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We wished to test the hypothesis that colonic loading with fecal material leads to delayed gastric emptying. Twelve healthy male volunteers were studied. Each of these subjects went through two randomized study periods of four days. In one of these, the subjects defecated upon urge, in the other period defecation was voluntarily suppressed. Gastric emptying of a semisolid meal (mashed potatoes) was measured with the noninvasive applied potential tomography technique. On day 3 no significant changes in gastric emptying were found, but on day 4 the emptying rate had decreased from 85.8 +/- 11.0%/hr (mean +/- SEM) to 70.3 +/- 10.9%/hr (P < 0.05) and the T50 had increased from 38.5 +/- 3.4 min to 46.2 +/- 4.0 min (P < 0.025). The duration of the lag phase (4.1 +/- 1.5 min) was not significantly altered by suppression of defecation. Our conclusion is that voluntary suppression of defecation delays gastric emptying in normal subjects. This "cologastric brake" may be involved in the pathogenesis of upper abdominal symptoms in constipated patients.

BACKGROUND: It is uncertain whether gastric emptying of fat is determined mainly by its physical characteristics or chemical composition. In particular, the intragastric distribution of extracellular fat and the importance of that distribution to gastric emptying of fat is controversial. The effects of posture on gastric emptying, intragastric distribution, and appetite after ingestion of a meal containing oil and aqueous phases was evaluated. METHODS: Eleven volunteers consumed 60 mL 99mTc-(V)-thiocyanate-labeled olive oil and 290 mL 113mIn-labeled soup while sitting and while lying in the left lateral decubitus position. Hunger before and after the meal was recorded. RESULTS: In the sitting position, oil emptied from the stomach more slowly (P < 0.01) whereas in the decubitus position oil emptied faster (P < 0.01) than the aqueous phase. Oil was preferentially retained in the proximal stomach when sitting (P < 0.01), and more oil was retained in the distal stomach in the decubitus position (P < 0.05). The amount of oil that emptied in the first 180 minutes was not different between the two postures. The aqueous phase emptied much more slowly (P < 0.01) in the decubitus position. At 120 minutes and 180 minutes, subjects were less hungry (P < 0.05) in the decubitus position. In the decubitus position, hunger at 120 minutes and 180 minutes was related to the retention of oil (r > or = 0.79; P < 0.01) in the stomach. CONCLUSIONS: These results indicate that (1) gravity has a major effect on the intragastric distribution and relatively little effect on total stomach emptying of oil, and (2) postprandial hunger is affected by posture and, in the decubitus position, is inversely related to the amount of oil that has entered the small intestine

Excessive supragastric belching, sometimes called aerophagia, is a rare behavioural disorder in which patients belch frequently, up to twenty times a minute. This is perceived by the patients as disturbing and interferes with social functioning and is likely to affect quality of life. Psychiatric disorders such as anxiety and depression are suggested to play a role. Methods: 21 patients (11 males, age 49 (28-78)) whose presenting symptom was excessive belching underwent impedance monitoring to confirm the diagnosis of supragastric belching. They were asked to fill in questionnaires regarding the presence and severity of their symptoms, quality of life (SF-36), reflux and dyspepsia related quality of life (QoLRaD) and the hospital anxiety and depression scale (HADS). Results: Impedance monitoring showed supragastric belching in all patients, concurrent with audible belches. On a scale 0-4 patients scored the frequency of the following symptoms: epigastric discomfort (4 iqr 3-4), heartburn (1 iqr 0-1), retrosternal pain (0 iqr 0-2), early satiety (0 iqr 0-2), bloating (0 iqr 0-3), nausea (0 iqr 0-2), belching (4 iqr 4-4) and vomiting (0 iqr 0-0). On a scale 0-5 patients scored the severity of the following symptoms: epigastric discomfort (3 iqr 2-4), heartburn (0 iqr 0-1), retrosternal pain (0 iqr 0-3), early satiety (0 iqr 0-3), bloating (0 iqr 0-3), nausea (0 iqr 0-2), belching (4 iqr 3-4) and vomiting (0 iqr 0-0). Compared to normative values, patients showed a decreased quality of life for the domains social functioning (64.3 ± 17.8), mental health (67.4 ± 16.5), vitality (47.6 ± 20.3), bodily pain (58.9 ± 21.7) and general health (44.8 ± 19.8) but not for physical functioning (75.5 ± 21.5) and physical (63.1 ± 40.0) and emotional role (81.0 ± 35.9). The QoLRaD scores were not decreased for any factor (emotional distress (4.7 iqr 4.2-6.2), sleep disturbance (5.0 iqr 3.8-6.3), food and drink problems (4.8 iqr 3.2-6.4), physical and social function (5.0 iqr 4.3-5.9), vitality (5.0 iqr 3.8-6.0)). The median HADS for anxiety (3 iqr 2-4) and/or depression (2 iqr 1-4) were not elevated and only 1 patient showed a score higher than 8 for anxiety (9) and another one for depression (10). Conclusions: In patients with excessive supragastric belching, quality of life is significantly decreased, in particular due to impairment of social function and vitality. Patients with excessive belching present a distinct symptom pattern which does not resemble reflux disease or functional dyspepsia, furthermore reflux symptoms and dyspepsia do not play a role in the observed reduction of quality of life. Depression and anxiety disorders are absent.

The effects of nifedipine (20 mg orally) on esophageal body resting tone and perception of esophageal distension were compared with those of placebo in 10 healthy volunteers, using a double-blind crossover design. A 3-cm silicon balloon positioned 10 cm above the lower esophageal sphincter was inflated with 2-20 ml of air, in 2-ml increments. The subjects scored their chest sensations, while pressure in the balloon was continuously recorded. In each experiment three series of measurements were made, at baseline and 15 and 30 min after administration of nifedipine or placebo. Bench tests were run to determine pressure-to-volume relationships for each of the balloons used in the study. Thirty minutes after nifedipine ingestion, a significant decrease in systolic blood pressure (from 112.6 +/- 2.3 to 99.0 +/- 2.0 mm Hg) was observed. Amplitude and duration of esophageal peristaltic contractions were significantly decreased by nifedipine (from 128.1 +/- 16.7 to 98.7 +/- 10.6 mm Hg and from 3.9 +/- 0.3 to 3.3 +/- 0.2 sec, respectively). With balloon volumes of 8 ml and higher, balloon pressures were higher with the balloon in the esophagus than on the bench, the difference being determined by the compliance of the esophagus. This difference rose from 18.5 +/- 6.8 to 40.2 +/- 7.2 mm Hg (8-20 ml) with placebo and from 23.1 +/- 3.7 to 35.9 +/- 5.8 mm Hg with nifedipine. No significant differences between nifedipine and placebo were found. The esophageal sensation scores increased linearly with increasing balloon volume from 6 ml onwards. Nifedipine had no significant effect on the perception of esophageal balloon distension.

Cerebral evoked potential recording was used to study the oesophagus-brain axis in 10 controls and 10 patients with non-cardiac chest pain with a manometric diagnosis of either nutcracker oesophagus or diffuse spasm and a positive edrophonium test. A series of 50 inflations (10/minute; inflation rate of 170 ml/second) of an intraoesophageal balloon (5 cm proximal to the lower oesophageal sphincter) was performed in each subject. Three different inflation volumes were used and were individually determined to cause no sensation, slight sensation, and definite sensation, respectively (volume ranges: 2-8 ml, 5-18 ml, and 8-22 ml). All signals were coded and their quality was scored on a scale from 0 (no recognisable pattern) to 5 (well defined potential of good quality) by four 'blinded' observers. The evoked potential quality scores and amplitude of the major peaks increased significantly (p less than 0.01) with increasing sensation, both in patients and in controls. In the patients, quality score and amplitude of all four peaks of the evoked potentials were lower (p less than 0.05) and latencies of two of the four peaks were longer (p less than 0.02) than in the controls. The volumes of air required to produce the various sensations were lower in the patients (p less than 0.01). When divided by the balloon volume, amplitude and quality of the evoked potential were no longer significantly different between the groups. These results suggest that the increased perception of oesophageal distension in patients with non-cardiac chest pain is caused by altered central processing rather than (functionally) abnormal receptors in the oesophageal wall.

The advent of pharmacological agents that inhibit TLESRs has increased the need for accurate objective identification and scoring of these events. The only current objective criteria were published over 10 years ago (Am.J.Physiol,1995;268:G128-13) and have not been subject to rigorous evaluation. Aims: To assess the performance of the TLESR criteria with regard to intraand inter-assessor variability and to improve them where necessary. Methods: Two 3-hour post-prandial esophageal manometric and pH recordings were performed at least 1 week apart in 20 healthy volunteers. Each recording was duplicated and all recordings were given a unique identifier, creating two datasets of 40 recordings. The recordings were analysed by 5 experienced observers for the occurrence of TLESRs based on their expert opinion. Scored TLESRs were also analysed for the presence of the original 4 criteria as well as inhibition of the crural diaphragm (ID), a prominent after-contraction (AC), acid reflux and an esophageal common cavity. Results: For TLESRs based on the observer's expert opinion, the overall inter-observer agreement was 59% (range 56-67%) and the intra-observer agreement 75% (60-89%). When TLESRs were restricted to those fulfilling the original criteria, inter-observer agreement fell to 46% (40-53%) and the intra-observer agreement to 60% (44-67%). Cleaning the recordings by removal of technically flawed sections (up to 20% of any one recording) improved inter and intra-observer agreement by 5%. Inclusion of additional criteria (ID and AC) for the identification of TLESRs in the second dataset resulted in interand intra-observer agreements of 62% (52-70%) and 69% (53-79%) respectively, close to those based on the observers expert opinion (64% (56-71%), 71% (61-80%). A consensus analysis performed collectively by 3 observers and based on the new criteria (original ± ID and AC) resulted in agreement between the paired recordings of 84%. The remaining disagreement was largely the result of technical difficulties with the recordings.Conclusions: The original criteria for the definition of TLESRs allows for substantial interand intra-observer variability. Incorporation of additional objective criteria reduces the variability. However, the highest level of intra-observer agreement can be achieved by consensus analysis.

Background and Aims: Studies describe adverse pulmonary effects in those who responded to the World Trade Center (WTC) disaster in New York City,with mention of aerodigestive symptoms (sx) described as GERD. Little is known about the mechanism of gastrointestinal sx in the WTC-exposed populations. The WTC Environmental Health Center (WTCEHC) was established to respond to health issues related to the attack on 9/11/01 and serves those exposed to WTC dust or fumes, including local residents, workers, and clean-up workers. We now report biopsy findings of post 9/11 refractory GERD-like sx. Methods: Participants were self-referred for medical sx and WTC exposure within the year after 9/11/2001. A standardized questionnaire was administered, including questions assessing the presence of heartburn and/or “acid indigestion.” Patients with sx were treated with proton pump inhibitors (PPIs); those with refractory sx were referred to a single gastroenterologist. Endoscopic results from patients evaluated between 1/11/07 and 10/23/08 are analyzed. Results: 160 patients were referred for endoscopy for refractory GERD-like symptoms. 33 patients whose sx resolved before their appointment were not endoscoped. 18 patients did not attend their appointment. 109 patients underwent endoscopy (mean age of 49.8, 48.6% male). 41.3% were white, 11.0% black, 8.3% Asian, 0.9% Native American, and 40% were undeclared. 64.2% of patients were Hispanic. Many patients (58.7%) had an income

The circular muscle fibers at the end of the esophagus are traditionally considered the lower esophageal sphincter. However, the first barrier to gastric reflux is actually the clasp/sling fiber complex of the stomach. Relaxation mediates transient lower esophageal sphincter relaxation underlying the pathophysiology of gastroesophageal reflux disease (GERD). This study determined the pharmacologic specificity of the nicotinic receptor mediated relaxation of pre-contracted strips of human and porcine clasp muscle fibers. Human specimens were obtained from organ transplant donors. Clasp fiber muscle strips were exposed to increasing carbachol concentrations (human) or acetylcholine with physostigmine to block cholinesterase (pig). At concentrations higher than 30 uM, abrupt relaxations were produced. After 60 minutes of repeated washing, strips were exposed to various ganglionic and neuromuscular nicotinic receptor antagonists for 30 minutes then rechallenged with cholinergic agonists. Results, as a percentage of relaxation in time control strips are shown in the figure below. The neuromuscular blockers d-tubocurarine, decamethonium (human) and pancuronium (pig) inhibited relaxation whereas the ganglionic blocker hexamethonium (human) and the alpha7 selective antagonist methyllycaconitine did not. Other ganglionic blockers such as MG624, NDNI and TMPH blocked these relaxations whereas mecamylamine was only partially effective in human tissue. These results indicate that the pharmacology of the nicotinic receptor mediating relaxation of the gastric clasp fibers may be unique and a potential target for development of selective agents for treatment of GERD.

Trefoil peptides are involved in mechanisms of defense and repair in the gastrointestinal tract. We have recently demonstrated a HIF-1 dependent induction of TFF genes by hypoxia in gastric epithelial cells but less is known about TFF genes regulation In Vivo. Nitric oxide has been shown to modulate HIF-1 activity in cellular models. AIM: To analyze the role of iNOS-derived NO on HIF-1α stabilization and the TFF2 mRNA expression in the damaged mucosa of aspirin-treated rats. MATERIALM b) significantly reduced the increase in TFF2 mRNA expression observed 3 and 6 h after aspirin administration, and delayed the fall of TFF2 mRNA expression at 24h; c) diminished HIF-1α immunostaining. CONCLUSIONS: iNOS-derived NO induces HIF-1α stabilization and TFF2 mRNA expression in the damaged mucosa of aspirin-treated rats. These results suggest that iNOS-derived NO may contribute to the recovery of the gastric mucosa by modulating the epithelial gene expression.

Nissen fundoplication is a commonly used antireflux operation. After this operation symptoms such as dysphagia, inability to belch and vomit, and gas bloating are frequently reported in the literature. In 32 patients who underwent Nissen fundoplication 3.5-18 years ago, postprocedure dysphagia was studied using conventional manometry and 24 h ambulatory pressure and pH recording. Our study indicates that dysphagia tends to decrease after surgery. Neither conventional nor ambulatory pressure recording revealed motor abnormalities that could be held responsible for the dysphagia. Therefore, the data do not support the concept that dysphagia is a major complication of Nissen fundoplication.

To the Editor: In a recent issue of Digestive Disease and Sciences, King et al. reported the results of a comparison of the esophageal acid perfusion test (APT) and ambulatory pH monitoring with symptom association analysis in patients with suspected gastroesophageal reflux disease [1]. Patients with a positive APT were found to have a significantly higher symptom index (SI), symptom sensitivity index (SSI), and symptom association probability (SAP) compared to patients with a negative APT. In previous studies comparing the outcome of APT and 24-hr pH monitoring, the association between these tests was found to be weak [2–5]. It was felt that the “endogenous Bernstein test” constituted by pH monitoring was at least as good as and more physiological than the APT, and the APT disappeared from the armamentarium of most gastroenterology services in the early nineties. In their paper, King et al. state that the APT is useful for the evaluation of esophageal acid sensitivity, in particular, in patients in whom a symptom-reflux association cannot be demonstrated by 24-hr pH-metry. In the words of the authors, “It is possible that the APT may detect acid sensitivity in some patients with false-negative 24-hr pH studies.” We agree that this is possible, but it is also possible that the APT yields false-positive results in some patients with truly negative 24-hr pH studies. Since the study by King et al. did not include healthy subjects, we do not know how many of these would have had a positive APT. Forty-eight of the 162 patients with a negative SI (29.6%) had a positive APT, and of the subgroup of 86 patients who

Our aim was to explore the use of intraluminal impedance recording for assessment of interdigestive transpyloric fluid movements. Twenty healthy volunteers were studied with a catheter allowing the recording of five antropyloroduodenal impedance signals simultaneously with six pressure signals. Patterns induced by air were verified by standard ultrasound. Transpyloric Doppler ultrasound was used to validate impedance patterns associated with transpyloric fluid transports. Impedance changes caused by air (short-lived increases) occupied 14 ± 12% of the time in the antrum and 0.8 ± 0.5% in the duodenum ( P < 0.005). All fluid transport events lasting >4 s were recorded by both Doppler and impedance techniques. Transpyloric fluid transport was observed in all three phases of the antral migrating motor complex. The total number of transport events was significantly higher ( P < 0.05) in phase II (18 ± 7) than in phases I (2.6 ± 2) and III(6.1 ± 3). Retrograde transport was observed mainly in antral phase I (54% of fluid movements, compared with 2.5% in phase II and 18.5% in phase III, P < 0.05). During phase II, 80 ± 13% of the impedance changes were associated with manometric events and 72 ± 9% of the antral contractions were associated with transpyloric fluid transport. Prolonged assessment of interdigestive transpyloric fluid transport events using intraluminal measurement of impedance is possible. Manometrically detectable contractions are the most frequent, but not the only, driving forces of these events.

"Ihe mechanism of excessive belching in aerophagia is hitherto poorly understood. In an attempt to clarif}~ the pathophysiology ot excessive belching, w'e used intraesophageal electro cal impedance mor~itoring (a relatively new technology making it possible to monitor the passage of air through the esophagus, either in aboral or oral direction) in 2 male patients wnh aerophagia (age 43 and 61) and in 11 heahhy voh.mteers (4 m, 7 f, age 18-43). A 6channd amhnlatory m~pedance system was used, each recording segment being 2 cm long. The recording segments were located at 0-2, 2-4, 4-6, 10-12, 14q6, 17-19 cm above the upper horde* of the I.ES Each recording cl'~nnel was sampled at 1000 Hz. In all, a protocol was carried out consistitg of a tasting recording period of 45 minutes, followed by a standardized meal (967 kCal) and a 90 minutes postprandial period. Three distinct patterns of passage of air could be discerned. Pattern A, consisting of a sudden increase in impedance followed by a decrease moving in aboral direction reflected the passage of a certain amount ot air swallowed together with a boh.ls, in pattern B, more sporadically waves oi sudden high increments of impedance travelled t~om the distal to the proximal esophagus representing venting of gas from the stomach (normal belching) 9 Patterns A and B were encountered as oiten in controls as in the patients, in pattern C, only encountered in patients (53x and 38x, resp.) and coinciding with observed belching, sudden, high increments of esophageal in~pedance were recorded on all mipedance channels, beginning at the most proximal recording segment and very rapidly mos'ing distally along the esophagus, implicating the passage of air in aboral direction The aboral movement of air was immediately followed by clearance of the air boh]s in opposite direction This pattern of rapid influx and e~flux of air in the esophagus can be referred to as esophageal belching and was the mechanism of excessive belching in the patients with aerophagia Conclusion: belchmg in aerophagia is the result ot a mechanism distinctly different from regular belching.

Recent studies indicate that nocturnal recovery of gastric acid secretion, termed "nocturnal acid breakthrough" (NAB), occurs despite treatment with twice daily proton pump inhibitors (PPI). This observation raises concerns about the therapeutic efficacy of PPI. Aims: I) Determine the prevalence of NAB at our center. 2) Compare the clinical and endoscopic findings of patients (pts) with and without NAB. 3) Evaluate whether pts with NAB have concomitant esophageal acid breakthrough (EAB). Methods: We reviewed the records of consecutive pts with GER on twice daily PPI referred for 24-hr pH testing. Data obtained included demographics, indications for the study, and endoscopy (EGD) findings. The pH tracings were analyzed for NAB (gastric pH ~4 lasting ;::,1 hour after nocturnal dose of PPI was taken) and concomitant EAB (esophageal pH ~4.0 lasting ;::,10 min.). In addition, the esophageal pH tracing was examined for the number of episodes and % time pH ~4 during the period of NAB. GER was diagnosed if 24-hr pH showed abnormal acid contact time (% time pH~4: upright ;::'8.1, supine ;::'3.4, and total ;::'5.5). Results: 23 pts (7M, 16F), mean age 62 (20-82), were referred for pH testing while taking PPI twice daily. All subjects took their PPI before meals except for one patient who consumed PPI at bedtime and was removed from the study. The remaining 22 pts are the subjects of this report. Indications for the study: persistent GER symptoms n=16 (73%), atypical GER n=6 (27%): chest pain n=3, cough n=3. See table for results. NAB was noted in all NAB( +) patients during the first 6 hrs after evening dose of PPI. Duration of NAB: mean 273 min (72-530). Conclusions: I) 64% of pts with GER-related symptoms taking twice daily PPI have NAB. 2) This phenomenon occurs in pts with typical and atypical GER symptoms. 3) The majority (96%) of pts on twice daily PPI have minimal or no esophagitis on EGD. 4) Concomitant EAB rarely occurs at the time of NAB. 5) Abnormal esophageal acid contact time was more common in pts with NAB than those without it. 6) The role of NAB in GER warrants further investigation.