The sphincter mechanism at the lower end of the esophagus: an overview.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R K Mittal.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Esophagogastric junction (EGJ) pressure is the major barrier to gastroesophageal reflux. Recent studies suggest that contraction of the crural diaphragm increases esophagogastric junction pressure. Whether this increase in EGJ pressure is important in the prevention of gastroesophageal reflux is not known. Our aim in this study was to determine the effects of crural myotomy on the occurrence of gastroesophageal reflux. METHODS: The spontaneous and stress gastroesophageal reflux before and after a surgical crural myotomy in four cats was studied. Spontaneous gastroesophageal reflux was recorded in the awake cats through a pH probe, placed via an esophagostomy, for periods of 12-24 hours. Stress reflux was studied during periods of airway obstruction and abdominal compression in anesthetized animals using the technique of simultaneous esophageal manometry and pH monitoring. RESULTS: There was a significant increase in the frequency of spontaneous acid reflux after crural myotomy. In anesthetized animals, there was an increase in the EGJ pressure during airway obstruction, which was abolished by a crural myotomy. Abdominal compression caused a reflex contraction at the EGJ that was not affected by crural myotomy. The crural myotomy resulted in a significant increase in the frequency of acid reflux during airway obstruction but not during abdominal compression. CONCLUSIONS: It is concluded that the crural diaphragm is important in the prevention of gastroesophageal reflux and its dysfunction leads to an increased incidence of gastroesophageal reflux.
Explore the source record for details and available documents.
Treatment for esophageal perforation has traditionally been surgery, but development of more effective antibiotics and parenteral nutrition has led to a cautious trend toward nonoperative management. The goal of this investigation was to identify relevant presenting features that would guide a physician in making the therapeutic choice between medical and surgical therapy. Twenty-five consecutive patients with esophageal perforation--20 iatrogenic and five spontaneous--were reviewed. Treatment was medical in 12 cases and surgical in 13. The findings indicate that many patients with esophageal perforation can be treated medically. The following guidelines are suggested for selecting nonoperative treatment: (1) clinically stable patients; (2) instrumental perforations detected before major mediastinal contamination has occurred or perforations with such a long delay in diagnosis that the patient has already demonstrated tolerance for the perforation without the need for surgery; and (3) esophageal disruptions well contained within the mediastinum or a pleural loculus.
A 31-year old female with chronic constipation was referred for treatment of a paradoxical contraction of the external anal sphincter (EAS) muscle during straining to defecate. The patient was dependent on laxative use and the digital removal of feces. The present program emphasized biofeedback training of the EAS utilizing the inexpensive, noninvasive procedure of disposable surface electrodes placed on the anal verge. Outcome of treatment resulted in an 89% decrease in laxatives used, complete termination of the digital removal of feces, and a notable decrease in EAS tension. The patient was able to maintain these gains at an 8 month follow-up.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Transient relaxation of the lower esophageal sphincter (LES) is observed fairly frequently during prolonged continuous monitoring of the LES. The aim of this study was to test whether the presence of a catheter in the pharynx through the stimulation of mechanoreceptors may induce transient LES relaxation. LES and esophageal pressure recordings were obtained for 1 hour in six subjects with a manometric catheter placed via a gastrostomy tube. Swallowing was monitored by submental electromyographic recording. Additional recordings were obtained in these subjects with a catheter placed in the pharynx for 1 additional hour. Transient LES relaxations were recorded in both study periods, i.e., with and without a catheter in the pharynx. The frequency of transient LES relaxations was significantly higher in the presence of manometric catheters in the pharynx (6.4 +/- 2.2 vs. 2.0 +/- 1.1 total LES relaxations). The frequency of transient LES relaxation during the first and second hour after placement of the manometric catheter in a group of seven healthy subjects was not significant different. It is concluded that the pharynx is one of the sites that may mediate the induction of transient LES relaxation.
Explore the source record for details and available documents.
The sphincteric function of the crural diaphragm has been difficult to measure in humans. The authors recently reported the use of a Dent sleeve device to measure esophagogastric junction pressure during contraction of the crural diaphragm. However, the major limitation of the conventional sleeve device is its slow response rate, and sustained diaphragmatic contractions of 6-8 seconds must be induced to measure the true pressure. In this article, the principles of a reverse-perfused sleeve device and the theoretical basis for its fast response rate are reported. The reverse-perfused sleeve is validated in an in vitro model of the lower esophageal sphincter. Furthermore, in vivo studies were performed in seven healthy human subjects. Standardized Muller maneuvers and straight-leg raises were performed to induce diaphragmatic contractions. Pressure increases of 50-150 mm Hg during diaphragmatic contractions were attained in less than 1 second. The delay between the actual contraction of the diaphragm as measured by simultaneously recorded crural diaphragm electromyography and pressure recorded by the sleeve was only 0.25-0.50 seconds. Increasing the rate of infusion of the sleeve from 0.5 to 1.0 mL/min did not further improve the response rate of the reverse perfused sleeve. It was concluded that the reverse-perfused sleeve is a considerable improvement over the conventional sleeve for quantitating the sphincteric function of the crural diaphragm. The role of the crural diaphragm in reflux esophagitis may be easily investigated using a reverse-perfused sleeve device.
Nocturnal gastro-oesophageal reflux may be important in the pathogenesis of reflux oesophagitis. This study aimed to determine whether: (1) gastro-oesophageal reflux occurs during sleep in patients with reflux oesophagitis and, if so, to explore the mechanism, and (2) the sleep pattern of patients with oesophagitis is different from that of control subjects. After a standard evening meal, simultaneous manometric, oesophageal pH, and polysomnographic recordings were obtained in 11 patients with endoscopic oesophagitis and 11 control subjects. Patients with gastrooesophageal reflux disease had significantly more total reflux episodes throughout the nocturnal monitoring period than control subjects (105 v 6). Ninety two of 105 episodes of gastro-oesophageal reflux in patients occurred during the awake state and 10 during sleep stage II. A number of reflux episodes occurred during brief periods of arousal from the various sleep stages. Of the 105 reflux events recorded in patients, 42 were induced by transient lower oesophageal sphincter relaxation, 20 by stress reflux, 22 by free reflux mechanisms, and in 21 the mechanism was unclear. The sleep pattern and the time spent in each sleep stage was not different between the two groups. It is concluded that the awake state is crucial for the occurrence of nocturnal reflux episodes in normal subjects as well as in patients with reflux oesophagitis and that the difference between the frequency of gastro-oesophageal reflux between normal subjects and patients cannot be explained by different sleep patterns.
We studied eight patients with gastro-oesophageal reflux disease to compare the frequency and mechanism of reflux in the upright and supine positions. Simultaneous oesophageal manometry and pH studies were performed on two separate days in each subject in the fasting and postprandial periods. The frequency of reflux tended to be higher in the upright position. The most prevalent mechanism of reflux in either position was transient relaxation of the lower oesophageal sphincter. The frequency of transient lower oesophageal sphincter relaxation was higher in the upright than in the supine position. There was no difference in the total reflux time, acid clearance time, and number of reflux episodes lasting longer than five minutes in the two positions. We suggest that daytime reflux (upright) may be as important as night time (supine) reflux in the pathogenesis of reflux oesophagitis and needs to be considered when treating patients with reflux disease.
Our aim in this study was to determine the effect of variations in intrabolus pressure on esophageal peristalsis. In five cats, intrabolus pressure was altered by increasing intragastric pressure to 20-45 mmHg by use of a pressure cuff to compress the abdomen. In each cat, increases in intragastric pressure were associated with comparable increases in pressure of the esophageal bolus while the bolus was in the distal esophagus during esophageal peristalsis. Secondary peristalsis induced by a 5-ml injection of barium into the proximal esophagus was recorded by synchronized videofluoroscopy and esophageal manometry. Graded increases in intrabolus pressure caused an increased prevalence of ineffective, incomplete peristaltic sequences that did not completely clear barium from the esophagus. At intragastric pressures greater than 45 mmHg, 63% of the peristaltic sequences were incomplete. Increases in intrabolus pressure elicited by increased intragastric pressure also caused 1) slowing of the peristaltic wave in the distal esophagus, 2) increased pressure wave duration in the distal esophagus, 3) increased esophageal diameter, and 4) increased duration of lower esophageal sphincter opening. The incidence of retrograde bolus escape was inversely related to the difference between peristaltic wave amplitude and intrabolus pressure. A pressure difference of greater than 20 mmHg prevented retrograde barium escape at all esophageal levels, whereas a difference of less than 20 mmHg was generally associated with retrograde escape of barium in the distal esophagus. We conclude that an increase in intrabolus pressure causes an increase in esophageal distension that is transduced into alterations of esophageal peristalsis by either a myogenic or neural mechanism.
The aim of this study was to characterize lower esophageal sphincter (LES) longitudinal muscle contraction during changes in LES pressure in opossums. LES pressure was used as a marker of LES circular muscle contraction. Longitudinal muscle contraction was measured by strain gauge transducers. For precise placement of the strain gauge on the LES, the high-pressure zone was identified using a manometric-laser illumination technique. Measurements were made during 1) spontaneous LES pressure fluctuations, 2) LES pressure changes induced by pharmacological agents, and 3) LES relaxation induced by vagal nerve stimulation. These studies show that 1) spontaneous LES pressure fluctuations correlated with spontaneous changes in LES longitudinal muscle contraction; 2) pharmacologically induced contraction and relaxation of LES pressure correlated with contraction and relaxation of LES longitudinal muscle, respectively; 3) a close temporal relationship existed between changes in LES longitudinal muscle contraction and LES pressure that occurred spontaneously or were induced pharmacologically; and 4) vagal stimulation caused LES longitudinal muscle contraction and LES pressure relaxation. We propose that LES longitudinal muscle may play a role in the modulation of intraluminal LES pressure.
Explore the source record for details and available documents.