming at clearing the esophagus of the refluxed acid. The esophageal pressure and electromyographic (EMG) activity response to esophageal sphincter balloon distension in increments of 2 mL of saline was recorded in 17 healthy volunteers (10 men, 7 women, mean age 43.6 +/- 11.2 years). The test was repeated in 10 of 17 volunteers while the esophageal sphincter was being anesthetized. The response of the esophageal pressure and electromyographic activity to lower esophageal acidification was also tested. Lower esophageal sphincter balloon distension with 2 mL of saline produced esophageal pressure increase to a mean of 34.2 +/- 5.3 cm H2O (p < 0.001). Increase of the balloon distending volume produced results similar to the 2-mL distension (p > 0.05). The esophageal electrical activity increased on esophageal balloon distension; the increase was similar with distensions of 2 mL up to 10 mL. There was no esophageal pressure or electrical activity response to distension of the anesthetized lower esophageal sphincter or to lower esophageal sphincter acidification. During gastroesophageal reflux episodes, the lower esophageal sphincter dilatation and not acidification appears to initiate increased esophageal peristalsis, which clears the esophagus of the refluxed acid. The increased esophageal peristalsis on lower esophageal sphincter dilatation is suggested to be reflex in nature and is mediated through the "sphincteroesophageal excitatory reflex." This reflex may be of diagnostic significance in esophageal motility disorders; however, this point needs further studies.

Esophageal Visceral Sensitivity to Bile Salts in Patients with Functional Heartburn and in Healthy Control Subjects

Patients with nonerosive gastroesophageal reflux disease often have relatively low esophageal acid exposure and respond suboptimally to gastric acid suppression. In these patients, other constituents of gastric contents may induce esophageal symptoms. We have demonstrated that gastric contents can cause heartburn when the gastric pH >4. (Aliment Pharm Ther 14:129-134, 2000). The aim of this study was to determine relative sensitivities to chenodeoxycholic and ursodeoxycholic acids, and 0.1 N HCl, administered as provocative perfusion tests. Patients with functional heartburn and healthy control subjects were evaluated. Patients underwent a modified Bernstein acid infusion test and esophageal Barostat balloon distention. Time and volume to pain were recorded. Barostat balloon distention was performed using our standard protocol. Stepwise distentions were performed and pain was recorded. Sensitivity to chenodeoxycholic acid (Cheno) and Ursodeoxycholic acid (Urso) were assessed similarly to the Bernstein test using 2 mM concentrations of each, followed immediately by 5 mM if no pain was reported with 2 mM. Volume of bile acid infusion and length of time until pain was induced were assessed and compared to the same endpoints for acid sensitivity. "Total" time and "total" volume to induce pain were calculated for Cheno and Urso. Least-squares means were generated and two-tailed t-tests and regression analyses were performed (P < 0.05 level of significance). Ten functional heartburn patients and six healthy controls were evaluated (3 M, 13 F; age range, 19 to 56 years). Since five of six controls had pain with acid infusion (hypersensitive), all subjects were analyzed as one group. Only three subjects (all controls) had no pain with infusion of 2 mM Cheno and received the follow-up infusion of 5 mM. These same three subjects tolerated the maximum infusion (150 ml and 15 min) of 5 mM Cheno. Nine subjects did not have pain with 2 mM Urso and received the follow-up infusion of 5 mM Urso (five functional heartburn, four controls). Significantly more subjects tolerated the maximum bile acid infusion of 2 mM Urso vs 2 mM Cheno (nine vs three; P < 0.05, Chi-square test). The pain threshold (volume and time) for Urso was significantly higher than that for Cheno and acid (P < 0.05), and the pain threshold for Cheno was significantly higher than that for acid (P < 0.05). Conclusions are as follows: (1) Bile acids differ in their ability to induce pain. (2) Changing bile acid composition by treatment with Urso may change symptom presentation and symptom severity in patients with bile acid-induced esophageal pain.

Investigation of esophageal balloon distension test for unexplained (NCCP) chest pain

Purpose: Although balloon distension test has been used for identifying esophageal visceral hypersensitivity, there is limited data and in small number of patients and its clinical utility is not fully known. Our aim was to prospectively assess symptoms, biomechanical and sensory properties in patients with unexplained chest pain and the yield of this test.

Oesophageal motor and sensitivity abnormalities in non-obstructive dysphagia.

To evaluate oesophageal sensitivity to balloon distension in patients with non-obstructive dysphagia (NOD), and to determine its relationship with the motility pattern in response to food ingestion. Twenty-one healthy volunteers and 19 consecutive patients complaining of NOD with normal standard manometry were included. An oesophageal sensitivity test was carried out before the manometry study with liquid and solid swallows. The median threshold to distension was 9 ml in control subjects and 5 ml in patients (P < 0.002). Dysphagia or odynophagia were reproduced in 15/19 (78.9%) patients during manometry with solid swallows only. The percentage of swallows with abnormal motility patterns was higher in patients than control subjects (P < 0.001). Compared with control values, sensitivity abnormality was defined by a distension threshold of < 6 ml. Motor abnormality was defined by > 19% of swallows occurring with one or more abnormal motor profiles. A total of 8/19 (42%) patients presented with the association of an abnormal sensitivity threshold and an abnormal motor pattern; 5/19 (26%) presented with isolated motor abnormalities; 4/19 (21%) patients presented with isolated abnormal sensitivity thresholds; and 2/19 (11%) patients presented without any abnormality. Manometry with solid swallows and oesophageal balloon distension are useful in characterizing NOD.

Catecholaminergic neurons in rat dorsal motor nucleus of vagus project selectively to gastric corpus.

Nitric oxide synthase-immunoreactive (NOS-IR) neurons in the rat caudal dorsal motor nucleus of the vagus (DMV) project selectively to the gastric fundus and may be involved in vagal reflexes controlling gastric distension. This study aimed to identify the gastric projections of tyrosine hydroxylase-immunoreactive (TH-IR) DMV neurons, whether such neurons colocalize NOS-IR, and if they are activated after esophageal distension. Gastric-projecting neurons were identified after injection of retrograde tracers into the muscle wall of the gastric fundus, corpus, or antrum/pylorus before removal and processing of the brain stems for TH- and NOS-IR. A significantly higher proportion of corpus- compared with fundus- and antrum/pylorus-projecting neurons were TH-IR (14% compared with 4% and 2%, respectively, P < 0.05). Colocalization of NOS- and TH-IR was never observed in gastric-projecting neurons. In rats tested for c-Fos activation after intermittent esophageal balloon distension, no colocalization with TH-IR was observed in DMV neurons. These findings suggest that TH-IR neurons in the caudal DMV project mainly to the gastric corpus, constitute a subpopulation distinct from that of nitrergic vagal neurons, and are not activated on esophageal distension.

Roles of central glutamate, acetylcholine and CGRP receptors in gastrointestinal afferent inputs to vagal preganglionic neurones

It is unknown which neurotransmitter receptors are involved in the transfer of sensory information from the digestive tract to the brainstem. We examined the potential involvement of central glutamate, acetylcholine, and CGRP receptors in vagal pathways arising from gut chemo- and mechanosensitive afferents. Unitary recordings were made from 21 vagal preganglionic efferent neurones. Neuronal discharge showed either excitation or inhibition in response to oesophageal balloon distension (1–2 ml), gastric distension (40–60 ml in whole stomach or 20 ml in proximal stomach), cholecystokinin-8s (100 pmol close intra-arterially) and bradykinin (18 nmol close intra-arterially). Effects of glutamatergic non-NMDA, muscarinic M 1, and CGRP 1 receptor antagonism on efferent responses were investigated using CNQX (75–155 nmol i.c.v.), pirenzepine (2.5–5.0 μmol/kg i.v.), and hCGRP 8-37 (3.2–6.4 nmol i.c.v.), respectively. CNQX, pirenzepine, and hCGRP 8-37, respectively, altered efferent responses in 65%, 23% and 41% of neurones. When both CNQX and hCGRP 8-37 were administered, a further 58% of responses were reduced. CNQX and hCGRP 8-37 reduced a proportion of efferent responses to all stimuli whereas pirenzepine selectively reduced only efferent responses to gastric distension. We conclude that central CGRP 1 and non-NMDA receptors are involved in mediating a range of upper gastrointestinal mechano- and chemo-sensitive afferent inputs onto vagal efferents. M 1 receptors, on the other hand, are selectively involved in neurotransmission from gastric mechanoreceptors.

Determination of biomechanical properties in guinea pig esophagus by means of high frequency ultrasound and impedance planimetry.

Impedance planimetry and high-frequency ultrasound were used to determine circumferential stress and strain from measurements of luminal cross-sectional area and wall thickness during balloon distension of the guinea pig esophagus in vitro (N = 30). The excised esophagus was mounted on two plastic tubes in an organ bath containing oxygenated calcium-free Krebs-Ringer solution with 10(-2) M MgCl2 to abolish smooth muscle contractile activity. One of the plastic tubes was movable in order to stretch the esophagus longitudinally by 15% (elongated state). The impedance planimetry probe was placed with the balloon inside the lumen of the esophagus. A 20-MHz ultrasound transducer was mounted above the esophagus and provided scans in the transverse and longitudinal directions. The luminal cross-sectional area at the highest applied pressure of 2.9 kPa was 13.3 +/- 0.3 mm2 in the resting state. In the elongated state the luminal cross-sectional area at the highest pressure was 12.5 +/- 0.1 mm2 (P < 0.02). The wall thickness decreased from 990 +/- 21 microm at 0 kPa to 640 +/- 9 microm at 2.9 kPa at in vitro length. In the elongated state, the values were 940 +/- 32 microm to 480 +/- 13 microm (P < 0.01). The stress-strain relation was exponential (sigma = alpha(ebetaepsilon - 1), r2 > 0.98, P < 0.01). The circumferential elastic modulus calculated at a Green strain of 0.95 was 44.5 +/- 10.5 kPa in the in vitro state and 81.7 +/- 13.1 kPa in the elongated state. The elastic modulus differed between the resting and elongated states (P < 0.02).

Identification and characterization of cerebral cortical response to esophageal mucosal acid exposure and distention

Background & Aims: Esophageal acid exposure is a common occurrence in healthy individuals and patients with esophagitis. Clinically, perception of this exposure ranges from no perception to severe heartburn and chest pain. Cerebral cortical response to esophageal mucosal contact to acid has not been systematically studied. The aim of this study was to elucidate cerebral cortical response to esophageal acid exposure in normal individuals by functional magnetic resonance imaging (FMRI). Methods: We studied 10 normal healthy volunteers. Cortical FMRI response to 10 minutes of intraesophageal perfusion of 0.1N HCl (1 mL/min) was determined, and the results were compared with those of saline infusion and balloon distention. Results: Acid perfusion did not induce heartburn or chest pain but increased FMRI signal intensity by 6.7% ± 2.0% over the preperfusion values. No increase was detected for saline infusion. FMRI signal intensity to balloon distention was similar to that of acid perfusion. Activation latency, activation to peak, and the deactivation periods for response to acid perfusion were significantly longer than those of balloon distention ( P < 0.05). Conclusions: Contact of esophageal mucosa with acid, before inducing heartburn, evokes a cerebral cortical response detectable by FMRI. Temporal characteristics of this response are significantly different from those induced by esophageal balloon distention. GASTROENTEROLOGY 1998;115:1353-1362

Chest pain of esophageal origin

One third to one half of patients presenting with chest pain have no evidence of coronary artery disease and are characterized as having non-cardiac chest pain. In a large subset of these patients, the esophagus can be the source of the symptoms. This paper summarizes recent progress in our understanding of chest pain of esophageal origin. The value of esophageal diagnostic evaluation in patients with chest pain and normal coronary arteries remains controversial. Symptomatic gastroesophagel reflux is the most common cause of chest pain of esophageal origin. The use of impedance planimetry has provided a better insight in the mechanisms underlying hypersensitivity to esophageal balloon distension. The high prevalence and likely role of panic disorder in patients with chest pain of non -cardica origin has been confirmed. Further investigations towards factors underlying atypical chest pain should include not only a gastrointestinal but also a psychological work-up. Finally, recent reports indicate the contribution of the esophagus to chest pain events in patients with known coronary artery disease.

Is there an irritable bladder in the irritable bowel syndrome?

In this prospective case controlled study 16 premenopausal women with documented irritable bowel syndrome were recruited from the gastroenterology clinic and 16 premenopausal controls without symptoms of irritable bowel syndrome were recruited from the gynaecology clinic. All women answered a standardised bowel and urinary symptom questionnaire and underwent twin channel subtracted cystometry. Women with irritable bowel syndrome also underwent oesophageal balloon distension studies for perception and pain. Oesophageal and bladder sensory thresholds were compared. Urinary frequency and urgency and the urodynamic finding of detrusor instability were significantly more common in women with irritable bowel syndrome (P < 0.05). We were unable to demonstrate a relationship between first sensation of bladder fullness and oesophageal perception or between maximum bladder capacity and oesophageal pain thresholds. These findings suggest that there is an irritable bladder in the irritable bowel syndrome and support the concept that irritable bowel syndrome is part of a generalised disorder of smooth muscle.

Vagal efferent fibre responses to gastric and oesophageal mechanical and chemical stimuli in the ferret

Gastric and oesophageal afferent inputs to vagal efferent fibres were investigated in Urethane anaesthetized ferrets. Mechanical, chemical, and pharmacological stimuli were tested and efferent activity recorded from single cervical vagal fibres. Fibres showed either no basal discharge or low frequency, irregular patterns of resting discharge; only those which showed >50% excitation or inhibition of basal activity with both gastric distension and oesophageal balloon distension were studied further. These responses were rapid and maintained only for the duration of the stimuli. 18/32 efferent fibres tested also showed changes in discharge in response to acid infused slowly into the distal oesophagus. These responses were larger after repeated acid infusions. Subsequent intra-oesophageal capsaicin elicited a similar response in 7/8 fibres. These responses were reproducible with repeated capsaicin infusions in 2/4 fibres and desensitized in 2/4 fibres. 2 capsaicin-responsive fibres were unresponsive to oesophageal acidification. 4/12 fibres tested responded to close intraarterial injections of capsaicin and 9/12 to close intraarterial bradykinin. These responses were brief and of short latency. Vagal efferent responses to mechanical and chemical stimuli above were unchanged after the NK-1 receptor antagonist CP96,345 (4 mg/kg i.v.). Subsequently, bilateral vagotomy caudal to the recording site abolished the basal activity in 4/7 fibres. In the 3 fibres where spontaneous activity remained, none of these responded to oesophageal distension or intra-oesophageal acid (2/2 fibres tested) after vagotomy, whereas 2/2 fibres tested still responded to gastric distension. The response of 1 fibre to intraarterial bradykinin and capsaicin was unchanged by vagotomy. We conclude that vagal efferent neurones respond to gastro-oesophageal mechanical inputs and also receive convergent input from oesophageal acid-sensitive and gastrointestinal bradykinin- and capsaicin-sensitive afferents. These afferent inputs are not mediated via NK-1 receptors. There also exists a nonvagal afferent input onto vagal efferent neurones which is probably spinal and likewise non NK-1 receptor mediated.

Esophageal and lower esophageal sphincter response to balloon distention in patients with achalasia.

Achalasia is characterized by absent or incomplete lower esophageal sphincter (LES) relaxation and aperistalsis in the smooth muscle esophageal body in response to swallowing. The esophageal and LES response to distention has not previously been studied. I aimed to characterize the responses to esophageal balloon distention in achalasia patients in comparison to controls. Sixteen consecutive achalasia patients and 11 healthy volunteers underwent standard esophageal manometry followed by graded midesophageal balloon distention during which LES (as measured by the Dent sleeve) and esophageal body pressures were monitored. Subject perception of distention was also recorded using a standardized scoring system. The LES relaxation response to esophageal balloon distention was markedly impaired in achalasia patients, irrespective of whether the patient had radiological evidence of a dilated or nondilated esophagus. However, phasic contractions proximal to the distending balloon were preserved. The esophageal body responses below the balloon were inconsistent in both groups, and not significantly different from one another. Pain-sensation scores were significantly lower in achalasia patients at the highest distending volumes, but this difference was attributable to the subgroup of patients with a dilated esophagus. Distention-induced LES relaxation is markedly impaired in achalasia patients in keeping with loss of intrinsic inhibitory innervation. Preservation of the proximal excitation suggests that extrinsic vagal reflexes are intact.

Esophageal sensation in spinal cord-injured patients: balloon distension and cerebral evoked potential recording.

We sought to determine the esophageal sensory function in patients with a C6 or C7 spinal cord injury. A balloon was repetitively distended 10 cm above the lower esophageal sphincter in five patients and nine normal control subjects. Sensation was reported on a scale from 0 to 2 with progressive distension to pain threshold (level 2). Cortical responses were recorded from midline scalp electrodes. Blinded determinations of quality and reproducibility of the potentials were performed. All subjects experienced sensation with esophageal balloon distension. Volumes to sensation showed a trend toward a higher sensory threshold in patients but were significant only for first sensation, not pain. In all subjects, a triphasic evoked potential response consisting of a negative-positive-negative complex was noted with distension but not with sham distension. Characteristics (amplitude, latency, reproducibility, and quality) of the evoked potentials were not different in patient and control groups. These data suggest sensory pathways from the distal esophagus are intact in patients with a C6 or C7 spinal cord injury.