The relationship between gastric motility and nausea: Gastric prokinetic agents as treatments

Sanger, Gareth J.; Broad, John; Andrews, Paul

doi:10.1016/j.ejphar.2013.06.031

Cited by 53 publications

(33 citation statements)

References 50 publications

(48 reference statements)

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“…It may also exert an antiemetic effect through its prokinetic properties within the GI tract itself, potentially mediated through antagonism of D 2 receptors and agonism of 5-HT 4 receptors (Sanger et al, 2013; Tonini et al, 1995). Metoclopramide, given in doses of 10 mg, has been shown to an effective prophlaxis against PONV (Carlisle and Stevenson, 2006; De Oliveira et al, 2012).…”

Section: Pharmacological Therapiesmentioning

confidence: 99%

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting

Horn¹,

Wallisch²,

Homanics³

et al. 2014

European Journal of Pharmacology

188

130

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Clinical research shows that postoperative nausea and vomiting (PONV) is caused primarily by the use of inhalational anesthesia and opioid analgesics. PONV is also increased by several risk predictors, including a young age, female sex, lack of smoking, and a history of motion sickness. Genetic studies are beginning to shed light on the variability in patient experiences of PONV by assessing polymorphisms of gene targets known to play roles in emesis (serotonin type 3, 5-HT3; opioid; muscarinic; and dopamine type 2, D2, receptors) and the metabolism of antiemetic drugs (e.g., ondansetron). Significant numbers of clinical trials have produced valuable information on pharmacological targets important for controlling PONV (e.g., 5-HT3 and D2), leading to the current multi-modal approach to inhibit multiple sites in this complex neural system. Despite these significant advances, there is still a lack of fundamental knowledge of the mechanisms that drive the hindbrain central pattern generator (emesis) and forebrain pathways (nausea) that produce PONV, particularly the responses to inhalational anesthesia. This gap in knowledge has limited the development of novel effective therapies of PONV. The current review presents the state of knowledge on the biological mechanisms responsible for PONV, summarizing both preclinical and clinical evidence. Finally, potential ways to advance the research of PONV and more recent developments on the study of postdischarge nausea and vomiting (PDNV) are discussed.

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Section: Pharmacological Therapiesmentioning

confidence: 99%

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting

Horn¹,

Wallisch²,

Homanics³

et al. 2014

European Journal of Pharmacology

188

130

View full text Add to dashboard Cite

show abstract

“…However, other physiological changes may be associated with the pre-emetic stress response, including alterations in heart rate variability (Doweck et al, 1997; Kim et al, 2011; Kim et al, 2005) and a release of vasopressin from the posterior pituitary (Fisher et al, 1982; Robertson, 1976; Rowe et al, 1979; Sorensen et al, 1985). Along with these physiological responses are a number of perceptions with accompanying behavioral changes (Graybiel et al, 1968; Muth et al, 1996), including an awareness that stomach emptying is imminent, loss of appetite (Farmer et al, 2015; Heer et al, 2006; Hiura et al, 2012; Lackner, 2014; Sanger et al, 2013), anxiety and foreboding (Coelho et al, 2015; Fox et al, 1988; Lackner, 2014; Tarbell et al, 2014), as well as lethargy and disinterest in engaging in routine activities (Graybiel et al, 1976; Lackner, 2014; Lawson et al, 1998; Matsangas et al, 2014; Van Ombergen et al, 2015). The latter disengagement responses were first documented by Graybiel (Graybiel et al, 1976), and later described by others, who referred to them as the “sopite syndrome” (Graybiel et al, 1976; Lackner, 2014; Lawson et al, 1998; Matsangas et al, 2014; Van Ombergen et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

What is nausea? A historical analysis of changing views

Balaban

Yates

2017

Autonomic Neuroscience

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The connotation of “nausea” has changed across several millennia. The medical term ‘nausea’ is derived from the classical Greek terms ναυτια and ναυσια, which designated the signs and symptoms of seasickness. In classical texts, nausea referred to a wide range of perceptions and actions, including lethargy and disengagement, headache (migraine), and anorexia, with an awareness that vomiting was imminent only when the condition was severe. However, some recent articles have limited the definition to the sensations that immediately precede emesis. Defining nausea is complicated by the fact that it has many triggers, and can build-up slowly or rapidly, such that the prodromal signs and symptoms can vary. In particular, disengagement responses referred to as the “sopite syndrome” are typically present only when emetic stimuli are moderately provocative, and do not quickly culminate in vomiting or disengagement from the triggering event. This review considers how the definition of “nausea” has evolved over time, and summarizes the physiological changes that occur prior to vomiting that may be indicative of nausea. Also described are differences in the perception of nausea, as well as the accompanying physiological responses, that occur with varying stimuli. This information is synthesized to provide an operational definition of nausea.

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“…Two main pathways may be involved in drug‐induced nausea and vomiting/pica: direct activation, by circulating drugs, of neurons within the area postrema (without blood‐brain barrier and known as the chemoreceptor trigger zone); activation of vagal afferents located in the stomach and small intestine, sensitive to distension and to the chemical nature of the luminal environment. Distension of the gastric antrum and duodenum, and dysrhythmic gastric movements can induce nausea and vomiting but paradoxically, gastric motor quiescence is also associated with nausea . Inhibition of gastric motility (with relaxation of the proximal stomach, gastric dysrhythmia, and delayed gastric emptying) has been included amongst the physiological changes often referred to as “prodromata of vomiting” .…”

Section: Discussionmentioning

confidence: 99%

Radiographic dose‐dependency study of loperamide effects on gastrointestinal motor function in the rat. Temporal relationship with nausea‐like behavior

Vera

Girón

Martín-Fontelles

et al. 2019

Neurogastroenterology Motil

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Background Loperamide is a potent mu opioid receptor agonist available over the counter to treat diarrhea. Although at therapeutic doses loperamide is devoid of central effects, it may exert them if used at high doses or combined with drugs that increase its systemic and/or central bioavailability. Recently, public health and scientific interest on loperamide has increased due to a growing trend of misuse and abuse, and consequent reports on its toxicity. Our aim was to evaluate in the rat the effects of increasing loperamide doses, with increasing likelihood to induce central effects, on gastrointestinal motor function (including gastric dysmotility and nausea‐like behavior). Methods Male Wistar rats received an intraperitoneal injection of vehicle or loperamide (0.1, 1, or 10 mg kg−1). Three sets of experiments were performed to evaluate: (a) central effects (somatic nociceptive thresholds, immobility time, core temperature, spontaneous locomotor activity); (b) general gastrointestinal motility (serial X‐rays were taken 0‐8 hours after intragastric barium administration and analyzed semiquantitatively, morphometrically, and densitometrically); and (c) bedding intake (a rodent indirect marker of nausea). Animals from sets 1 and 3 were used to evaluate gastric dysmotility ex vivo at 2 and 4 hours after administration, respectively. Key Results Loperamide significantly induced antinociception, hypothermia, and hypolocomotion (but not catalepsy) at high doses and dose‐dependently reduced gastrointestinal motor function, with the intestine exhibiting higher sensitivity than the stomach. Whereas bedding intake occurred early and transiently, gastric dysmotility was much more persistent. Conclusions and inferences Our results suggest that loperamide‐induced nausea and gastric dysmotility might be temporally dissociated.

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The relationship between gastric motility and nausea: Gastric prokinetic agents as treatments

Cited by 53 publications

References 50 publications

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting

What is nausea? A historical analysis of changing views

Radiographic dose‐dependency study of loperamide effects on gastrointestinal motor function in the rat. Temporal relationship with nausea‐like behavior

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