Preservation of postural control of transient lower oesophageal sphincter relaxations in patients with reflux oesophagitis.
INTRODUCTION: In normal subjects, transient lower oesophageal sphincter relaxations (TLOSRs) and gas reflux during belching are suppressed in the supine position. Supine reflux, however, is a feature of reflux disease. AIMS: To investigate whether postural suppression of TLOSRs and gas reflux is impaired in patients with reflux disease. PATIENTS: Ten patients with erosive oesophagitis. METHODS: Oesophageal manometry was performed during gastric distension with 750 ml carbon dioxide. Measurements were made for 10 minutes before and after distension in both sitting and supine positions. RESULTS: In the sitting position gastric distension substantially increased the rate of gas reflux (median (interquartile range)), as evidenced by increases in oesophageal common cavities from 1 (0-1)/10 min to 7 (5-10)/10 min and TLOSRs from 1 (1-1.5)/10 min to 6 (2.5-8)/10 min. However, this effect was suppressed in the supine position in all but one patient (TLOSRs 0 (0)/10 min to 1 (0-4.5)/10 min, common cavities 0 (0)/10 min to 0.5 (0-2)/10 min). CONCLUSIONS: Postural suppression of TLOSRs and gas reflux is generally preserved in reflux disease. (+info)
The effect of hiatus hernia on gastro-oesophageal junction pressure.
BACKGROUND: Hiatus hernia and lower oesophageal sphincter hypotension are often viewed as opposing hypotheses for gastro-oesophageal junction incompetence. AIMS: To examine the interaction between hiatus hernia and lower oesophageal sphincter hypotension. METHODS: In seven normal subjects and seven patients with hiatus hernia, the squamocolumnar junction and intragastric margin of the gastro-oesophageal junction were marked with endoscopically placed clips. Axial and radial characteristics of the gastro-oesophageal junction high pressure zone were mapped relative to the hiatus and clips during concurrent fluoroscopy and manometry. Responses to inspiration and abdominal compression were also analysed. RESULTS: In normal individuals the squamocolumnar junction was 0.5 cm below the hiatus and the gastro-oesophageal junction high pressure zone extended 1.1 cm distal to that. In those with hiatus hernia, the gastro-oesophageal junction high pressure zone had two discrete segments, one proximal to the squamocolumnar junction and one distal, attributable to the extrinsic compression within the hiatal canal. Inspiration and abdominal compression mainly augmented the distal one. Simulation of hernia reduction by algebraically summing the proximal segment pressures with the hiatal canal pressures restored normal maximal pressure, radial asymmetry, and dynamic responses of the gastro-oesophageal junction. CONCLUSIONS: Hiatus hernia reduces lower oesophageal sphincter pressure and alters its dynamic responsiveness by spatially separating pressure components derived from the intrinsic lower oesophageal sphincter and the extrinsic compression of the oesophagus within the hiatal canal. (+info)
A manometric assessment of oesophagogastrostomy.
Intraluminal pressures were recorded in 14 patients who had undergone oesophagogastrectomy. Seven of these had a mid-thoracic and seven a high cervical oesophagogastrostomy. The incidence of postoperative reflux complications in each group was noted. No pressure gradient across the anastomosis was detected in any patient but the upper oesophageal sphincter was shown to be retained as a functioning unit in all cases. It is considered that the thoracic anastomosis provides no demonstrable barrier to reflux. In addition, a high cervical oesophagogastrostomy does not adversely affect the upper oesophageal sphincter. The wider application of this latter procedure may be associated with a decreased incidence of postoperative reflux complications. (+info)
Effect of motilin on the lower oesophageal sphincter.
The effect of motilin on lower oesophageal sphincter (LES) pressure has been studied in unanesthetised specially trained dogs using an infusion manometric technique. Motilin produced significant rises in resting pressure and contractions of the LES after doses ranging from 0-009 mug/kg to 0-05 mug/kg. Doses greater than 0-05 mug/kg resulted in repetitive high amplitude contractions. Atropine 30 mug/kg completely abolished the effect of the lower doses of motilin. Higher doses of motilin in atropinised dogs still caused a small rise in baseline pressure and contractile activity still appeared. Hexamethonium 2 mg/kg resulted in both a diminished rise in LES pressure and the disappearance of contractions after motilin. Hexamethonium and atropine together completely abolished the LES response to motilin. We conclude that motilin increases LES pressure by acting on preganglionic cholinergic neurones to release acetylcholine which excites other cholinergic neurones supplying the circular muscle of the LES. (+info)
Responses of the competent and incompetent lower oesophageal sphincter to pentagastrin and abdominal compression.
Responses of the lower oesophageal sphincter (LOS) to pentagastrin, given by continuous intravenous infusion in doses ranging between 0 and 9 mug/kg/h, and to external abdominal compression were measured by infused catheters in healthy subjects and in a group of patients with reflux oesophagitis. In separate experiments, pressures were measured both by sensors stationary within the LOS, and by repeated continuous withdrawals of sensors from stomach to distal oesophagus. In normal subjects, doses of pentagastrin within the physiological range (0.9 mug/kg/h) produced modest but statistically significant increases in LOS pressure. By comparison, sphincteric responses in patients with oesophagitis were small and a dose of 4-5 mug/kg/h was the lowest that produced a significant increase in LOS pressure. During abdominal compression increases in LOS pressure did not significantly exceed increases in intragastric pressure in either patients or normal subjects. This was so at all doses of pentagastrin that were tested. Hence, there was no evidence of synergism between the effects of pentagastrin and abdominal compression upon the LOS. We infer from our findings that gastrin does play a modest role in the physiological regulation of human LOS tone. Relative insensitivity of the incompetent LOS to pentagastrin represents, we believe, sphincteric muscle failure. Our results are not consistent with the hypothesis that LOS incompetence is due to loss or impairment of an adaptive response of the LOS to alterations in intra-abdominal pressure. (+info)
Cholinergic blockade inhibits gastro-oesophageal reflux and transient lower oesophageal sphincter relaxation through a central mechanism.
BACKGROUND: Atropine, an anticholinergic agent with central and peripheral actions, reduces gastro-oesophageal reflux (GOR) in normal subjects and patients with gastro-oesophageal reflux disease (GORD) by inhibiting the frequency of transient lower oesophageal sphincter relaxation (TLOSR). AIMS: To compare the effect of methscopolamine bromide (MSB), a peripherally acting anticholinergic agent, with atropine on the rate and mechanism of GOR in patients with GORD. METHODS: Oesophageal motility and pH were recorded for 120 minutes in 10 patients with GORD who were studied on three separate occasions. For the first two recording periods, either atropine (15 microg/kg bolus, 4 microg/kg/h infusion) or saline were infused intravenously. MSB (5 mg orally, four times daily) was given for three days prior to the third recording period. RESULTS: Atropine significantly reduced basal LOS pressure (12.6 (0.17) mm Hg to 7.9 (0.17) mm Hg), and the number of TLOSR (8.1 (0.56) to 2.8 (0. 55)) and reflux episodes (7.0 (0.63) to 2.0 (0.43)) (p<0.005 for all comparisons). MSB reduced basal LOS pressure (12.6 (0.17) to 8.7 (0. 15) mm Hg, p<0.005), but had no effect on the frequency of TLOSR (8. 1 (0.56) to 7.5 (0.59)) and reflux episodes (7.0 (0.63) to 4.9 (0. 60)) (p>0.05). CONCLUSION: In contrast to atropine, MSB has no effect on the rate of TLOSR or GOR in patients with GORD. Atropine induced inhibition of TLOSR and GOR is most likely mediated through a central cholinergic blockade. (+info)
Lack of effect of spearmint on lower oesophageal sphincter function and acid reflux in healthy volunteers.
BACKGROUND: Spearmint is commonly used as an antispasmodic and as a flavouring in several medications including antacids. It can produce heartburn, presumably by lowering lower oesophageal sphincter (LES) tone, but the mechanism has not previously been objectively examined. AIM: To study the effect of spearmint on LES function, acid reflux and symptoms. METHODS: In healthy volunteers, a Dent Sleeve and a pH electrode were placed in the distal oesophagus. They were then given spearmint either in a flavouring (0.5 mg), or a high (500 mg) dose, or a placebo, using a double-blind randomized crossover design. LES pressure, oesophageal pH and symptoms were recorded for 30 min before and after administration. RESULTS: LES pressure was not affected by spearmint, either high dose (19.6 vs. 16.0 mmHg), flavouring dose (20.2 vs. 19.8 mmHg) or placebo (20.5 vs. 19.2 mmHg, all N.S.). There were no differences in reflux occurrence following high dose (mean = 0.65 vs. 0.85 episodes), low dose (0.4 vs. 0.5 episodes) or placebo (0.7 vs. 1.10 episodes, all N.S.). There was a significant increase in mean symptom scores following high-dose spearmint (0 vs. 0.35, P = 0.03), but not low dose (0 vs. 0.2) or placebo (0 vs. 0.5, both N.S.). One subject reported symptoms with placebo, one with low dose, and six with high dose; all without increased reflux episodes or decreased sphincter pressure. CONCLUSION: Spearmint has no effect on LES pressure or acid reflux. Flavouring doses of spearmint do not produce more symptoms than placebo while high doses can be associated with symptoms, presumably from direct mucosal irritation but not reflux. (+info)
Activation of outward K+ currents: effect of VIP in oesophagus.
1. Electrical field stimulations (EFS) of the opossum and canine lower oesophageal sphincters (OLOS and CLOS respectively) and opossum oesophageal body circular muscle (OOBCM) induce non-adrenergic, non-cholinergic (NANC) relaxations of any active tension and NO-mediated hyperpolarization. VIP relaxes the OLOS and CLOS and any tone in OOBCM without major electrophysiological effects. These relaxations are not blocked by NOS inhibitors. Using isolated smooth muscle cells, we tested whether VIP acted through myogenic NO production. 2. Outward currents were similar in OOBCM and OLOS and NO increased them regardless of pipette Ca2+(i), from 50-8000 nM. L-NAME or L-NOARG did not block outward currents in OLOS at 200 nM pipette Ca2+. 3. Outward currents in CLOS cells decreased at 200 nM pipette Ca2+ or less but NO donors still increased them. VIP had no effect on outward currents in cells from OOBCM, OLOS or CLOS under conditions of pipette Ca2+ at which NO donors increased outward K+ currents. 4. We conclude, VIP does not mimic electrophysiological effects of NO donors on isolated cells of OOBCM, OLOS or CLOS. VIP relaxes the OLOS and CLOS and inhibits contraction of OOBCM by a mechanism unrelated to release of myogenic NO or an increase in outward current. 5. Also, the different dependence of outward currents of OOBCM and OLOS on pipette Ca2+ from those of CLOS suggests that different K+ channels are involved and that myogenic NO production contributes to K+ channel activity in CLOS but not in OLOS or OOBCM. (+info)