Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effect of esophageal acid perfusion on salivation in patients with reflux esophagitis and in normal subjects. Serial 10-min saliva collections were obtained by expectoration during perfusion of the esophagus with water, and then 0.1 N HCl (pH 1.2) for 50 min or 0.01 N HCl (pH 2.1) for 120 min. Within 1-5 min of beginning 0.1 N HCl perfusion, all 8 patients with esophagitis developed heartburn accompanied by an increase in saliva flow. By the time the severity of heartburn required discontinuation of HCl perfusion (10-40 min), saliva flow had increased nearly fourfold. With 0.1 N HCl perfusion, 8 of 10 volunteers developed mild heartburn after 22 +/- 3 min (mean +/- SE), whereas 0.01 N HCl induced heartburn in 6 of 10 volunteers after 57 +/- 12 min of perfusion. Saliva flow increased concurrently with the onset of heartburn and doubled in those volunteers who developed heartburn. Saliva flow did not change in those volunteers who were without heartburn. We conclude that esophageal acid perfusion unaccompanied by heartburn does not affect salivation. However, saliva flow increases concurrently with the onset of heartburn, a phenomenon called "water brash" when clinically evident. The increased saliva flow that accompanies heartburn may act as an endogenous antacid that serves as a protective response to symptomatic gastroesophageal reflux.
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PMID:Salivary response to esophageal acid in normal subjects and patients with reflux esophagitis. 367 54

To determine if hiatus hernia (HH) contributes to the delayed clearance of acid from the esophagus in patients with gastroesophageal reflux (GER), we performed simultaneous esophageal pH recordings and radionuclide studies in three study populations: 12 GER patients with HH, 5 GER patients with no HH, and 8 subjects with HH but no GER symptoms. Acid clearance was measured at 5 cm. above the manometrically located lower esophageal sphincter (LES) after injecting a 15-ml. bolus of 0.1 N HCl at 15 cm. above the LES. The acid was labeled with 200 mu Ci of 99mTc-sulfur colloid. Acid clearance was also measured at 10 cm. above the LES after injection of a 15-ml. bolus of 0.1 N HCl at 20 cm. above the LES. Acid clearance at 5 cm. above the LES was faster in GER patients with no HH compared to GER patients with HH and asymptomatic HH subjects. Acid clearance was faster at 10 cm. than 5 cm. above the LES in all HH and non-HH subjects studied. In non-HH subjects, each swallow resulted in an increase in pH (a monophasic pH response) at 5 and 10 cm. above the LES. In symptomatic as well as asymptomatic HH subjects, swallows resulted in an initial fall followed by a rise in pH at 5 cm. above the LES (a biphasic pH response). Radionuclide studies showed reflux of the isotope-labeled acid into the esophagus followed by clearance (a biphasic response) accompanying swallows in 15 of the 20 HH subjects. Swallow-induced reflux was not detected by radionuclide scanning in non-HH subjects. Based on these observations, we conclude that during acid clearance a small amount of acid is trapped in the HH sac and refluxes into the esophagus during subsequent swallows when there is relaxation of the LES, and these repeated episodes of acid reflux from the HH account for the delayed acid clearance observed in GER patients with HH.
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PMID:Identification and mechanism of delayed esophageal acid clearance in subjects with hiatus hernia. 378 Nov 81

There is much evidence to suggest that peristaltic function is defective in esophagitis patients and that this defect may contribute to prolonged acid exposure, promoting esophageal mucosal injury. Abnormal peristalsis may also be related to the generation of reflux symptoms. We evaluated primary peristalsis and its relationship to symptoms under basal conditions and during saline and HCl perfusion in 15 symptomatic reflux patients with gross esophagitis and 15 healthy controls. In the basal state, LES pressure (15.3 vs 25.1 mm Hg) and peristaltic amplitude (74.2 vs 104.8 mm Hg) were significantly lower in subjects with gastroesophageal reflux disease (GERD) (P less than 0.05). During HCl perfusion, peristaltic amplitude and duration increased slightly, and peristaltic velocity slightly decreased similarly in both groups. There was no difference in the incidence of nonpropagated, segmental, or swallow-initiated simultaneous contractions, or change in resting intraesophageal pressure during HCl perfusion in control and GERD groups. This study identified abnormal contractile amplitude as a specific defect in the primary peristaltic wave of esophagitis patients but does not support a role for acid-induced motility changes in the generation of symptoms in GERD.
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PMID:Esophageal motor function and response to acid perfusion in patients with symptomatic reflux esophagitis. 399 56

To determine a possible mechanism for the association between gastroesophageal reflux and obstructive pulmonary disease, we quantitatively compared the short latent airway response after acid infusion into the trachea or esophagus in 13 anesthetized adult cats. Total lung resistance was calculated from synchronous measurements of air flow and intrapleural pressure differences from those at end expiratory level. Tracheal infusion of as little as 0.05 ml of 0.2 N HCl evoked an average 4.65-fold increase in total lung resistance from baseline in all animals tested (p less than 0.005). Intratracheal saline had no effect. The response to intratracheal acid infusion was rapidly adapting, pH dependent, and vagally mediated. Infusion of a much larger volume of 10 ml of 0.2 N HCl into the esophagus produced an average 1.47-fold increase in total lung resistance from baseline (p less than 0.05). No change was seen with intraesophageal saline. In contrast to intratracheal acid infusion, a clearly significant increase in resistance was seen in only 8 of 13 animals tested after intraesophageal acidification. When it occurred, the response was sustained for at least 60 s after acid infusion. The magnitude of the response was not augmented by the presence of severe esophagitis. These studies strengthen the concept that reflex pathways in the trachea and esophagus may explain a causal relationship between gastroesophageal reflux and obstructive pulmonary diseases. The results support the view that microaspiration into the trachea is a much more likely mechanism for bronchospasm associated with gastroesophageal reflux than simple acid reflux into the esophagus.
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PMID:Comparison of airway responses following tracheal or esophageal acidification in the cat. 646 75

Nocturnal asthma has been associated with nighttime gastroesophageal reflux (GER). To establish whether the presence of acid in the lower esophagus causes bronchoconstriction, nine children with nocturnal asthma and GER underwent intraesophageal acid-infusion challenges during sleep. The patients were divided into two groups on the basis of presence or absence of a positive Bernstein test for esophagitis. The test was considered positive if acid infusion produced symptoms of heartburn. On two occasions, at approximately midnight and 4 to 5 A.M., 30 ml of normal saline was infused over 15 min into the distal esophagus followed by a similar infusion of 0.1N HCl. Respiration was continuously monitored by inductance plethysmography along with clinical evaluation. The saline and midnight acid infusions had no effect in either patient group; however, with the 4 to 5 A.M. acid infusion, all the patients with a positive Bernstein test developed significant changes in their respiratory pattern indicative of bronchoconstriction as well as overt clinical wheezing. In the patients with a negative Bernstein test, the 4 to 5 A.M. acid infusion had no effect. It is concluded that during sleep the presence of acid in the lower esophagus can trigger bronchoconstriction in asthmatic children with a positive Bernstein test and that these children appear to be more susceptible to the bronchoconstrictive effects of intraesophageal acid at 4 to 5 A.M. than at midnight.
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PMID:Respiratory response to intraesophageal acid infusion in asthmatic children during sleep. 661 53

The pathogenesis of oesophagitis associated with ethanol ingestion was studied experimentally by perfusing isolated rabbit oesophagus in situ with 20% and 40% (v/v) ethanol. Since ingestion of ethanol increases duodenogastric and gastro-oesophageal reflux, the effects of HCl and bile salts (in combination with ethanol) were also investigated. The severity of oesophageal mucosal damage was assessed by using transmucosal potential difference, net ion fluxes of H+ and Na+, and mucosal permeability to two neutral molecules of different sizes, 3H-H2O and 14C-erythritol, as indicators of mucosal integrity. Macroscopic changes in the mucosa were also recorded. The results showed that the lower ethanol concentration (20%) is relatively harmless to the oesophageal mucosa. Furthermore, addition of 20% ethanol did not intensify the effects on the mucosa caused by HCl or bile salts alone. In contrast, the stronger ethanol solution (40%) did cause significant mucosal damage when used alone, and this damage was further potentiated by the presence of HCl.
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PMID:Ethanol-induced mucosal injury in rabbit oesophagus. 666 35

The lower esophageal sphincter (LES) is observed as a zone with higher esophageal pressure by manometric studies and considered to save a barrier against gastric pressure. Mechanisms to prevent GER have still not been fully understood. Manometric studies and pH studies were performed in dogs and in infants. The following results were obtained: Experimental studies Increasing gastric pressure with 0.1 N HCl, LES relaxation was elicited by increased esophageal pressure after GER was detected by pH measurement. LES pressure increased with increased abdominal pressure and decreased with elevated intraesophageal pressure after intraluminal injection of normal saline. Inflation of the esophagus with air caused GER when gastric pressure elevated with 0.1 N HCl. Clinical studies Manometric studies were performed in 63 infants with or without GER. Infants with GER had higher esophageal pressure, lower LES pressure and shorter LES than infants without GER (p less than 0.001). In conclusion, these studies may indicate that relaxation of LES caused by increased intraesophageal pressure induces GER in infants.
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PMID:[Experimental and clinical studies of gastroesophageal reflux (GER) in infants]. 667 64

The purpose of this study was to determine the relationship of lower esophageal sphincter (LES) pressure and the volume of acid placed into the stomach required to induce gastroesophageal reflux in man. LES pressure was recorded continuously and by station pull-through by three radially oriented catheters in both symptomatic and asymptomatic subjects during the graded infusions of 0.1 N HCl acid into the stomach. Symptomatic subjects had a mean LES pressure of 7.5 +/- 0.7 mm Hg and refluxed at a volume of 140.0 +/- 21.0 ml. Fifty-five percent of asymptomatic subjects refluxed at a mean volume of 380.0 +/- 24.7 ml, and had a mean LES pressure of 13.8 +/- 0.4 mm Hg. Asymptomatic nonrefluxers at a volume of 500 ml of 0.1 N HCl acid had a mean LES pressure of 18.9 +/- 1.1 mm Hg. The mean LES pressure and acid volumes showed statistical significance between the three groups (P less than 0.01). There was an excellent overall correlation between LES pressure and acid volume required to produce reflux in all subjects (r = 0.91, P less than 0.001). Following reflux, asymptomatic but not symptomatic subjects showed a significance increase in LES pressure. These studies suggest that: (1) LES pressure does provide an accurate index of the gastroesophageal antireflux mechanism, provided that acid volume is considered; and (2) asymptomatic subjects showing acid reflux have higher LES pressures, reflux at higher volumes, and develop an LES contractile response after the reflux episode.
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PMID:Lower esophageal sphincter pressure as an index of gastroesophageal acid reflux. 729 81

Aggressive factors operating within the esophageal lumen during gastroesophageal reflux are balanced by adequately mobilized protective mechanisms. Esophageal mucosal protection operates at three different although complementary dimensions: (1) preepithelial, (2) epithelial and (3) postepithelial. Since aggressive factors predominantly operate within the esophageal lumen, preepithelial defense is pivotal in mucosal protection. The preepithelial barrier is significantly enhanced by the quantity and the quality of salivary organic components such as salivary mucin, nonmucin protein, salivary epidermal growth factor (EGF) and salivary prostaglandin E2. The rate of secretion of salivary mucin, nonmucin protein and EGF under the impact of intraesophageal mechanical (bolus) and chemical (HCl/pepsin) stimulation, mimicking the natural gastroesophageal reflux scenario, is significantly impaired in patients with RE, whereas the rate of salivary PGE2 output remains essentially unchanged. Salivary secretory response to esophageal mechanical and chemical stimuli in terms of organic components, mediated by the esophagosalivary reflex pathway, exhibits a significant impairment in patients with reflux esophagitis.
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PMID:Do salivary organic components play a protective role in health and disease of the esophageal mucosa? 755 68

A healthy neonatal piglet model was developed to investigate the effects of simulated gastro-esophageal reflux (GER) on airway protective mechanisms in different sleep states. Piglets were chosen for the model because there are similarities in esophageal morphology, development of the cardiorespiratory system and sleep-wakefulness cycle between the piglet and the human infant. Unanesthetized piglets were instrumented and trained to sleep in a radiolucent, temperature-controlled box. Physiologic recordings of sleep (electroencephalogram, 'ear-o-gram', behavioral observations), cardiorespiratory function (end-tidal CO2, O2 saturation, heart rate, respiratory movements), swallowing (pharyngeal or esophageal pressures) and GER (signaled by a fall in esophageal pH) were displayed and stored on a computer. An image intensifier was used for radiographic observations. The outputs from the computer and image intensifier were synchronized and recorded on videotape. The method enabled simultaneous physiologic and radiographic observations to be made during the simulation of GER by the injection of normal NaCl, distilled water or HCl (pH 2 and 3) into either the pharynx or different sites in the esophagus. The piglet model appears to accurately reflect the normal physiologic responses of the healthy sleeping neonate.
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PMID:A method for simultaneous physiological and radiographic recordings from sleeping neonatal piglets. 767 62


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