Increase In Intragastric Pressure Research Articles

Gastric accommodation: pathogenetic role and clinical significance

The article presents a literature review of modern Russian and foreign publications devoted to the study of gastric accommodation. It has been shown that accommodation of the proximal stomach plays an important role in its adaptation to food intake. This process is carried out in two stages with the participation of parasympathetic and paracrine regulation; the effects of nutrients when they enter the duodenum also play an important role. Methods for assessing gastric accommodation include gastric barostat, gastric scintigraphy with food load, drinking tests, single-photon emission computed tomography, magnetic resonance imaging and ultrasound examination of the stomach, intragastric manometry. Violation of gastric accommodation leads to an excessive increase in intragastric pressure and the occurrence of symptoms most often found in functional dyspepsia, gastroesophageal reflux disease and diabetic gastropathy. Approaches to the treatment of gastric accommodation disorders are at the development stage, the possibilities of diet therapy, pharmacological and non-drug correction are being discussed.

When symptoms are more than reflux.

45 year-old male patient with history of heartburn and regurgitation of non-acid food in the immediate postprandial period, with no symptomatic improvement after anti-acid treatment. The patient underwent an upper endoscopy that was unremarkable. A high-resolution impedance manometry (HRIM) was performed according to Chicago Protocol 4.0, as well as an additional solid test meal, with findings of rumination syndrome (RS) (figure 1). The study was completed with a 24-hour impedance pH monitoring that showed, in the immediate postprandial period, episodes of reflux that reached the proximal sensor followed by a normal swallow (figure 2). Abdominophrenic biofeedback was started with clinical improvement and anti-acid treatment was maintained at once a day. Discussion: RS is diagnosed by a complete clinical history, using the Rome IV or DSM-5 criteria (figure 3). Due to lack of knowledge of the disease and the fact that regurgitation can be present in other conditions including gastroesophageal reflux disease and achalasia, most patients undergo multiple tests and visit several physicians before reaching the diagnosis1. The gold standard investigation for RS, in cases where there are diagnostic doubts, is HRIM with solid meal administration, that shows a sudden increase in intragastric pressure > 30 mmHg concurrent with a drop in impedance and both simultaneous lower and upper esophageal sphincter relaxation, that may or may not be followed by re-swallowing food2. Rumination episodes can appear spontaneously (type 1) or may be preceded by a reflux episode (type 2) or a supragastric belch (type 3)3. 24-hour impedance pH monitoring cannot confirm de diagnosis, but during rumination, in the majority of episodes, the refluxed material reaches the proximal esophagus2.

Gas leakages from gastrointestinal endoscopy system-its visualization and semi-quantification utilizing schlieren optical system in the swine models.

Background and aimsWith the global epidemic of SARS-CoV-2, there has been a growing concern regarding the risk of aerosol exposure to healthcare workers and patients during medical/surgical interventions. The Schlieren device is capable of visualizing fine gas-flows by using refractive index differences in the medium. We aimed to reveal the existence of gas leakage from gastro-intestinal endoscopy system by utilizing Schlieren device and to clarify the factors which relates to the amount of gas leakage.MethodsThe experiments were performed on the excised swine stomach while maintaining a constant pressure environment in the stomach. The System Schlieren (SS100,KatoKoken) was used to visualize possible gas leakages from forceps plugs of endoscopy. We attempted to semi-quantify the leakage by referring to the image of the gas from the forceps plug and by measuring the initial velocity and diffusion area of the leakage.ResultsRegardless of the type of forceps plugs, a certain amount of leakage was detected during both insertion and removal of forceps. The initial velocity and the diffusion area of the leakage increased with the increase in intragastric pressure. Semi-quantitative comparison showed that there was a difference in the amount of gas leakage among various forceps plugs. Furthermore, the amount of gas leakage was significantly greater in the forceps plugs that were used repeatedly.ConclusionIt was possible to visualize gas leakages from the gastrointestinal endoscope system using the Schlieren optical device. Avoiding too high intragastric pressure and not using deteriorated plugs may reduce the risk of aerosol exposure.Supplementary InformationThe online version contains supplementary material available at 10.1007/s00464-022-09668-y.

How a modified Nissen procedure works: a mechanistic study using intraoperative esophageal high-resolution manometry.

We aimed at demonstrating how a modified Nissen procedure works by analyzing intraoperatively the variations of the low esophageal sphincter pressure values using high resolution manometry. This study included 15 patients with documented gastroesophageal reflux disease who underwent a laparoscopic modified Nissen procedure. Data regarding the changes in the pressure values were recorded at each step of the procedures using high resolution manometry and after the progressive insufflation of air in the stomach. Categorical data were compared between the preoperative and postoperative periods using Fisher's test, and continuous data were compared using Mann-Whitney U non-parametric test. Preoperative versus postoperative variations in continuous data were assessed using Wilcoxon's non-parametric test for paired data. Intraoperative manometric data showed a rise of basal LES pressure until the creation of the wrap. An evident increase of pressure values was recorded after gastric air insufflation, as consequence of the increase of intragastric pressure. No intraoperative and postoperative complications were observed. All patients experienced a significant reduction in terms of intensity and frequency of gastroesophageal reflux symptoms and no patients complained of dysphagia. Intraoperative high resolution manometry was feasible in all patients and demonstrated that the modified Nissen procedure works by increasing the LES pressure in response to gastric distension, without impeding the progression of the bolus into the stomach.

Endoscopic gastric plication for the treatment of GERD and underlying class I obesity.

Endoscopic gastric plication for the treatment of GERD and underlying class I obesity.

Современные возможности применения прокинетиков в лечении больных с гастроэзофагеальной рефлюксной болезнью

Aim of the lecture. To present modern approaches to prokinetic treatment at gastroesophageal reflux disease (GERD) to gastroenterologists. Summary. GERD belongs to acid-related diseases, because detrimental action of hydrochloric acid on esophageal mucosa plays major role in its pathogenesis. However esophageal and stomach motility disorders, e.g.: increase in frequency of transient lower esophageal sphincter relaxations, decrease of esophageal clearance and increase of intragastric pressure play important role in GERD development as well. These factors along with the not uncommon resistance of GERD patients to the proton pump inhibitors (PPI) caused by nonacidic refluxes require prokinetic administration. Most commonly prokinetics are prescribed as supplemental to PPI treatment. At the present time the optimal prokinetic drug, with proved efficacy at GERD and other diseases associated to gastrointestinal dysmotility is itopride hydrochloride (Ganaton®). Conclusion. Taken into account important role of esophageal and stomach dysmotility in GERD pathogenesis, prokinetics can be recommended for comprehensive disease treatment, especially at PPI inefficacy.

Rumination Syndrome: The Forgotten Offender

Rumination syndrome is an under-diagnosed and not well-understood condition. It's a repetitive and effortless habit that becomes a subconscious process, which affects children and adults that are developmentally challenged as well as healthy patients of all ages. It carries social stigmata and impacts one's health. We describe a case of a middle-aged woman suffering from this for majority of her life and once successfully diagnosed, she underwent biofeedback therapy and diaphragmatic breathing technique with remarkable improvement in her quality of life. A 68 year-old female with history of GERD presented with chronic regurgitations for > 48 years with re-mastication afterwards, negatively impacting her social life. Extensive work up was unremarkable including upper endoscopy, barium esophagram and gastric emptying study. Esophageal manometry showed normal contraction amplitude and LES profile. 24-hour pH-impedance reflux testing on acid suppression showed poor gastric acid control and slightly abnormal upright acid exposure (1.6%). One-hour high-resolution manometry-impedance study after consuming a provocative meal, with advancing the catheter distally into the proximal stomach, revealed total of 39 episodes of regurgitation (Figure 1). Episodes were preceded by increase in intra-gastric pressure (>30 mmHg), and were followed immediately by normal swallows to clear up the regurgitated food and were typical for rumination syndrome. Biofeedback was implemented, and diaphragmatic breathing technique was used as adjunctive modality for therapy. 6 months later, she had significant improvement in her social life with remarkable relief of symptoms. A Likert scale was used to quantify symptoms reduction (Figure 2). Rumination syndrome is often misdiagnosed for other upper gastrointestinal disorders (GERD, functional dyspepsia, eating disorders like bulimia, gastroparesis and chronic intestinal pseudo-obstruction). It involves involuntary increase in gastric pressure followed by opening of LES and increase in the intra-esophageal pressure to the same extent as gastric (common-cavity phenomenon). Rumination syndrome can be diagnosed with clinical symptomatology according to Rome IV criteria (Figure 3). Combined esophageal manometry-impedance testing is helpful in confirming the diagnosis. Biofeedback and behavioral modification therapy with diaphragmatic breathing proved to be useful in management of this chronic condition.Figure: High-resolution esophageal impedance-manometry showing sudden increase in intra-gastric and intra-esophageal pressure followed by a normal swallow to clear the regurgitated food (Left-hand side). Conventional manometry shows increase intra-gastric and esophageal pressure followed by normal swallow (Right-hand side).Figure: Patient's symptom improvement on Likert scale 1, 2 and 5 months through treatment. On a scale from 0-5, where 0 represents no symptoms and 5 represents severe symptoms, patient had 50% decrease in regurgitation, resolution of heartburn, 75% decrease in belching, 2/3 decrease in acid taste in mouth and resolution on bloating sensation with use of biofeedback and diaphragmatic breathing.Figure: Rome IV criteria for Rumination Syndrome

Rumination

Rumination syndrome is one of the functional gastroduodenal disorders. Effortless and repetitive regurgitation of recently ingested food from the stomach to the oral cavity followed by rechewing and reswallowing or spitting are the characteristic clinical features. This disorder is believed to be uncommon, but many patients with this disorder are overlooked by their physicians. Rumination might be caused by a reversal of the gastric contents through the esophagogastric junction, which is initiated by an increase in intragastric pressure. The characteristic symptoms are sufficient for the diagnosis of rumination syndrome. Postprandial high resolution esophageal impedance manometry can detect gastric pressurization exceeding 30 mmHg associated with the return of ingested material into the proximal esophagus, which is a pathognomonic finding of rumination syndrome. An extensive explanation of the condition and the underlying mechanism is the first step of the treatment of rumination syndrome. Behavioral therapy through diaphragmatic breathing is the mainstay of treatment. Further studies on the long term effects of biofeedback therapy as well as a proper strategy for refractory rumination syndrome are needed.

Rumination syndrome: pathophysiology, diagnosis, and treatment.

Rumination syndrome is a functional gastrointestinal disorder characterized by effortless and repetitive regurgitation of recently ingested food from the stomach to the oral cavity followed by either re-swallowing or spitting. Rumination is thought to occur due to a reversal of the esophagogastric pressure gradient. This is achieved by a coordinated abdominothoracic maneuver consisting of a thoracic suction, crural diaphragm relaxation and an increase in intragastric pressure. Careful history is important in the diagnosis of rumination syndrome; patients often report "vomiting" or "reflux" and the diagnosis can therefore be missed. Objective testing is available with high resolution manometry or gastroduodenal manometry. Increase in intra-gastric pressure followed by regurgitation is the most important characteristic to distinguish rumination from other disorders such as gastroesophageal reflux. The mainstay of the treatment of rumination syndrome is behavioral therapy via diaphragmatic breathing in addition to patient education and reassurance. The purpose of this review was to critically appraise recent key developments in the pathophysiology, diagnosis and therapy for rumination syndrome. A literature search using OVID (Wolters Kluwer Health, New York, NY, USA) to examine the MEDLINE database its inception until May 2016 was performed using the search terms "rumination syndrome," "biofeedback therapy," and "regurgitation." References lists and personal libraries of the authors were used to identify supplemental information. Articles published in English were reviewed in full text. English abstracts were reviewed for all other languages. Priority was given to evidence obtained from randomized controlled trials when possible.

A Case of Rumination Documented by Using High-resolution Impedance Manometry

A 40-year-old male with normal intelligence was referred for oral malodor. He first noticed his oral malodor because his wife had pointed out his bad breath about 7 years ago. He undertook some periodontal treatment such as scaling. His medical history was unremarkable. Esophagogastroduodenoscopy was performed and then revealed reflux esophagitis of minimal changes. His primary care physician started treatment with pantoprazole and mosapride. However, his oral malodor did not decrease. The patient reported frequent postprandial regurgitation and reswallowing of the regurgitated material. Under the clinical impression of rumination syndrome, high-resolution impedance manometry (HRIM) was performed after the patient was provided with some meal. HRIM revealed reflux event that was associated with an increase in intragastric pressure (gastric strain), which was compatible with rumination (Figure). The patient was instructed to take inspiratory and expiratory breaths with the abdominal muscles, keeping the chest motionless. He was encouraged to practice the diaphragmatic breathing during and after eating. He also was given baclofen of 10 mg preprandially for 4 weeks. He eventually reported decreased frequency of regurgitation and heard improved oral malodor from his wife 8 weeks later. Figure High-resolution impedance manometry of a patient with rumination syndrome. Two rumination episodes (black arrows) are observed as a rise in the intragastric pressure on the high-resolution manometry color plot associated with retrograde intra-esophageal ... HRIM is useful to diagnose rumination especially in case of diagnostic uncertainty or poor patient's acceptance on a possible diagnosis.1 Diaphragmatic breathing is known as the mainstay of treatment. Baclofen is reported to increase postprandial pressure of lower esophageal sphincter and to inhibit transient lower esophageal sphincter relaxations.2 Therefore baclofen is considered to be potentially beneficial in the treatment of rumination.3

Mechanism of hyperphagia contributing to obesity in brain-derived neurotrophic factor knockout mice

Global-heterozygous and brain-specific homozygous knockouts (KOs) of brain-derived neurotrophic factor (BDNF) cause late- and early-onset obesity, respectively, both involving hyperphagia. Little is known about the mechanism underlying this hyperphagia or whether BDNF loss from peripheral tissues could contribute to overeating. Since global-homozygous BDNF-KO is perinatal lethal, a BDNF-KO that spared sufficient brainstem BDNF to support normal health was utilized to begin to address these issues. Meal pattern and microstructure analyses suggested overeating of BDNF-KO mice was mediated by deficits in both satiation and satiety that resulted in increased meal size and frequency and implicated a reduction of vagal signaling from the gut to the brain. Meal-induced c-Fos activation in the nucleus of the solitary tract, a more direct measure of vagal afferent signaling, however, was not decreased in BDNF-KO mice, and thus was not consistent with a vagal afferent role. Interestingly though, meal-induced c-Fos activation was increased in the dorsal motor nucleus of the vagus nerve (DMV) of BDNF-KO mice. This could imply that augmentation of vago-vagal digestive reflexes occurred (e.g., accommodation), which would support increased meal size and possibly increased meal number by reducing the increase in intragastric pressure produced by a given amount of ingesta. Additionally, vagal sensory neuron number in BDNF-KO mice was altered in a manner consistent with the increased meal-induced activation of the DMV. These results suggest reduced BDNF causes satiety and satiation deficits that support hyperphagia, possibly involving augmentation of vago-vagal reflexes mediated by central pathways or vagal afferents regulated by BDNF levels.

Temperature Can Influence Gastric Accommodation and Sensitivity in Functional Dyspepsia with Epigastric Pain Syndrome

Functional dyspepsia-epigastric pain syndrome (FD-EPS) is characterized pathophysiologically by visceral hypersensitivity, but the effect of the temperature stimulation on gastric function has been seldom studied. The purpose of this study was to investigate the effects of liquid nutrients at different temperatures on the gastric accommodation, sensitivity, and gastric-wall compliance of healthy subjects (HS) and FD-EPS patients. Ten FD-EPS patients (Roma III criteria) and ten HS were recruited into the study. Intragastric pressure (IGP) and gastric perfusion were measured and compared following the administration of liquid nutrients at 37 °C on day 1 and at 8 °C on day 2. Seven patients developed abdominal discomfort or abdominal pain after being given cold liquid nutrient. The administration of liquid nutrient at 8 °C resulted in an increase of IGP in HS (P=0.044), a significant decrease in gastric perfusion (P<0.0001), a marked increase in IGP (P=0.015), and a dramatic reduction in gastric wall compliance (P=0.012) in patients compared to the effects of liquid nutrient at 37 °C. In addition, IGP in patients was lower than that in HS at 37 °C liquid nutrient (P=0.036), and the gastric perfusion volume in patients at maximal satiety was also significantly reduced at 8 °C liquid nutrient compared with HS (P=0.017). Cold stimulation can increase the IGP in HS and FD-EPS patients, elevate the visceral sensitivity and reduce the gastric volume of FD-EPS patients. FD-EPS patients who are sensitive to cold may develop epigastric discomfort or pain.

Reflex Increase in the Gastroesophageal Junction High Pressure Zone Pressure During Sedated Endoscopy With Gastric Distension in Normal Volunteers

Background: Gastric distension is a strong trigger for transient lower esophageal sphincter relaxation. In addition, it has been shown in prior unsedated studies that as the stomach is distended the pressure and length within the Gastroesophageal Junction High pressure Zone (GEJHPZ) decreases (Ayazi, Shahin MD et al, Annals of Surgery: July 2010 Volume 252 Issue 1 pp 57-62) Purpose: To evaluate the GEJHPZ pressure during gastric distension. Methods: Five normal volunteers (56.2 Yrs, 4F and 1M) were evaluated during upper endoscopy. A custom made manometry catheter with pressure ports spaced 3mm apart was attached to an Olympus ultrathin endoscope (GIF-N 180). Simultaneous manometry and endoscopy was recorded on an MMS swallowing work station. The endoscopy was performed under conscious sedation with Midazolam and Fentanyl. The endoscope was retroflexed to visualize the manometry catheter placed across the entire GEJHPZ. Baseline sphincter and gastric pressures were measured. Air was then insufflated into the stomach through the air channel of the endoscope with the air flow settings set at low (20ml/sec). Gastric and GEJHPZ pressures were measured continuously during air insufflation until a peak pressure was attained or the sphincter relaxed. All the pressures reported were relative to the gastric baseline pressure. To analyze the data, the start time was selected based on the lowest pressure at or just before the start of air insufflation, and the end point was selected where the pressure reached the peak within the GEJHPZ or just before sphincter relaxation. The duration to reach the peak pressure varied widely from subject to subject so the total duration was converted into 100% and then divided into 5 equal zones and an average pressure was calculated for each zone in the subjects. The peak and baseline pressures within the stomach and GEJHPZ were compared to each other using a paired student T test. The slope of the pressure change was determined. Results: The intragastric pressure increased from a mean of 6.19 mmHg to 12.34 mmHg at a slope of 1.09 (p=0.123). The GEJHPZ pressure increased from a mean 12.16 mmHg to 63.68 mmHg at a slope of 9.47 (p≤0.001). Conclusions: During sedated endoscopy, contrary to prior unsedated studies, gastric distension elicits a marked and significant reflex increase in the pressure and tone within the GEJHPZ as measured by intersphincteric pressure measurements using ultra-high resolution manometry. We measured the absolute change and the slope of the change of the pressures in both the stomach and the GEJHPZ during distension of the stomach with air. We believe that this gastric/GEJHPZ reflex is an important mechanism that protects the esophagus from reflux of gastric contents during increases in intragastric pressure.

Response to Air Insufflation in Patients with Non-Erosive Gastro-Oesophageal Reflux Disease (NERD)

This study compared changes in intragastric pressure (IGP) in response to a gastric distension stimulus caused by air insufflation in 25 patients with non-erosive gastro-oesophageal reflux disease (NERD) and 34 healthy volunteers (controls). In four NERD patients, IGP responses were also measured before and after oral treatment with 10 mg rabeprazole daily for 2 weeks. The rate of increase in IGP at the start of insufflation was significantly higher in NERD patients than in controls. The time to appearance of symptoms (i.e. time to threshold) was significantly shorter in NERD patients than in controls. Direct measurement of IGP showed that visceral hypersensitivity and impaired fundal relaxation are both characteristic of NERD. Administration of rabeprazole led to a marked prolonging of time to threshold, indicating that treatment could alleviate this hypersensitivity.

Gastric Pneumatosis in a Premature Neonate

Gastric pneumatosis is extremely rare during infancy. It has been reported in association with necrotizing enterocolitis or congenital abnormalities such as pyloric stenosis. Here, we report a case of gastric pneumatosis in a premature neonate on synchronized nasal intermittent positive pressure ventilation. No pneumatosis was noted in the rest of the bowel or esophagus. There could have been mild damage in the gastric mucosa, either related to the placement of the feeding tube or secondary to the use of indomethacin or both. The condition was further aggravated by noninvasive ventilation. An increase in intragastric pressure resulted in the submucosal dissection of air followed by the development of gastric pneumatosis. Conservative management strategies, including the use of a nasogastric tube for decompression and the withholding of feeding, successfully managed the gastric pneumatosis in our patient. An uneventful recovery was made after conservative management. Prompt recognition and evaluation of this condition were essential for making the diagnosis.

T1683 An Increase in Intra-Gastric Pressure is Associated With a Higher Proximal Extent of Gastroesophageal Reflux in Healthy Volunteers

T1683 An Increase in Intra-Gastric Pressure is Associated With a Higher Proximal Extent of Gastroesophageal Reflux in Healthy Volunteers

S2057 Diabetes-Induced Changes in the Expression of Proteins Involved in the Regulation of Sustained Mlc 20 Phosphorylation and cGMP Levels in Gastrointestinal Smooth Muscle

The gastrointestinal complications of diabetes mellitus include nausea, vomiting, increase in intragastric pressure and delay in gastric emptying. Several studies showed that the changes in gastric emptying in diabetes are associated with the loss of enteric neurons and interstitial cells of Cajal, and dysfunction of neuronal nitric oxide synthase activity. We have previously shown that in gastrointestinal smooth muscle sustained MLC20 phosphorylation and contraction are dependent on inhibition of MLC phosphatase, which is mediated by RhoA-dependent pathway involving phosphorylation of MYPT1 (at Thr696) by Rho kinase and CPI-17 (at Thr38) by PKC. Smooth muscle relaxation is dependent on stimulation of cAMP and cGMP levels and activation of cAMPand cGMP-dependent protein kinases. The levels of cAMP and cGMP are regulated mainly by phosphodiesterase (PDE) 4D5 and PDE5, respectively. We hypothesized that diabetes induces changes in the expression of proteins involved in the maintenance of smooth muscle tone and regulation of cGMP levels. Aim. To determine the expression of PDE5, CPI-17 and Rho kinase as well as agonist-induced Rho kinase activity in gastric smooth muscle from control and diabetic animal models.Methods. Gastric smooth muscle was isolated from spontaneously type II diabetic ob/ob mice and type I diabetic rats. Type I diabetes was induced in rats by intravenous injection of streptozotocin. The rats were kept for 9 weeks and induction of diabetes was ascertained by the determination of blood glucose concentrations. Expression of CPI-17, Rho kinase and PDE5 was measured by immunoblot analysis and acetylcholine-induced Rho kinase activity was measured by immunokinase assay. Results. Expression of CPI-17, Rho kinase and PDE5 are significantly higher in gastric smooth muscle from both models of diabetic animals than from control animals. Consistent with the increased expression of Rho kinase, acetylcholine-induced Rho kinase activity was also significantly higher in smooth muscle from both models of diabetic animals than from control animals. Conclusion. This study identified mechanisms for increased smooth muscle tone and decreased smooth muscle relaxation in diabetes that are directly attributable to changes in smooth muscle physiology. The mechanisms involved increased expression of proteins involved in the regulation of sustained MLC20 phosphorylation (CPI-17 and Rho kinase) and cGMP levels (PDE5). Upregulation CPI-17 and Rho kinase could contribute to increased intragastric pressure, whereas upregulation of PDE5 could contribute to rapid hydrolysis of cGMP and decreased relaxation leading to delay in gastric emptying.

PTH-040 The effect of salivary nitrite on gastric emptying

Introduction Human saliva has a high nitrite concentration from the entero-salivary recirculation of dietary nitrate. Swallowed nitrite reacts with acidic gastric juice forming nitric oxide (NO). Increasing NO bioactivity, by inhibiting phosphodiesterase, enhances gastric accommodation and delays gastric emptying. Aims To determine (1) whether nitrite in saliva affects gastric emptying and (2) whether nitrite in saliva alters postprandial intragastric pressure (IGP). Methods 20 healthy subjects (11 males) were studied. On four separate days high-resolution manometry was performed during 15 min fasting and for 90 min following a standardised meal. Post-prandially, solutions of 0, 0.286, 2 and 14 mmol/l potassium nitrite were infused into the oral cavity. Solutions were randomised and double-blinded. Saliva was collected at baseline, 30, 60 and 90 min after the meal. Salivary nitrite concentrations were quantified by Griess reaction. Gastric emptying was assessed by means of a specially designed breath test. 14C labelled sodium acetate was incorporated, during baking, into a rolled oats flapjack which constituted part of our standardised meal. Following consumption of the flapjack, breath samples were taken at regular intervals. The quantity of 14C appearing in breath per unit time (μmol/minute) was calculated. A generalised linear regression method was used to estimate gastric half-emptying times (T½). Mean IGP was defined relative to atmospheric pressure as the lowest mean pressure recorded in the six most distal manometry sensors. Results are medians and ranges. Results Salivary nitrite concentrations at 60 min were 24.35 μmol/l (3.86–65.46), 80.42 μmol/l (20.88–158.79), 358.4 μmol/l (118.2–726.6) and 2694 μmol/l (600–8087) for the solutions containing 0, 0.286, 2 and 14 mmol/l nitrite, respectively. There was no significant difference in the rate of gastric emptying (T½) between the control solution (103.5 min, 56.2–239.1) and those containing 0.286 mmol/l (113.4 mins, 68.7–254.8, p=0.56), 2 mmol/l (121.7 min, 39.8–270.0, p=0.93) and 14 mmol/l (114.4 mins, 79.1–390.1, p=0.75). There was no difference in the increase in IGP recorded between the control solution (4.06 mm Hg, −2.64–7.31) and those containing 0.286 mmol/l (4.42 mm Hg, −4.55–8.45, p=0.61), 2 mmol/l (4.66 mm Hg, −0.94-9.16, p=0.27) and 14 mmol/l (4.24 mm Hg, −2.12–8.17, p=0.81) potassium nitrite. Conclusion Despite an excellent range of salivary nitrite concentrations, extending over and beyond the normal physiological range, no difference in the rate of gastric emptying or postprandial rise in IGP was seen. This suggests salivary nitrite does not affect gastric emptying.

Investigation of specificity of auricular acupuncture points in regulation of autonomic function in anesthetized rats

Auricular acupuncture has been used for various autonomic disorders in clinical practice. It has been theorized that different auricular areas have distinct influence on autonomic functions. The present study aims to examine the effects of acupuncture stimulation at different auricular areas on cardiovascular and gastric responses. In male Sprague–Dawley rats anesthetized with pentobarbital sodium, five auricular areas, which were located at the apex of the helix (A 1), the middle of the helix (A 2), the tail of the helix (A 3), the inferior concha (A 4) and the middle of the antihelix (A 5), had been selected for stimulation with manual acupuncture (MA) and different parameters of electroacupuncture (EA). A mild depressor response (6%–12% decrease from baseline) was evoked from A 1, A 3 and A 4 by MA and from all five areas by EA (100 Hz–1 mA). The biggest depressor response (− 18.4 ± 3.1 mmHg, p < 0.001) was evoked from A 4. A small bradycardia was evoked by MA from A 4 and by EA at A 3, A 4 and A 5. Increase in intragastric pressure (8–14 mmH 2O) was evoked by MA from A 1, A 3 and A 4 and by EA at A 2. These results show that similar patterns of cardiovascular and gastric responses could be evoked by stimulation of different areas of the auricle. The present results do not support the theory of a highly specific functional map in the ear. Rather, there is a similar pattern of autonomic changes in response to auricular acupuncture, with variable intensity depending on the area of stimulation.

Diabetes induces sex-dependent changes in neuronal nitric oxide synthase dimerization and function in the rat gastric antrum

Diabetic gastroparesis is a disorder that predominantly affects women. However, the biological basis of this sex bias remains completely unknown. In this study we tested the hypothesis that a component of this effect may be mediated by the nitrergic inhibitory system of the enteric nervous system. Age-matched male and female Sprague-Dawley rats were studied 8 or 12 wk after streptozotocin (55 mg/kg body wt ip)-induced sustained hyperglycemia and compared with controls. Solid gastric emptying (GE) studies were performed in all the groups. Changes in gastric antrum neuronal nitric oxide synthase (nNOS) mRNA and protein levels were analyzed by real-time PCR and Western immunoblotting, respectively. nNOS dimerization studies were performed using low-temperature SDS-PAGE. In vitro nitrergic relaxation (area under curve/mg tissue wt) was studied after the application of electric field stimulation in an organ bath. Changes in intragastric pressure (mmHg.s) in freely moving rats in the presence or absence of N(G)-nitro-l-arginine methyl ester (nitric oxide synthase inhibitor) were examined by an ambulatory telemetric method. After diabetes induction, GE is delayed in both male and female rats. However, diabetic females exhibited significant delayed GE than in diabetic males. Compared with male controls, gastric nNOS expression and nitrergic relaxation were substantially elevated in healthy female control rats, accompanied by significantly reduced intragastric pressure. The active dimeric form and dimer-to-monomer ratio of nNOSalpha were also higher in healthy females compared with male rats (P < 0.05). Diabetic females, but not males, showed significant (P < 0.05) impairment in both gastric nNOSalpha dimerization and nitrergic relaxation, accompanied by an increase in intragastric pressure. Our data provide evidence that females may have a greater dependency on the nitrergic mechanisms in health. Furthermore, diabetes seems to affect the nitrergic system to a greater extent in females than in males. Together, these changes may account for the greater vulnerability of females to diabetic gastric dysfunction.