The Contribution of Intrabolus Pressure to Symptoms Induced by Gastric Banding

Background & Aims: Mechanisms that ultimately lead to dysphagia are still not totally clear. Patients with laparoscopic gastric banding (LAGB) often complain about dysphagia, regurgitation and heartburn. Our aim was to evaluate the contribution of intrabolus pressure to symptoms of gastric banding.Methods: This study investigated 30 patients with LAGB before and 3 months after conversion to Roux-en-Y gastric bypass (RYGB), evaluating symptoms with a 7-point-Likert-scale and esophageal peristalsis, esophageal bolus transit and intrabolus pressure changes using combined impedance-manometry.Results: Conversion from LAGB to RYGB leads to a significant reduction in dysphagia (1.9 ± 0.4 vs. 0.0 ± 0.0; p< 0.01) and regurgitation (4.2 ± 0.4 vs. 0.1 ± 0.1; p< 0.01) symptom scores. For liquid swallows we found a modest but significant correlation between the intensity of dysphagia and intrabolus pressure (r=0.11; p<0.05) and the intensity of regurgitation and intrabolus pressure for viscous swallows (r=0.12, p<0.05) in patients with LAGB. There was a significant (p< 0.05) reduction in intrabolus pressure at 5 cm above LES before (liquid 10.6 ±1.0; viscous 13.5 ± 1.5) and after (liquid 6.4 ± 0.6; viscous 10.5 ± 0.9) conversion from LAGB to RYGB.Conclusion: Current data suggest that intraesophageal pressure during bolus presence in the distal esophagus contributes to the development but not to the intensity of dysphagia and regurgitation.

Coordinated gastric and sphincter motility evoked by intravenous CCK-8 as monitored by ultrasonomicrometry in rats

Gastric and sphincter motility evoked by intravenous injection of CCK-8 were investigated in urethane-anesthetized rats. Digital ultrasonomicrometry was used to monitor pyloric (PYL), antral (ANT), corpus (COR), and lower esophageal sphincter (LES) movements while simultaneously measuring intragastric pressure (IGP) and, in some experiments, subdiaphragmatic intraesophageal pressure (sIEP). Intracrystal distances (ICD) were measured continuously between pairs of piezoelectric crystals affixed to the serosa of PYL, ANT, COR (circular and longitudinal), and LES. Consecutive intravenous injections of CCK-8 (0.3, 1, and 3 μg/kg) at 30-min intervals caused dose-dependent simultaneous tonic contractions of PYL and ANT, LES opening, and drops in IGP with peak changes at 3 μg/kg of -17.9 ± 2.1, -7.7 ± 2.5, 6.5 ± 1.4, and -29.2 ± 3.8%, respectively, whereas intravenous saline had no effect. Rhythmic contractile activity was inhibited by CCK-8. COR responses were not significantly different from vehicle controls for most metrics, and the direction of response for circular COR varied between preparations, although not for repeated trials in a single preparation. During the LES response to CCK-8, sIEP rose in parallel with drops in IGP, indicating formation of a common cavity. Recovery of LES ICD after intravenous CCK occurred more rapidly than recovery of PYL ICD, suggesting the importance of preventing simultaneous patency of gastroesophageal and gastroduodenal passages. The CCKA receptor antagonist devazepide (500 μg/kg intravenous) inhibited motion responses evoked by intravenous CCK-8. These data revealed CCK-8-induced gastric and sphincter activity consistent with retropulsion of gastric content.

Upper esophageal sphincter function during gastroesophageal reflux events revisited

Upper esophageal sphincter (UES) function during gastroesophageal reflux events is not completely elucidated because previous studies addressing this issue yielded conflicting results. We reexamined the UES pressure response to intraluminal esophageal pressure and pH changes induced by reflux events. We studied 14 healthy, asymptomatic volunteers (age 49 ± 6 yr) and 7 gastroesophageal reflux disease patients (age 48 ± 5 yr). UES pressure, intraesophageal pressure, and pH were monitored at the distal, middle, and proximal esophagus concurrently in the supine position 1 h before and 2 h after a 1,000-calorie meal. A total of 321 reflux events were identified by the development of abrupt reflux-induced intraesophageal pressure increase (IPI); 285 events occurred in patients and 36 in control subjects. In control subjects 33 of 36 and in patients 252 of 285 IPI events were associated with a pH drop. Among patients and control subjects, 99% and 100%, respectively, of all IPI events irrespective of pH drop were associated with abrupt increase in UES pressure (34 ± 2 and 27 ± 6 mmHg, respectively). The average percentage of maximum UES pressure increase over prereflux values ranged between 66% and 96% (control subjects) and 34% and 122% (patients). IPIs induced by both acidic and nonacidic reflux events evoke strong UES contractile responses.

Vagovagal reflex motility patterns of the rat esophagus

Esophageal reflex motility and its neural correlates were investigated in 94 urethan-anesthetized adult male albino rats. When distended by means of a stationary balloon, the cervical and thoracic esophageal portion responded with a single pressure wave (type I response), whereas the diaphragmatic (intercrural) segment exhibited rhythmic contractions (type II response). Balloon deflation resulted in an off response aboral to the balloon. Bilateral cervical vagotomy or systemicd-tubocurarine abolished all types of reflex responses. Both type I and type II responses were associated with multiunit discharges in the central subnucleus of the solitary tract complex (NTSC) and the compact formation of the nucleus ambiguus (AMBC). Type I discharges, consisting of single bursts, and type II discharges, consisting of rhythmic 0.6-Hz bursts, preceded intraesophageal pressure waves in a fixed phase relationship, persisted after contralateral vagotomy, and were eliminated by ipsilateral vagotomy. During neuromuscular paralysis, peak intraburst discharge rates were reduced in both the NTSC and AMBC, with a concomitant decrease in rhythmicity. It is concluded that bolus-evoked peristalsis of the rat esophagus is 1) segmentally organized; 2) effected by a bilateral uncrossed reflex arc consisting of vagal viscerosensory, NTSC premotor, and AMBC motoneurons innervating the striated muscle tunic and 3) strongly facilitated by reafferent feedback.

Initiation of esophageal secondary peristalsis by slow fluid infusion in the opossum: effect of hydrochloric acid

We investigated the mechanisms of slow fluid infusion-induced secondary peristalsis and the effects of hydrochloric acid on this response. In 13 chronically esophagostomized opossum, acidic and neutral barium sulfate were infused into the distal esophagus at a rate of 1.1 ml/min, while recording the esophageal dimension by videofluoroscopy and esophageal intraluminal pressure concurrently. The effects of atropine, tetrodotoxin, capsaicin, and bilateral cervical vagotomy on the response to slow fluid infusion were examined. Acidic barium initiated secondary peristalsis more frequently and at shorter latency with less increase of preperistaltic intraesophageal pressure than neutral barium (P < 0.05). Atropine abolished secondary peristalsis initiated by neutral barium. For acidic barium, atropine decreased the incidence of secondary peristalsis, increased the latency for initiation of secondary peristalsis, and initiated secondary peristalsis more distally (P < 0.05). Tetrodotoxin or vagotomy and capsaicin abolished activation of secondary peristalsis. We concluded that secondary peristalsis can be stimulated in response to slow distension by minute amounts of fluid. This peristalsis is atropine and capsaicin sensitive and vagally mediated. The presence of acid significantly lowers the threshold for stimulation of secondary peristalsis induced by slow fluid distension. This effect seems to be atropine resistant.