scholarly journals Prokinetics in the management of upper gastrointestinal motility disorders: an Indian expert opinion review

2021 ◽  
Vol 8 (9) ◽  
pp. 1442
Author(s):  
Ramesh Roop Rai ◽  
V. G. Mohan Prasad
Keyword(s):  
Delayed Gastric Emptying ◽  
Functional Gastrointestinal Disorders ◽  
Primary Concern ◽  
Motility Disorders ◽  
Expert Opinions ◽  
Indian Context ◽  
The Central Nervous System ◽  
Intestinal Motility Disorders ◽  
Upper Gastrointestinal ◽  
Gi Motility

Functional gastrointestinal disorders (FGIDs) are disorders of gut-brain interaction. Nearly 40% of individuals globally suffer from FGIDs and have chronic fluctuating symptoms. Of all GI conditions, 30-45% are referable to intestinal motility disorders. Prokinetics act by different mechanisms and are effective in FGIDs with delayed gastric emptying or postprandial distress. When choosing a prokinetic, safety is the primary concern, particularly with regard to the central nervous system and cardiovascular risk. Here, we review the efficacy and safety of prokinetics in functional GI motility disorders and provide expert opinions for the use of prokinetics to manage upper GI motility disorders in the Indian context. 

scholarly journals Efficacy of Sparex in the management of intestinal motility disorders

2016 ◽  
pp. 110-115
Author(s):  
E. P. Yakovenko ◽  
N. A. Agafonova ◽  
A. N. Ivanov ◽  
A. V. Yakovenko
Keyword(s):  
Intestinal Motility ◽  
Motility Disorders ◽  
Intestinal Motility Disorders

scholarly journals Role of estrogen and stress on the brain-gut axis

2019 ◽  
Vol 317 (2) ◽  
pp. G203-G209 ◽  
Author(s):  
Yanyan Jiang ◽  
Beverley Greenwood-Van Meerveld ◽  
Anthony C. Johnson ◽  
R. Alberto Travagli
Keyword(s):  
Functional Gastrointestinal Disorders ◽  
Clinical Problem ◽  
Visceral Sensitivity ◽  
Physiological Mechanisms ◽  
Acute And Chronic Stress ◽  
Highly Correlated ◽  
The Brain ◽  
Gi Motility

Symptoms of functional gastrointestinal disorders (FGIDs), including fullness, bloating, abdominal pain, and altered gastrointestinal (GI) motility, present a significant clinical problem, with a reported prevalence of 25%–40% within the general population. More than 60% of those affected seek and require healthcare, and affected individuals report a significantly decreased quality of life. FGIDs are highly correlated with episodes of acute and chronic stress and are increased in prevalence and reported severity in women compared with men. Although there is evidence that sex and stress interact to exacerbate FGID symptoms, the physiological mechanisms that mediate these sex-dependent disparities are incompletely understood, although hormonal-related differences in GI motility and visceral sensitivity have been purported to play a significant role in the etiology. In this mini review, we will discuss brain-gut axis control of GI motility and sensitivity, the influence of estrogen on GI motility and sensitivity, and stress modulation of the brain-gut axis.

Central Nervous System Processing of Human Visceral Pain in Health and Disease

Physiology ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 109-114 ◽  
Author(s):  
Anthony R. Hobson ◽  
Qasim Aziz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Visceral Pain ◽  
Functional Gastrointestinal Disorders ◽  
Functional Brain Imaging ◽  
Gastrointestinal Disorders ◽  
The Past ◽  
Body Of Knowledge ◽  
The Central Nervous System ◽  
Health And Disease

To understand the pathophysiology of anomalous pain in functional gastrointestinal disorders, we must increase our understanding of how the central nervous system processes visceral pain. Over the past decade, novel application of functional brain imaging and electrophysiological techniques has given us the opportunity to study these processes in humans, and this review summarizes the current body of knowledge.

scholarly journals Effect of Chaihu Shugan Powder-Contained Serum on Glutamate-Induced Autophagy of Interstitial Cells of Cajal in the Rat Gastric Antrum

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Ren-Qian Tan ◽  
Zhi Zhang ◽  
Jing Ju ◽  
Jiang-Hong Ling
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Interstitial Cells Of Cajal ◽  
Underlying Mechanism ◽  
Control Group ◽  
Motility Disorders ◽  
Transmission Electron ◽  
Cells Of Cajal ◽  
Bcl2 Expression ◽  
Gi Motility

Gastrointestinal (GI) motility disorder is caused by excessive autophagy of the interstitial cells of Cajal (ICC). Chaihu Shugan Powder (CSP) is a traditional Chinese medicine with therapeutic benefits in GI motility disorders; however, the underlying mechanism of its therapeutic effect in GI disorders, especially autophagy of ICC, remains unclear. Thus, this study investigated the effects of CSP-contained serum on glutamate-induced autophagy in rat gastric ICC, exploring its underlying mechanism. In vitro cultured rat stomach ICC were identified by fluorescence microscopy and then stimulated with glutamate (5 mmol/L) for 3 h to establish the autophagy model. These cells were then treated with 10% CSP-containing serum or the autophagy inhibitor 3-methyladenine (3-MA; 5 mmol/L) for 24 h. The control group was cultured with only 10% serum containing physiological saline. The viability of ICC was measured by the CCK-8 assay. The ultrastructure and autophagosomes of ICC were observed using transmission electron microscopy. LC3 expression was detected by immunofluorescence, and LC3, Beclin1, Bcl2, and PI3KC3 expression was detected by western blot analysis. Transmission electron microscopy showed abundant endoplasmic reticulum, mitochondria, and other organelles in the control group, whereas the cells in the autophagy model control group had clear autophagic vacuoles, which were not apparent in both CSP and 3-MA groups. ICC viability was significantly increased by CSP and 3-MA interventions (P < 0.01), accompanied by a decrease in LC3 fluorescence (P < 0.01). Moreover, the expression levels of LC3II/I, Beclin1, and PI3KC3 were significantly decreased (all P < 0.01) with CSP and 3-MA treatment, while Bcl2 expression level was higher than that of the model group (P < 0.01). Thus, CSP can reduce autophagic damage by enhancing Bcl2 expression and downregulating the expression of LC3, Beclin1, and PI3KC3 to protect ICC. These results highlight the potential of CSP in the treatment of GI motility disorders.

Surgical treatment and outcomes of severe pediatric intestinal motility disorders requiring parenteral nutrition

2013 ◽  
Vol 48 (2) ◽  
pp. 333-338 ◽  
Author(s):  
Mikko P. Pakarinen ◽  
Annika Kurvinen ◽  
Antti I. Koivusalo ◽  
Tarja Ruuska ◽  
Heikki Mäkisalo ◽  
...  
Keyword(s):  
Surgical Treatment ◽  
Parenteral Nutrition ◽  
Intestinal Motility ◽  
Motility Disorders ◽  
Intestinal Motility Disorders

scholarly journals Approaches to the Modulation of Abdominal Pain

1999 ◽  
Vol 13 (suppl a) ◽  
pp. 66A-70A ◽  
Author(s):  
Emeran A Mayer ◽  
Tony Lembo ◽  
Lin Chang
Keyword(s):  
Disease Model ◽  
Functional Gastrointestinal Disorders ◽  
Great Majority ◽  
Gastrointestinal Disorders ◽  
Dorsal Horn Neurons ◽  
Afferent Nerves ◽  
Calcitonin Gene ◽  
High Prevalence ◽  
The Central Nervous System ◽  
Neurokinin 1

Despite their high prevalence and significant economic impact on the health care system, functional gastrointestinal disorders have evaded successful therapy. Conventional medical therapies are based on inadequate disease models, and the great majority of published treatment trials are flawed in their design, permitting no conclusions to be drawn about the true efficacy of any particular treatment. During the past several years, a new, comprehensive disease model based on alterations in brain-gut interactions has rapidly evolved. Even though the precise mechanisms and sites underlying these alterations remain incompletely understood, plausible targets for the development of effective pharmacological treatments are receptors on peripheral terminals of visceral afferent nerves (opioids and serotonin), ion channels and receptors on dorsal horn neurons within the spinal cord (opioids, glutamate, calcitonin gene-related peptide and neurokinin-1), and supraspinal targets in the brainstem within the limbic system and in the prefrontal cortex (serotonin, catecholamines, dopamine and acetylcholine). Regardless of the primary pathophysiology underlying functional gastrointestinal disorders (ie, central versus peripheral), different pharmacological strategies targeted at different sites in the periphery or within the central nervous system may become effective therapies in the future.

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