Gastrointestinal Motility Disturbances Research Articles

Effects of Bifidobacterium lactis BLa80 on fecal and mucosal flora and stem cell factor/c-kit signaling pathway in simulated microgravity rats.

Simulated microgravity environment can lead to gastrointestinal motility disturbance. The pathogenesis of gastrointestinal motility disorders is closely related to the stem cell factor (SCF)/c-kit signaling pathway associated with intestinal flora and Cajal stromal cells. Moreover, intestinal flora can also affect the regulation of SCF/c-kit signaling pathway, thus affecting the expression of Cajal stromal cells. Cajal cells are the pacemakers of gastrointestinal motility. To investigate the effects of Bifidobacterium lactis (B. lactis) BLa80 on the intestinal flora of rats in simulated microgravity and on the gastrointestinal motility-related SCF/c-kit pathway. The internationally recognized tail suspension animal model was used to simulate the microgravity environment, and 30 rats were randomly divided into control group, tail suspension group and drug administration tail suspension group with 10 rats in each group for a total of 28 days. The tail group was given B. lactis BLa80 by intragastric administration, and the other two groups were given water intragastric administration, the concentration of intragastric administration was 0.1 g/mL, and each rat was 1 mL/day. Hematoxylin & eosin staining was used to observe the histopathological changes in each segment of the intestine of each group, and the expression levels of SCF, c-kit, extracellular signal-regulated kinase (ERK) and p-ERK in the gastric antrum of each group were detected by Western blotting and PCR. The fecal flora and mucosal flora of rats in each group were detected by 16S rRNA. Simulated microgravity resulted in severe exfoliation of villi of duodenum, jejunum and ileum in rats, marked damage, increased space between villi, loose arrangement, shortened columnar epithelium of colon, less folds, narrower mucosal thickness, reduced goblet cell number and crypts, and significant improvement after probiotic intervention. Simulated microgravity reduced the expressions of SCF and c-kit, and increased the expressions of ERK and P-ERK in the gastric antrum of rats. However, after probiotic intervention, the expressions of SCF and c-kit were increased, while the expressions of ERK and P-ERK were decreased, with statistical significance (P < 0.05). In addition, simulated microgravity can reduce the operational taxonomic unit (OTU) of the overall intestinal flora of rats, B. lactis BLa80 can increase the OTU of rats, simulated microgravity can reduce the overall richness and diversity of stool flora of rats, increase the abundance of firmicutes in stool flora of rats, and reduce the abundance of Bacteroides in stool flora of rats, most of which are mainly beneficial bacteria. Simulated microgravity can increase the overall richness and diversity of mucosal flora, increase the abundance of Bacteroides and Desulphurides in the rat mucosal flora, and decrease the abundance of firmicutes, most of which are proteobacteria. After probiotics intervention, the overall Bacteroidetes trend in simulated microgravity rats was increased. B. lactis BLa80 can ameliorate intestinal mucosal injury, regulate intestinal flora, inhibit ERK expression, and activate the SCF/c-kit signaling pathway, which may have a facilitating effect on gastrointestinal motility in simulated microgravity rats.

Effects of Repeated Cisplatin and Monosodium Glutamate on Visceral Sensitivity in Rats.

Cisplatin, a chemotherapeutic drug, is known for causing gastrointestinal disorders and neuropathic pain, but its impact on visceral sensitivity is unclear. Monosodium glutamate (MSG) has been shown to improve gastrointestinal dysmotility and neuropathic pain induced by cisplatin in rats. This study aimed to determine if repeated cisplatin treatment alters visceral sensitivity and whether dietary MSG can prevent these changes. Male Wistar HAN rats were treated with saline or cisplatin (2 mg/kg/week, ip) for 5 weeks, and visceral sensitivity to intracolonic mechanical stimulation was recorded after the final cisplatin administration (week 5) and one-week post-treatment (week 6). In a second cohort, rats treated with cisplatin or saline also received MSG (4 g/L) in their drinking water, and visceral sensitivity was evaluated on week 6. Finally, the untouched distal colon was obtained from a third cohort of animals one week after treatment to assess immunocyte infiltration. Cisplatin significantly increased colonic mechanical sensitivity on week 6 but not on week 5. MSG did not prevent cisplatin-induced visceral hypersensitivity on week 6 and even exacerbated it. On week 6, compared with the control, cisplatin (with or without MSG) did not modify the colonic infiltration of eosinophils, macrophages, neutrophils, or mast cells. Although MSG seems to be useful in ameliorating some of the adverse effects of cisplatin, such as gastrointestinal motility disturbances or neuropathic pain, it does not alleviate visceral pain.

Segmental regulation of intestinal motility by colitis and the adaptive immune system in the mouse ileum and colon.

Gastrointestinal motility disturbances are a hallmark of inflammatory bowel disease (IBD); however, their mechanisms remain unclear. This study utilized a dextran sulfate sodium (DSS)-induced colitis mouse model, deficient in mature B and T lymphocytes, to assess intestinal motility and the role of the adaptive immune system in health and IBD. In healthy mice, the absence of adaptive lymphocytes reduced acetylcholine (ACh) sensitivity in the ileum. During colitis, it decreases motility by reducing the intensity and frequency of spontaneous contractions while increasing cholinergic responsiveness. In the proximal colon, adaptive immunity deficiency led to increased contractility and reduced ACh sensitivity in homeostasis, while colitis reduced contractile capacity. In the mid-colon, immune-deficient mice have reduced ACh sensitivity in homeostasis and exacerbated contractile responses during colitis. In the distal colon, adaptive immunity loss reduced contractility in health and cholinergic responsiveness during colitis. These motility alterations were associated with altered acetylcholinesterase and M2/M3 muscarinic receptor expression. Notably, adaptive lymphocyte deficiency resulted in reduced tissue damage and lower TNF-α expression in the colon during colitis paralleling intestinal motility changes. Overall, the adaptive immune system critically regulates motility and inflammation across different intestinal segments in IBD.

Alterations in gastrointestinal motility assessed by high-resolution antroduodenal manometry in patients with severe disorders of gut-brain interaction.

Data are limited regarding gastrointestinal motility disturbance in disorders of gut-brain interaction (DGBI). This study aimed to characterize antroduodenal motor alterations in patients with high-resolution antroduodenal manometry (HR-ADM). HR-ADM was performed in patients with severe DGBI and compared with healthy volunteers (HV). HR-ADM used a commercially available probe composed of 36 electronic sensors spaced 1 cm apart and positioned across the pylorus. Antral and duodenal motor high-resolution profiles were analyzed, based on the frequency, amplitude, and contractile integral/sensor (CI/s) calculated for each phase of the migrating motor complex (MMC). Eighteen HV and 64 patients were investigated, 10 with irritable bowel syndrome (IBS), 24 with functional dyspepsia (FD), 15 with overlap IBS-FD, and 15 with other DGBI. Compared with HV, patients had a lower frequency of phase II duodenal contractions (27 vs. 51 per hour; P = 0.002) and a lower duodenal phase II contraction amplitude (70 vs. 100 mmHg; P = 0.01), resulting in a lower CI/s of phase II (833 vs. 1,901 mmHg·cm·s; P < 0.001) in the duodenum. In addition, the frequency of phase II propagated antroduodenal contractions was lower (5 vs. 11 per hour; P < 0.001) in patients compared with HV. Interestingly, the antral CI/s of phase III was decreased in FD patients but not in IBS patients. Patients with severe DGBI display alterations in antral and intestinal motility assessed by commercially available HR-ADM. Whether these alterations may explain symptom profiles in such patients remains to be confirmed (NCT04918329 and NCT01519180).NEW & NOTEWORTHY Gastrointestinal dysmotility has been assessed poorly in disorders of gut-brain interaction (DGBI), especially with high-resolution antroduodenal manometry. Plots of DGBI patients showed lower duodenal contractions during phase II regarding amplitude, frequency, and contractile integral/sensor (CI/s) compared with healthy volunteers. A lower frequency of propagated antroduodenal contractions was also reported. Finally, antral CI/s was lower in patients with functional dyspepsia during phase III. Further studies are needed to assess the clinical significance of these alterations.

Анестетик лідокаїн пригнічує холінергічні скорочення тонкої кишки миші та спричиняє порушення шлунково-кишкового тракту людини

Lidocaine is one of the components of multimodal low-opioid anesthesia, which is commonly used in surgical procedures, especially in cardiac surgery. Lidocaine has been used in medicine for a long time as a local anesthetic, but after the invention of the method of its intravenous administration, questions arose about its possible side effects on the visceral system, in particular on the motility of the gastrointestinal tract. Therefore, the aim of our work was to investigate the main aspects of the use of lidocaine-based opioid-free anesthesia and its side effects and also to study the effect of lidocaine on the contractile activity of small intestine smooth muscle, namely the mouse ileum. We recorded the contractile activity of smooth muscles of the ileum of mice using the tensiometry method and found that lidocaine at the clinically relevant concentration range, i.e. 1.5, 3, and 5 μg/ml, inhibited carbachol-induced contractions by 16, 27 and 37%, respectively (n = 7). To determine the side effects of opioid-free anesthesia, we studied 60 patients with coronary artery disease undergoing coronary artery stenting with the administration of anesthesia based on lidocaine solution at different concentrations (1 and 2 mg/kg). The side effects included nausea and vomiting, which may indicate а disturbance of gastrointestinal motility, as well as numbness of the limbs, cheeks, tongue, etc. These results contribute to a better understanding of the spectrum of action of lidocaine, a popular anesthetic in surgery, on the visceral system and become an important basis for the future development of new schemes for the use of local anesthetics in clinical practice, particularly in surgical procedures.

Effects of Banxia Xiexin Decoction on apoptosis of interstitial cells of Cajal via regulation of MiR-451-5p: An in vivo and in vitro study

Ethnopharmacological relevanceBanxia Xiexin Decoction (BXD) is a traditional Chinese medical formula applied to gastrointestinal (GI) motility disorders. Previous studies showed that miR-451-5p was down-regulated in rats with GI motility disorders induced by gastric electrical dysrhythmia. Interstitial cells of Cajal (ICCs) are pacemakers for GI motility, while loss of ICCs is responsible for GI motility disturbance. Thus, the underlying interaction mechanisms for BXD regulating ICCs apoptosis via miR-451-5p remain to be explored. Aim of the studyIn this work, the main objectives were to examine the efficacy of BXD on ICCs via miR-451-5p both in GI motility disorders rats model and in vitro, as well as the potential contributions of SCF/c-kit signaling. Materials and methodsRats with gastric electrical dysrhythmia were established in male SD rats by using a single-day diet and a double fasting method (drinking diluted hydrochloric acid water during the period) for 4 weeks. The gastric slow wave (GSW) recording, RT-qPCR, and western blot were performed to examine the effects of BXD on ICCs apoptosis in rats with GED and miR-451-5p expression. In vitro assays included CCK-8, flow cytometry analysis, RT-qPCR, and western blot were applied to investigate the potential molecular mechanism of BXD on ICCs apoptosis via miR-451-5p. ResultsBXD promoted gastric motility, reduced ICCs apoptosis, and elevated miR-451-5p in GED rats. In addition, miR-451-5p was significantly up-regulated in ICCs after BXD treatment compared with that in ICCs with miR-451-5p inhibitor transfection. Meanwhile, high miR-451-5p expression with either BXD treatment or miRNA mimics enhanced ICCs proliferation and inhibit apoptosis. Moreover, overexpression of miR-451-5p can reverse G0/G1 arrest in ICCs by BXD treatment. Further, SCF and c-kit protein levels were detected to demonstrate that modulation of miR-451-5p by BXD treatment was involved in this signaling. ConclusionsThrough this study, we demonstrated that BXD could promote ICCs proliferation and inhibit apoptosis via miR-451-5p and may involve the modulations of SCF/c-kit signaling, thus suggesting a new therapy basis for GI motility dysfunction from the perspective of modulation of ICCs apoptosis by targeting miR-451-5p.

Colostomy as a definitive treatment in an ALS patient with acute colonic Pseudo-obstruction refractory to medical management, a case report

BackgroundAmyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease, and ALS patients may experience disturbed gastrointestinal motility often resulting in acute colonic pseudo-obstruction (ACPO). There is currently a paucity in the literature to guide the treatment of patients with both ALS and ACPO.Case presentationHere we describe a 39-year-old male patient with advanced ALS who developed ACPO. His condition was refractory to both medical and procedural managements including polyethylene glycol, senna, and docusate suppository, metoclopramide, linaclotide, erythromycin, prucalopride, neostigmine, and repeated colonoscopies. He ultimately underwent successful colostomy for palliation. Here we report the peri-operative multidisciplinary approach taken with this case, the surgical procedures, the potential risks, and the outcome.ConclusionThe patient is delighted with the result and requested publication of this case to raise awareness of constipation in ALS patients and promote the consideration of colostomy as a treatment option for patients with ileus resistant to conservative management. Ultimately, a multidisciplinary team approach is required to properly assess the risks and benefits to achieve good clinical outcomes.

Disorders of Gastrointestinal Motility in Diabetes Mellitus: An Unattended Borderline Between Diabetologists and Gastroenterologists

Gastrointestinal (GI) symptoms represent an important and often poorly appreciated reason of morbidity in diabetes mellitus. Diabetes can affect nearly all parts of the GI tract; however, data on the prevalence of ‘diabetic gastroenteropathy’ are inconsistent. The significance of disturbed GI motility in diabetes across the patient spectrum and pathophysiological basis also remain inadequately defined. Fluctuating glucose levels, altered drug pharmacokinetics, variable absorption of nutrients, and impaired quality of life are important consequences of GI dysfunction. Diabetic gastroparesis is the best characterised manifestation of GI motility disorder in diabetes. Since there is a poor correlation between subjective GI symptoms and objective motility findings, a diagnosis of delayed emptying in diabetes requires a proper measurement of gastric emptying. There are fewer studies on intestinal motility in diabetes than those on the stomach. Several established modalities exist for the assessment of gastroenteropathy but the lack of standardisation, exposure to radiation, advanced data interpretation, and high cost limit their widespread use. While existing therapeutic choices for the management of diabetic gastroenteropathy are suboptimal, many potential novel agents are in progress. Both endocrinology and gastroenterology specialties working together will facilitate screening and treating patients with diabetes and GI dysmotility.

Intestinal microbiome: role in functional gastrointestinal disorders and contemporary diagnostic options

The most common problems that paediatricians and paediatric gastroenterologists encounter in their practice include functional gastrointestinal disorders. These are a group of chronic and/or recurrent conditions caused by any combination of gastrointestinal motility disturbances and visceral hypersensitivity with abnormal processing of stimuli in the central nervous system which manifest with abdominal pain, nausea and vomiting or disorders of defecation, among other problems. The symptoms cannot be assigned to any other clinical condition despite proper diagnostic investigation. The aetiology of functional gastrointestinal disorders is multifactorial. Recently, the role of the intestinal microbiota as an important environmental factor in the pathogenesis of such disorders has been investigated. In this article, the latest data regarding the composition of the microbiome (a collection of microbiota genes) of the human gastrointestinal tract are discussed and the methods used to determine it in detail are described. Currently, molecular biology techniques have the highest diagnostic value, which are based on genetic material sequencing. Due to their extraordinary efficacy, they are superseding classic microbiological tests. In addition, the publication presents factors which affect the composition of the gastrointestinal microbiome. These include, for example, mode of birth, method of infant feeding, diet at later stages of life, place of residence, physical activity and antibiotics intake. The research to date demonstrated that dysbiosis is one of the factors contributing to the pathogenesis of many diseases, including irritable bowel syndrome. Attempts at modifying the composition of the microbiome by, for example, the administration of probiotics, should therefore have a distinctly positive effect on patients with functional gastrointestinal disorders.

Pharmacomagnetography to evaluate the performance of magnetic enteric-coated tablets in the human gastrointestinal tract

A magnetic enteric-coated tablet containing diclofenac sodium was produced, and its performance under physiological and disturbed gastrointestinal motility was assessed through pharmacomagnetography analysis. In vitro studies were performed using conventional methods and in vivo studies were conducted on healthy volunteers before (control) and after domperidone administration. The magnetic tablet's gastrointestinal (GI) transit and disintegration process were monitored using the Alternating Current Biosusceptometry sensors combined with drug plasmatic concentration. The Gastric Residence Time, Colon Arrival Time, Small Bowel Transit Time, Disintegration Time and the pharmacokinetics parameters were calculated. The pH-dependent polymers used to coat the magnetic tablets were able to avoid the premature drug release on gastric or small intestine simulated medium. Gastric Residence Time was accelerated compared with the control group (p < 0.01). No significant differences were found regarding small bowel transit, colon arrival, disintegration process, or pharmacokinetics parameters. A strong correlation between magnetic monitoring and pharmacokinetics parameters analysis was determinant to evaluate the efficiency in the drug delivery at a specific site in the human gastrointestinal tract. In addition, a tablet with a damaged coating was used as a proof of concept to show the suitability of our methodology to evaluate the tablet. Our study showed that pharmacomagnetography is a multi-instrumental approach towards assessing drug delivery and bioavailability.

Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress.

Central injection of corticotrophin-releasing factor (CRF) mimics the effect of stress on gastrointestinal (GI) responses, including inhibition of GI motility. This study was designed to explore the effects of electroacupuncture (EA) on disordered jejunal motility in a rat model of stress induced by intracisternal (IC) injection of CRF. A stress model was established by IC injection of CRF in Sprague-Dawley rats. GI motility was evaluated by assessing gastric emptying (GE), gastrointestinal transit (GIT) and jejunal motility in vivo. EA was performed at ST36. The functional roles of CRF receptor subtype 1 and subtype 2 (CRFr1 and CRFr2) were examined by IC administration of the corresponding selective CRF antagonists. Protein expression of CRFr1 and CRFr2 in the hypothalamus and jejunum was detected by Western blotting. IC injection of CRF significantly inhibited GE, GIT and jejunal motility. EA treatment remarkably improved the disturbed GI motility. Intriguingly, the disordered jejunal motility induced by central CRF was abolished by IC injection of a selective CRFr2 antagonist, indicating the essential role of central CRFr2 in mediating the stress-induced jejunal motor disorder. EA at ST36 decreased central and peripheral expression of CRFr2, which might be one of the potential mechanisms underlying the beneficial effect of EA on jejunal dysmotility in this rat model of stress. This study suggested that EA at ST36 could ameliorate disordered jejunal motility induced by stress, and that this might be associated with the down-regulation of CRFr2.

Sex‐Differences in Gastric Smooth Muscle Function: Role of G Protein‐Coupled Estrogen Receptor

The regulation of gastrointestinal (GI) motility by estrogen and its receptors has been a topic of great interest owing to sexual dimorphism that exists in motility disorders. Scientific and clinical evidence establishes the fact of GI motility disturbances during estrous cycle but, there is a gap in the knowledge and understanding of estrogen and its receptors role in GI motility physiology during these cycles. Estrogen activates classical nuclear receptors ERα, ERβ and atypical 7‐transmembrane G protein‐coupled estrogen receptor (GPER or GPR30) to initiate both genomic and non‐genomic effects. GPER is involved in the several rapid cellular signaling events. The pleiotropic effects manifested by GPER action include regulation of body weight, glucose homeostasis, anti‐inflammation, anti‐nociception, and vascular muscle relaxation. Ablation of GPER leads to increase in mean arterial pressure in female mice, whereas treatment with GPER‐specific agonist G‐1 lowers arterial blood pressure in hypertensive and ovariectomized female rats. The role of GPER in mediating estrogen effects on GI smooth muscle is unknown.AimTo understand the role of GPER in gastric smooth muscle function in male and female mice.MethodsMuscle strips and muscle cells were isolated from the stomachs of control and GPER knockout mice. Expression of GPER was analyzed by qRT‐PCR and western blot. cAMP levels in response to estrogen and G‐1 was measured by radioimmunoassay. Relaxation was measured in organ bath studies in muscle strips and by scanning micrometry in isolated muscle cells.ResultsExpression of GPER (mRNA and protein) in the gastric smooth muscle was higher in female mice compared to male mice. 17β‐estradiol and G‐1 caused an increase in cAMP levels and inhibited acetylcholine‐induced muscle contraction (i.e., caused muscle relaxation) in gastric muscle strips and isolated muscle cells from both female and male mice, however, the increase in cAMP levels and the amount of relaxation was significantly greater in gastric muscle from female mice compared to male mice. The effect of 17β‐estradiol and G‐1 on muscle relaxation was concentration‐dependent. Relaxation was blocked by the GPER specific antagonist G15 (10 μM) in gastric muscle from control mice and absent in gastric muscle from GPER knockout mice. Relaxation was higher in proestrus and estrus phases compared to diestrus phase in female mice and this is consistent with higher expression of GPER in proestrus and estrus phases compared to diestrus phase.ConclusionActivation of GPER causes relaxation via cAMP/PKA pathway in gastric smooth muscle from female and male mice. Greater relaxation in gastric smooth muscle from female mice is due to higher expression of GPER in female mice compared to male mice. Pilot studies suggests that higher expression of GPER in the stomach of female mice is due to differential regulation of GPER expression by epigenetic mechanisms.Support or Funding InformationSupported by grants from VETAR (SM); IACUC approval AD10001201

Opioid utility function: methods and implications.

Opioids are complex drugs that produce profit (most importantly analgesia) as well as a myriad of adverse effects including gastrointestinal motility disturbances, abuse and addiction, sedation and potentially lethal respiratory depression (RD). Consequently, opioid treatment requires careful evaluation in terms of benefit on the one hand and harm on the other. Considering benefit and harm from an economic perspective, opioid treatment should lead to profit maximization with decision theory defining utility as (profit - loss). We here focus on the most devastating opioid adverse effect, RD and define opioid utility U = P(benefit) - P(harm), where P(benefit) is the probability of opioid-induced analgesia and P(harm) the probability of opioid-induced RD. Other utility functions are also discussed including the utility U = P(benefit AND NOT harm), the most wanted opioid effect, i.e., analgesia without RD, and utility surfaces, which depict the continuum of probabilities of presence or absence of analgesia in combination with the presence or absence of RD. Utility functions are constructed from pharmacokinetic and pharmacodynamic data sets, although pragmatic utility functions may be constructed when pharmacokinetic data are not available. We here discuss utilities of several opioids including the partial mu-opioid-receptor agonist buprenorphine, the full opioid receptor agonists fentanyl and alfentanil, and the bifunctional opioid cebranopadol, which acts at mu-opioid and nociception/orphanin FQ-receptors. We argue that utility functions give clinicians the opportunity to make an informed decision when opioid analgesics are needed for pain relief, in which opioids with a positive utility function are preferred over opioids with negative functions. Furthermore, utility functions of subpopulations will give an extra insight as a utility functions measured in one subgroup (e.g., patients with postoperative pain, good opioid responders) may not be mirrored in other patient subgroups (e.g., neuropathic pain patients, poor opioid responders).

Abnormal gut motility in inflammatory bowel disease: an update.

There is substantial evidence linking disturbed gastrointestinal motility to inflammation. Thus, it is not surprising that abnormalities of gastrointestinal motility play a role in inflammatory bowel disease (IBD), affecting patient outcomes. We performed a review of the literature to investigate the relationship between abnormal gut motility and IBD. With an extensive literature search, we retrieved the pertinent articles linking disturbed gut motility to IBD in various anatomical districts. The evidence in the literature suggests that abnormal gastrointestinal motility plays a role in the clinical setting of IBD and may confuse the clinical picture. Abnormal gut motility may be important in the clinical setting of IBD. However, additional data obtained with modern techniques (e.g., magnetic resonance imaging) are needed to individuate in a more precise manner gastrointestinal motor dysfunctions, to understand the nature of clinical manifestations and properly tailor the treatment of patients.

Nitrergic Enteric Neurons in Health and Disease-Focus on Animal Models.

Nitrergic enteric neurons are key players of the descending inhibitory reflex of intestinal peristalsis, therefore loss or damage of these neurons can contribute to developing gastrointestinal motility disturbances suffered by patients worldwide. There is accumulating evidence that the vulnerability of nitrergic enteric neurons to neuropathy is strictly region-specific and that the two main enteric plexuses display different nitrergic neuronal damage. Alterations both in the proportion of the nitrergic subpopulation and in the total number of enteric neurons suggest that modification of the neurochemical character or neuronal death occurs in the investigated gut segments. This review aims to summarize the gastrointestinal region and/or plexus-dependent pathological changes in the number of nitric oxide synthase (NOS)-containing neurons, the NO release and the cellular and subcellular expression of different NOS isoforms. Additionally, some of the underlying mechanisms associated with the nitrergic pathway in the background of different diseases, e.g., type 1 diabetes, chronic alcoholism, intestinal inflammation or ischaemia, will be discussed.

Role of Gut Microbiota-Gut Hormone Axis in the Pathophysiology of Functional Gastrointestinal Disorders.

Gut microbiota exert a pivotal influence on various functions including gastrointestinal (GI) motility, metabolism, nutrition, immunity, and the neuroendocrine system in the host. These effects are mediated by not only short-chain fatty acids produced by microbiota but also gut hormones and inflammatory signaling by enteroendocrine and immune cells under the influence of the microbiota. GI motility is orchestrated by the enteric nervous system and hormonal networks, and disturbance of GI motility plays an important role in the pathophysiology of functional gastrointestinal disorders (FGIDs). In this context, microbiota-associated mediators are considered to act on specific receptors, thus affecting the enteric nervous system and, subsequently, GI motility. Thus, the pathophysiology of FGIDs is based on alterations of the gut microbiota/gut hormone axis, which have crucial effects on GI motility.

Pseudo-obstruction intestinale chronique de l’adulte

Chronic intestinal pseudo-obstruction is a rare disease stemming from numerous causes characterized by disturbances in gastrointestinal motility. Symptomatology is often misleading and topography is variable, thus putting the clinician in serious difficulty. Diagnosis is based on a body of arguments, ranging from the clinical examination to surgical biopsies in expert centers. Treatment is non-consensual and mostly symptomatic. It is based on the use of prokinetics and optimal nutritional support. In the most serious cases, surgery can be required. The etiological treatment should be that of the causal disease when it exists and when the etiology is identified. Results of such treatment are variable. Chronic intestinal pseudo-obstruction is a disease which remains poorly understood. Progress had been made in terms of diagnosis and treatment but it seems obvious that a better comprehension of physiopathological mechanisms is necessary in order to improve our practice.

Effects of Pacifier Use on Transition Time from Gavage to Breastfeeding in Preterm Infants: A Randomized Controlled Trial.

Nonnutritive sucking (NNS) has been identified as having many benefits for preterm infants. NNS may improve the efficacy of oral feeding, reduce the length of time spent in orogastric (OG) tube feeding, and shorten the length of hospital stays for preterm infants. This study aimed to assess the effect of pacifiers on preterm infants in the transition from gavage to oral feeding, their time to discharge, weight gain, and time for transition to full breastfeeding. A prospective, randomized controlled trial was conducted in our center. Ninety infants were randomized into two groups: a pacifier group (PG) (n = 45) and a control group (n = 45). Eligibility criteria included body weight less than or equal to 1,500 g, gestational age (GA) younger than 32 weeks, tolerating at least 100 kcals/kg/day by OG feeding, growth parameters appropriate for GA, and a stable clinical condition. Mean GAs were 29.2 ± 1.86 versus 28.4 ± 1.84 weeks (p = 0.46), and birth weights were 1,188.2 ± 272 versus 1,112.8 ± 267 g (p = 0.72) in the PG and CG groups, respectively. The time for transition to full oral feeding (38 ± 19.2 days), time to transition to full breastfeeding (38.1 ± 20 days), and time to discharge (48.4 ± 19.2 days) in the PG were significantly shorter compared with the control group (49.8 ± 23.6, 49.1 ± 22, 65.3 ± 30.6 days, respectively) (p < 0.05). For preterm infants with gastrointestinal motility disturbance, similar symptoms (regurgitation, vomiting, abdominal distension) (n = 6, 22%) in the PG were significantly lower than the control group (n = 21, 77.8%) (p < 0.05). In this study, we determined that the method of giving pacifiers to preterm infants during gavage feeding reduced the infants' transition period to oral feeding and the duration of hospital stay. In addition, the pacifiers could be used during gavage feeding and in the transition from gavage to oral/breastfeeding in preterm infants to encourage the development of sucking ability.

Pain therapy in intensive care patients

After intensive care unit (ICU) treatment, the recollection of experienced pain is one of the most burdensome aftermaths. In addition, pain has several negative physiological consequences. The majority of patients report moderate to severe pain while being treated on an ICU, often caused by diagnostic or therapeutic procedures. Pain and its functional consequences during ICU treatment should therefore be systematically recorded and treated. Due to their high analgesic potency, pharmacological pain therapy focuses on opioids; however, gastrointestinal motility disturbance and development of tolerance are disadvantages. When applying non-opioids, such as non-steroidal anti-inflammatory drugs (NSAID) and paracetamol, attention should be paid to their possible organ toxicity. Ketamine and α2-antagonists can complement the analgesic concept. Analogous to its perioperative administration, intravenous lidocaine in intensive care seems acceptable because of a favorable impact on opioid requirements and gastrointestinal motility. When using regional anesthesia the positive therapeutic effect and the possible complications need to be carefully weighed. Non-pharmaceutical procedures, especially transcutaneous electrical nerve stimulation (TENS), have proven successful in postoperative pain management. Even if only limited data from intensive care are available, atherapeutic attempt seems justifiable because of the low risk of complications.

Intravenous citrulline generation test to assess intestinal function in intensive care unit patients.

BackgroundAssessment of a quantifiable small intestinal function test is cumbersome. Fasting citrulline concentrations have been proposed as a measure of enterocyte function and elaborated into a citrulline generation test (CGT), which is applicable only when glutamine is administered orally. CGT is an oral test, limiting its use, for example, in critically ill patients.ObjectiveAssessment of normative values and feasibility of an intravenously performed CGT in intensive care unit (ICU) patients with presumed gastrointestinal motility disturbances, especially when performed intravenously.DesignCGT reference values were determined in 16 stable ICU patients using two different CGT methods, namely following either enteral or intravenous glutamine administration and both with simultaneous arterial and venous plasma citrulline sampling at six time-points. Plasma amino acid analysis was performed using reverse-phase high-performance liquid chromatography.ResultsThe median total generation of citrulline in 90 min (CGT iAUCT90) was markedly higher with arterial citrulline sampling compared with venous citrulline sampling, being 724±585 and 556±418 µmol/L/min for enteral glutamine, respectively (p=0.02) and 977±283 and 769±231 µmol/L/min for intravenous glutamine, respectively (p=0.0004). The median slope (time-dependent increase) for plasma arterial and venous citrulline during the CGT was 0.20±0.16 and 0.18±0.12 µmol/L/min for enteral glutamine, respectively (p=0.004) and 0.22±0.16 and 0.19±0.05 µmol/L/min for intravenous glutamine, respectively (p=0.02).ConclusionIntravenous glutamine administration combined with arterial plasma citrulline sampling yielded the least variation in CGT characteristics in stable ICU patients. A 2-point measurement test had comparable test characteristics as a 6-point measurement CGT and seems promising.