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BACKGROUND: Stomach, small intestine, and colon have distinct patterns of contraction related to their function to mix and propel enteric contents. In this study, we aim to measure gut myoelectric activity in the perioperative course using external patches in an animal model. METHODS: Four external patches were placed on the abdominal skin of female Yucatan pigs to record gastrointestinal myoelectric signals for 3 to 5 d. Pigs subsequently underwent anesthesia and placement of internal electrodes on stomach, small intestine, and colon. Signals were collected by a wireless transmitter. Frequencies associated with peristalsis were analyzed for both systems for 6 d postoperatively. RESULTS: In awake pigs, we found frequency peaks in several ranges, from 4 to 6.5 cycles per minute (CPM), 8 to 11 CPM, and 14 to 18 CPM, which were comparable between subjects and concordant between internal and external recordings. The possible effect of anesthesia during the 1 or 2 h before surgical manipulation was observed as a 59% (±36%) decrease in overall myoelectric activity compared to the immediate time before anesthesia. The myoelectrical activity recovered quickly postoperatively. Comparing the absolute postsurgery activity levels to the baseline for each pig revealed higher overall activity after surgery by a factor of 1.69 ± 0.3. CONCLUSIONS: External patch measurements correlated with internal electrode recordings. Anesthesia and surgery impacted gastrointestinal myoelectric activity. Recordings demonstrated a rebound phenomenon in myoelectric activity in the postoperative period. The ability to monitor gastrointestinal tract myoelectric activity noninvasively over multiple days could be a useful tool in diagnosing gastrointestinal motility disorders.
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OBJECTIVES: This study aimed to investigate the integrative effects and mechanisms of transcutaneous electrical acustimulation (TEA) on postprocedural recovery from endoscopic retrograde cholangio-pancreatography (ERCP). MATERIALS AND METHODS: A total of 86 patients for elective ERCP were randomly ordered to receive TEA (n = 43) at acupoints PC6 and ST36 or Sham-TEA (n = 43) at sham points from 24 hours before ERCP (pre-ERCP) to 24 hours after ERCP (PE24). Scores of gastrointestinal (GI) motility-related symptoms and abdominal pain, gastric slow waves, and autonomic functions were recorded through the spectral analysis of heart rate variability; meanwhile, circulatory levels of inflammation cytokines of tumor necrosis factor-α (TNF-α) and interleukin (IL)-10 and GI hormones of motilin, ghrelin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) were assessed by enzyme-linked immunosorbent assay. RESULTS: 1) TEA, but not Sham-TEA, decreased the post-ERCP GI motility-related symptom score (2.4 ± 2.6 vs 7.9 ± 4.6, p < 0.001) and abdominal pain score (0.5 ± 0.7 vs 4.1 ± 2.7, p < 0.001) at PE24, and decreased the post-ERCP hospital day by 20.0% (p ï¼0.05 vs Sham-TEA); 2) TEA improved the average gastric percentage of normal slow waves and dominant frequency by 34.6% and 33.3% at PE24, respectively (both p < 0.001 vs Sham-TEA); 3) TEA, but not Sham-TEA, reversed the ERCP-induced increase of TNF-α but not IL-10 at PE24, reflected as a significantly lower level of TNF-α in the TEA group than in the Sham-TEA group (1.6 ± 0.5 pg/mL vs 2.1 ± 0.9 pg/mL, p ï¼ 0.01); 4) compared with Sham-TEA, TEA increased vagal activity by 37.5% (p ï¼ 0.001); and 5) TEA caused a significantly higher plasma level of ghrelin (1.5 ± 0.8 ng/ml vs 1.1 ± 0.7 ng/ml, p ï¼ 0.05) but not motilin, VIP, or CCK than did Sham-TEA at PE24. CONCLUSION: TEA at PC6 and ST36 accelerates the post-ERCP recovery, reflected as the improvement in GI motility and amelioration of abdominal pain, and suppression of the inflammatory cytokine TNF-α may mediate through both autonomic and ghrelin-related mechanisms.
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We explored the effect of Ninjinyoeito (NYT) on cisplatin-induced anorexia, which reduces cancer patient survival. Both gastrointestinal motility and plasma concentrations of gastrointestinal peptides were assessed. Nine-week-old ICR female mice received intraperitoneal cisplatin injections (10 mg/kg) and daily oral NYT doses of 300 mg/kg (NYT300) or 1000 mg/kg (NYT1000). Plasma levels of gastrointestinal peptides were measured at 3 and 6 days after cisplatin injection. Gastrointestinal motility was assessed by analyzing the concentration of phenol red marker within sections of the gastrointestinal tract. Cisplatin-injected mice showed a decrease in daily food intake, but this effect was attenuated on day 5 with NYT1000 administration. Although plasma ghrelin levels were reduced on day 3 in cisplatin-treated mice, NYT1000 administration ameliorated this decrease. However, there were no differences in ghrelin levels among all groups on day 6. Levels of peptide YY (PYY) were elevated in the plasma of cisplatin-injected mice on days 3 and 6. Administration of NYT300 and NYT1000 suppressed the increase in PYY levels on day 6 but not on day 3. Gastrointestinal motility was impaired on day 6 in cisplatin-treated mice, but NYT1000 administration attenuated this effect. Our results suggest that NYT improves cisplatin-induced anorexia by suppressing alterations in ghrelin and PYY levels and by increasing gastrointestinal motility. Therefore, NYT may be a promising candidate for alleviating cisplatin-induced anorexia.
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Naringenin (NRG) is widely found in citrus fruits and has anti-inflammatory, hypoglycemic, and immunomodulatory effects. Previous studies have shown that NRG promotes gastrointestinal motility in mice constipation models, but there are few systematic evaluations of its effects on normal animals. This study first clarified the promotive effects of NRG on gastric emptying and small intestine propulsion (p < 0.01). NRG can also regulate the release of gastrointestinal hormones, including enhancing gastrin (GAS) and motilin (MTL) (p < 0.01), while reducing vasoactive intestinal peptide (VIP) secretion (p < 0.01). Using NRG to stimulate the isolated stomach, duodenum, and colon showed similar promotive effects to those observed in vivo (p < 0.01). A Western blot analysis indicated that this effect may be mediated by increasing the expression of stem cell factor (SCF) and its receptor (c-Kit) in these three segments, thus regulating their downstream pathways. It is worth noting that NRG can also increase the proportion of beneficial bacteria (Planococcaceae, Bacteroides acidifaciens, Clostridia_UCG-014) in the intestine and reduce the quantity of harmful bacteria (Staphylococcus). These findings provide a new basis for the application of NRG.
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The orexigenic gut peptide ghrelin is an endogenous ligand for the growth hormone secretagogue receptor type 1a (GHSR1a). Systemic ghrelin administration has previously been shown to increase gastric motility and emptying. While these effects are known to be mediated by the vagus nerve, the cellular mechanism underlying these effects remains unclear. Therefore, the purpose of the present study was to investigate the signaling mechanism by which GHSR1a inhibits voltage-gated Ca2+ channels in isolated rat gastric vagal afferent neurons using whole-cell patch-clamp electrophysiology. The ghrelin pharmacological profile indicated that Ca2+ currents were inhibited with a log (Ic50)=-2.10 {plus minus} 0.44 and a maximal inhibition of 42.8 {plus minus} 5.0%. Exposure to the GHSR1a receptor antagonist (D-Lys3)-GHRP-6 reduced ghrelin-mediated Ca2+ channel inhibition (29.4 {plus minus} 16.7% vs 1.9 {plus minus} 2.5%, n=6, p=0.0064). Interestingly, we observed that activation of GHSR1a inhibited Ca2+ currents through both voltage-dependent and voltage-independent pathways. We also treated the gastric neurons with either pertussis toxin (PTX) or YM-254890 to examine whether the Ca2+ current inhibition was mediated by Gαi/o or Gαq/11 family of subunits. Treatment with both PTX (Ca2+ current inhibition=15.7 {plus minus} 10.6%, n=8, p=0.0327) and YM-254890 (15.2 {plus minus} 11.9%, n=8, p=0.0269) blocked ghrelin's effects on Ca2+ currents, as compared to control neurons (34.3 {plus minus} 18.9%, n=8). These results indicate GHSR1a can couple to both Gαi/o and Gαq/11 in gastric vagal afferent neurons. Overall, our findings suggest GHSR1a-mediated inhibition of Ca2+ currents occurs through two distinct pathways, offering necessary insights into the cellular mechanisms underlying ghrelin's regulation of gastric vagal afferents. Significance Statement This study demonstrated that in gastric vagal afferent neurons, activation of GHSR1a by ghrelin inhibits voltage-gated Ca2+ channels through both voltage-dependent and voltage-independent signaling pathways. These results provide necessary insight into the cellular mechanism underlying ghrelin regulation of gastric vagal afferent activity, which may benefit future studies investigating ghrelin mimetics to treat gastric motility disorders.
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Antispasmodic agents are crucial in managing gastrointestinal motility disorders by modulating muscle contractions and reducing symptoms like cramping and diarrhea. This study investigated the antispasmodic potential of different coffee bean extracts, including light coffee (LC), medium coffee (MC), and dark coffee (DC), on ileum contractions induced by potassium chloride (KCl), and elucidated their mechanisms of action using in vitro isolated tissue techniques. The results demonstrated that all coffee extracts reduced spontaneous contractions of rat ileum tissue in a dose-dependent manner. Among these, LC showed the most significant reduction in ileum contractions, particularly at higher concentrations. The key findings reveal that LC at 5 mg/mL significantly reduced CaCl2-induced contractions in isolated rat ileum tissue, indicating that LC may inhibit calcium influx or interfere with calcium signaling pathways. The presence of nifedipine, propranolol, and N-nitro-L-arginine methyl ester (L-NAME) have been confirmed in their involvement; they block calcium influx and calcium channels and activate ß-adrenergic pathways as part of LC's mechanism of action. The presence of their active compounds, particularly chlorogenic acid and caffeine, likely contributes to the observed antispasmodic effects. These findings suggest that LC exerts its antispasmodic effects by targeting key mechanisms involved in muscle spasms and intestinal motility, providing a potential for managing such conditions.
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(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.
Subject(s)
Appetite Regulation , Hypothalamus , Neuropeptide Y , Olive Oil , Palm Oil , Soybean Oil , Vagus Nerve , Animals , Vagus Nerve/drug effects , Vagus Nerve/physiology , Hypothalamus/metabolism , Hypothalamus/drug effects , Male , Olive Oil/pharmacology , Neuropeptide Y/genetics , Neuropeptide Y/metabolism , Palm Oil/pharmacology , Appetite Regulation/drug effects , Soybean Oil/administration & dosage , Soybean Oil/pharmacology , Rats, Wistar , Linseed Oil/pharmacology , Rats , Eating/drug effects , Plant Oils/pharmacology , Pro-Opiomelanocortin/genetics , Pro-Opiomelanocortin/metabolism , Nerve Tissue Proteins/genetics , Nerve Tissue Proteins/metabolism , Gastrointestinal Motility/drug effects , Gene Expression Regulation/drug effects , RNA, Messenger/metabolism , RNA, Messenger/geneticsABSTRACT
BACKGROUND: Gastric peroral endoscopic pyloromyotomy (G-POEM) is a promising therapeutic modality for refractory gastroparesis (GP). However, as characteristics of suitable patients for G-POEM remain unclear, antro-duodenal manometry (ADM) has been suggested to provide objective parameters for patient selection. The aim of the present study was to identify ADM parameters as predictors for treatment response after G-POEM in refractory GP. METHODS: Refractory GP patients who underwent a G-POEM between 2017 and 2022 were included. The following ADM parameters were mainly scored: antral hypomotility, pylorospasm, and the presence of neuropathic enteric patterns. Treatment response was defined as a GCSI-score decrease of ≥1 point 12 months after G-POEM. Explorative analyses were performed on potential predictors of response using logistic regression analysis. KEY RESULTS: Sixty patients (52 women, mean age 52 ± 14 years.) with refractory GP (33 idiopathic, 16 diabetic, 11 postsurgical) were included. Clinical response data were available for 52 patients. In 8 out of 60 patients, it was not feasible to advance the catheter beyond the pylorus. Abnormal ADM was found in 46/60 patients (77%). Antral hypomotility and pylorospasm were found in respectively 33% and 12% of patients. At least one neuropathic enteric dysmotility pattern was found in 58% of patients. No differences were found when comparing baseline ADM parameters between clinical response groups at 12 months follow-up. Following explorative analyses, no ADM parameters were identified to predict clinical response 12 months after G-POEM. CONCLUSIONS AND INFERENCES: No ADM parameters were identified as predictors of clinical response after G-POEM in refractory GP patients. Additionally, a high percentage of abnormal ADM tracings was found, in particular with relation to enteric dysmotility, while only a low percentage of patients showed antral hypomotility or pylorospasm.
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This review discusses the less-explored realm of DNA damage and repair within the enteric nervous system (ENS), often referred to as the "second brain." While the central nervous system has been extensively studied for its DNA repair mechanisms and associated neuropathologies, the ENS, which can autonomously coordinate gastrointestinal function, experiences unique challenges and vulnerabilities related to its genome integrity. The susceptibility of the ENS to DNA damage is exacerbated by its limited protective barriers, resulting in not only endogenous genotoxic exposures, such as oxidative stress, but also exogenous threats, such as ingested environmental contaminants, local inflammatory responses, and gut dysbiosis. Here, we discuss the evidence for DNA repair defects in enteric neuropathies, most notably, the reported relationship between inherited mutations in RAD21 and LIG3 with chronic intestinal pseudo-obstruction and mitochondrial gastrointestinal encephalomyopathy disorders, respectively. We also introduce the lesser-recognized gastrointestinal complications in DNA repair syndromes, including conditions like Cockayne syndrome. The review concludes by pointing out the potential role of DNA repair defects in not only congenital disorders but also aging-related gut dysfunction, as well as the crucial need for further research to establish direct causal links between DNA damage accumulation and ENS-specific pathologic phenotypes.
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There is a large pool of ideas in both mainstream and non-mainstream medicine on how diet can be manipulated in order to treat or prevent illnesses. Despite this, our understanding of how specific changes in diet influence the structure and function of the gastrointestinal tract is limited. This review aims to describe two areas that might provide key information on the integrity and function of the gastrointestinal tract. First, demystifying the "leaky gut syndrome" requires rational application and interpretation of tests of intestinal barrier function. Multiple ways of measuring barrier function have been described, but the inherent difficulties in translation from animal studies to humans have created misinterpretations and misconceptions. The intrinsic nature of intestinal barrier function is dynamic. This is seldom considered in studies of intestinal barrier assessment. To adequately understand the effects of dietary interventions on intestinal barrier function, background barrier function in different regions of the gut and the dynamic responses to stressors (such as psychological stress) should be assessed as a minimum. Second, intestinal ultrasound, which is now established in the assessment and monitoring of inflammatory bowel disease, has hitherto been poorly evaluated in assessing real-time intestinal function and novel aspects of structure in patients with disorders of gut-brain interaction. In conclusion, a more complete functional and structural profile that these investigations enable should permit a greater understanding of the effects of dietary manipulation on the gastrointestinal tract and provide clinically relevant information that, amongst other advantages, might permit opportunities for personalized health care delivery.
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Gulf War Illness (GWI) is characterized by a wide range of symptoms that manifests largely as gastrointestinal symptoms. Among these gastrointestinal symptoms, motility disorders are highly prevalent, presenting as chronic constipation, stomach pain, indigestion, diarrhea, and other conditions that severely impact the quality of life of GWI veterans. However, despite a high prevalence of gastrointestinal impairments among these veterans, most research attention has focused on neurological disturbances. This perspective provides a comprehensive overview of current in vivo research advancements elucidating the underlying mechanisms contributing to gastrointestinal disorders in GWI. Generally, these in vivo and in vitro models propose that neuroinflammation alters gut motility and drives the gastrointestinal symptoms reported in GWI. Additionally, this perspective highlights the potential and challenges of in vitro bioengineering models, which could be a crucial contributor to understanding and treating the pathology of gastrointestinal related-GWI.
Subject(s)
Bioengineering , Gastrointestinal Diseases , Persian Gulf Syndrome , Humans , Persian Gulf Syndrome/physiopathology , Persian Gulf Syndrome/complications , Bioengineering/methods , Bioengineering/trends , Gastrointestinal Diseases/physiopathology , Gastrointestinal Diseases/etiology , Gastrointestinal Diseases/complications , Gastrointestinal Tract/physiopathologyABSTRACT
BACKGROUND: Gastrointestinal (GI) motility disorders are common in clinical settings, but physicians still lack sufficient understanding and effective management of these conditions. METHODS: This research assessed Egyptian physicians' knowledge, practices, and attitudes towards GI motility disorders. A cross-sectional survey employing a self-administered questionnaire was carried out among physicians in Egypt. The questionnaire addressed various aspects of physicians' understanding, practices, and attitudes regarding GI motility disorders. Data analysis was conducted using descriptive statistics and presented as frequencies and percentages. RESULTS: A total of 462 physicians took part in the study. Although nearly two-thirds of them knew about GI motility studies, a notable proportion lacked adequate knowledge about GI motility disorders. Notably, 84.2% correctly identified dysphagia as a critical symptom suggestive of an upper GI motility disorder. However, 13.4% incorrectly linked hematemesis with an upper GI motility disorder, and 16.7% expressed uncertainty. In terms of practice, around half of the participants encountered a small number of patients with GI motility disorders (less than 5 per week or even fewer). Only 29.7% felt confident in managing patients with motility disorders. Most participating physicians expressed a willingness to participate in training programs focused on motility disorders. CONCLUSIONS: This study underscores a knowledge gap among Egyptian physicians concerning GI motility disorders. It suggests the necessity of tailored education and training programs to improve their competency and practice in this domain.
Subject(s)
Attitude of Health Personnel , Gastrointestinal Diseases , Gastrointestinal Motility , Health Knowledge, Attitudes, Practice , Humans , Egypt , Cross-Sectional Studies , Male , Female , Gastrointestinal Diseases/psychology , Gastrointestinal Diseases/therapy , Surveys and Questionnaires , Clinical Competence , Adult , Physicians/psychology , Middle Aged , Practice Patterns, Physicians'ABSTRACT
Stress has been linked to the development of irritable bowel syndrome (IBS), and various methods have been explored to model IBS in combination with other stimuli. However, it remains unclear whether stress alone can induce IBS in animals. This study aimed to investigate the impact of chronic unpredictable mild stress (CUMS) on gastrointestinal sensation and function in mice and assess the potential of CUMS as a modeling approach for IBS. To evaluate the mice's behavior, we conducted open field test, sucrose preference test and weighed the mice, revealing that CUMS indeed induced anxiety and depression in the mice and caused weight loss. Further analyses, including fecal analysis, a total gastrointestinal transport test, and a colon propulsion test, demonstrated that CUMS led to abnormal defecation and disruptions in gastrointestinal motility in the mice. Additionally, the abdominal withdrawal reflex test indicated an increase in visceral sensitivity in CUMS-exposed mice. Histological examination using hematoxylin and eosin staining revealed no significant histological alterations in the colons of CUMS-exposed mice, but it did show a minor degree of inflammatory cell infiltration. In summary, the findings suggest that CUMS can replicate IBS-like symptoms in mice, offering a novel top-down approach to modeling IBS.
Subject(s)
Disease Models, Animal , Gastrointestinal Motility , Irritable Bowel Syndrome , Stress, Psychological , Animals , Stress, Psychological/physiopathology , Stress, Psychological/complications , Male , Mice , Irritable Bowel Syndrome/physiopathology , Gastrointestinal Motility/physiology , Anxiety/physiopathology , Depression/physiopathology , Mice, Inbred C57BL , Behavior, Animal , Defecation , Colon/physiopathology , Colon/pathologyABSTRACT
We propose a novel strategy for tailoring the structure of fluorescent molecules to achieve emission at the tail end of the NIR-II window. The favorable spectroscopic properties and low cytotoxicity of YNs make them powerful tools for bioimaging. Notably, YN-4 exhibits a brightness 2.5 times greater than YN-3, 6 times that of IR-783, and 5 times that of ICG. This enhanced brightness enabled high-resolution imaging of mouse thoracic and abdominal cavities, tumor vasculature, and real-time monitoring of gastrointestinal motility using YN-4. Furthermore, covalent grafting of glucose onto the YN-Glu scaffold significantly improved tumor-targeting capability and facilitated tracking of glucose metabolism. This work aims to extend the application of fluorescent molecule imaging beyond the NIR-IIa window.
Subject(s)
Fluorescent Dyes , Indoles , Animals , Mice , Indoles/chemistry , Fluorescent Dyes/chemistry , Humans , Spectroscopy, Near-Infrared/methods , Optical Imaging , Carbocyanines/chemistry , Cell Line, Tumor , Glucose/metabolism , Glucose/chemistryABSTRACT
BACKGROUND: In 2018 diagnostic criteria for pediatric intestinal pseudo-obstruction (PIPO) were established. Neuromuscular dysfunction of the gastrointestinal tract is one of these, and often examined through antroduodenal manometry (ADM). There is little data on antroduodenal manometries in children. Our objectives were to retrospectively apply these criteria to children evaluated for suspected motility disorder, to reevaluate the ADM patterns and compare children who did and did not meet the PIPO criteria and also with healthy adults. METHODS: Children with a suspected gastrointestinal motility disorder previously investigated with 24-h 8-lead ADM were reevaluated by applying the 2018 ESPGHAN/NASPGHAN PIPO diagnostic criteria and the 2018 ANMS-NASPGHAN guidelines. ADM findings were compared between children who retrospectively fulfilled a PIPO diagnosis, children who did not, and a control group of healthy adults. KEY RESULTS: Of 34 children (age 7.9 (±5.1) years, 18 males), 12 retrospectively fulfilled the 2018 PIPO diagnostic criteria. Twenty-five children (10 in the PIPO group) had abnormal diagnostic findings on ADM, whereas 9 (2 in the PIPO group) had no such findings. A PIPO diagnosis implied a significantly higher degree of abnormal ADM patterns (2.33 vs. 1.23, p = 0.02). There were no major differences in quantitative ADM measurements between the groups except higher pressures in children. CONCLUSIONS AND INFERENCES: Children who retrospectively fulfilled a PIPO diagnosis had a significantly higher abundance of abnormal ADM findings compared with symptomatic children without PIPO and healthy adults. Our data indicate a need for set criteria for evaluation of ADM in children with suspected PIPO.
Subject(s)
Intestinal Pseudo-Obstruction , Manometry , Humans , Manometry/methods , Male , Child , Female , Retrospective Studies , Child, Preschool , Intestinal Pseudo-Obstruction/diagnosis , Intestinal Pseudo-Obstruction/physiopathology , Adolescent , Duodenum/physiopathologyABSTRACT
Achalasia esophagus and acute intestinal pseudo-obstruction are distinct gastrointestinal motility disorders rarely found together in the same patient. We present a case of a 96-year-old woman exhibiting symptoms of both conditions, including dysphagia, regurgitation, abdominal distension, nausea, vomiting, and constipation. Diagnostic evaluations revealed esophageal dilation with a "bird beak" sign on timed barium swallows and significant bowel dilation without mechanical obstruction on computed tomography scans. Treatment involved conservative measures for acute intestinal pseudo-obstruction and palliative approaches for achalasia esophagus. The coexistence of these disorders raises questions about potential shared pathophysiological mechanisms involving the enteric nervous system or smooth muscle dysfunction. Further research is warranted to elucidate these connections and improve management strategies for such complex cases.
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In the realm of gastroenterology, the inadequacy of current medical treatments for gastrointestinal (GI) motility disorders and inflammatory bowel disease (IBD), coupled with their potential side effects, necessitates novel therapeutic approaches. Neuromodulation, targeting the nervous system's control of GI functions, emerges as a promising alternative. This review explores the promising effects of vagal nerve stimulation (VNS), magnetic neuromodulation, and acupuncture in managing these challenging conditions. VNS offers targeted modulation of GI motility and inflammation, presenting a potential solution for patients not fully relieved from traditional medications. Magnetic neuromodulation, through non-invasive means, aims to enhance neurophysiological processes, showing promise in improving GI function and reducing inflammation. Acupuncture and electroacupuncture, grounded in traditional medicine yet validated by modern science, exert comprehensive effects on GI physiology via neuro-immune-endocrine mechanisms, offering relief from motility and inflammatory symptoms. This review highlights the need for further research to refine these interventions, emphasizing their prospective role in advancing patient-specific management strategies for GI motility disorders and IBD, thus paving the way for a new therapeutic paradigm.
Subject(s)
Gastrointestinal Motility , Inflammatory Bowel Diseases , Humans , Inflammatory Bowel Diseases/therapy , Gastrointestinal Motility/physiology , Vagus Nerve Stimulation/methods , Gastroenterology/methods , Gastrointestinal Diseases/therapy , Electroacupuncture/methods , Animals , Acupuncture Therapy/methodsABSTRACT
BACKGROUND: Low-intensity pulsed ultrasound (LIPUS) combined with acupoint can promote gastric motility of diabetic rats. The switch of gastric smooth muscle cell (GSMCs) phenotype was related to the diabetes-induced gastric dysfunction, but the mechanism is not clearly elucidated. This study was aimed at exploring the underlying mechanism of LIPUS stimulation application in diabetic gastroparesis rats. METHODS: In this study, Sprague-Dawley male rats were divided into three groups: control group (CON), diabetic gastroparesis group (DGP), and LIPUS-treated group (LIPUS). LIPUS irradiation was performed bilaterally at ST36 for 20 min per day for 4 weeks. The gastric emptying rate was measured by ultrasound examination. Contraction ability of GSMCs was assessed by muscle strip experiment. The expression of related proteins or mRNAs including α-SMA, SM22α, MHC, RhoA, Rock2, p-MYPT1, MYPT1, p-MLC, MLC, MALAT1, miR-449a, and DLL1 was detected by different methods such as western blotting, RT-qPCR, immunohistochemistry, and immunofluorescence staining, as appropriate. KEY RESULTS: (a) LIPUS stimulation at ST36 could improve the gastric motility dysfunction of diabetic rats. (b) LIPUS increased RhoA, Rock2, p-MYPT1, and p-MLC expression level. (c) MALAT1 and DLL1 contents were decreased, but the level of miR-449a was increased in the LIPUS group. CONCLUSIONS & INFERENCES: LIPUS may affect the contractile marker expression of gastric smooth muscle through the RhoA/Rock and MALAT1/miR-449a/DLL1 pathway to ameliorate DGP.
Subject(s)
Acupuncture Points , Diabetes Mellitus, Experimental , MicroRNAs , Muscle Contraction , Muscle, Smooth , RNA, Long Noncoding , Rats, Sprague-Dawley , Signal Transduction , Animals , Male , Rats , MicroRNAs/metabolism , MicroRNAs/genetics , Muscle, Smooth/metabolism , RNA, Long Noncoding/metabolism , RNA, Long Noncoding/genetics , Diabetes Mellitus, Experimental/metabolism , rho-Associated Kinases/metabolism , rho-Associated Kinases/genetics , Gastroparesis/metabolism , Gastroparesis/therapy , Ultrasonic Waves , rhoA GTP-Binding Protein/metabolism , Membrane Proteins/metabolism , Membrane Proteins/genetics , Stomach , Gastric Emptying/physiology , Ultrasonic Therapy/methods , Myocytes, Smooth Muscle/metabolism , rho GTP-Binding ProteinsABSTRACT
BACKGROUND AND AIM: To observe the clinical therapeutic effect and mental state of mindfulness-based cognitive therapy (MBCT) in patients with functional dyspepsia (FD). METHODS: In this study, 80 patients suffering from FD in an outpatient clinic were enrolled from January to December 2020. Patients were randomly allocated into the control group (conventional treatment) and observation group (MBCT treatment). Patients in the control group were prescribed rabeprazole and mosapiride, and patients in the observation group were given MBCT therapy in addition to the above drugs. After treatment for 8 weeks, the changes in gastrointestinal symptom scores, anxiety, depression, mindfulness and sleep quality and gastric emptying testing were compared between these two groups. RESULTS: The observation group showed strikingly lower gastrointestinal symptom scores, SAS, SDS, PSQI, and SCL-90 scale scores, and higher FFMQ scale scores than the control group (p < 0.05). There was no conspicuous change in gastric emptying monitoring (p > 0.05). CONCLUSIONS: MBCT therapy can improve patients' gastrointestinal symptoms, attenuate their anxiety and depression levels, and ameliorate their sleep quality.
Subject(s)
Anxiety , Cognitive Behavioral Therapy , Depression , Dyspepsia , Mindfulness , Humans , Dyspepsia/therapy , Dyspepsia/psychology , Female , Male , Mindfulness/methods , Adult , Middle Aged , Cognitive Behavioral Therapy/methods , Depression/therapy , Anxiety/therapy , Treatment Outcome , Gastric Emptying , Sleep QualityABSTRACT
Cannabinoids and their receptors play a significant role in the regulation of gastrointestinal (GIT) peristalsis and intestinal barrier permeability. This review critically evaluates current knowledge about the mechanisms of action and biological effects of endocannabinoids and phytocannabinoids on GIT functions and the potential therapeutic applications of these compounds. The results of ex vivo and in vivo preclinical data indicate that cannabinoids can both inhibit and stimulate gut peristalsis, depending on various factors. Endocannabinoids affect peristalsis in a cannabinoid (CB) receptor-specific manner; however, there is also an important interaction between them and the transient receptor potential cation channel subfamily V member 1 (TRPV1) system. Phytocannabinoids such as Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) impact gut motility mainly through the CB1 receptor. They were also found to improve intestinal barrier integrity, mainly through CB1 receptor stimulation but also via protein kinase A (PKA), mitogen-associated protein kinase (MAPK), and adenylyl cyclase signaling pathways, as well as by influencing the expression of tight junction (TJ) proteins. The anti-inflammatory effects of cannabinoids in GIT disorders are postulated to occur by the lowering of inflammatory factors such as myeloperoxidase (MPO) activity and regulation of cytokine levels. In conclusion, there is a prospect of utilizing cannabinoids as components of therapy for GIT disorders.