Modulation of emetic response by carotid baro- and chemoreceptor activations

Uchino, Masahiro; Kuwahara, Masayoshi; Ebukuro, Susumu; Tsubone, Hirokazu

doi:10.1016/j.autneu.2005.12.006

Cited by 14 publications

(15 citation statements)

References 61 publications

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“…Blocking either baro-or chemo-receptors by internal carotid artery ligation, or carotid body denervation, respectively, suppressed the emetic response (Uchino et al, 2006). In addition, during emesis, there is an activation of both baro- and chemo-receptors and the sensitivity of these reflexes is increased during retching and vomiting.…”

Section: Role Of Vagal Neurocircuitry In Nausea and Vomitingmentioning

confidence: 99%

“…It has been suggested that the predominance of the parasympathetic nervous system activity augments the emetic response, whereas predominance of sympathetic nervous system activity suppresses it. Studies in shrews and ferrets have demonstrated that arterial pressure increases during prodromal phase of retching, whereas heart rate decreases prior to retching, followed by a gradual increase (Andrews et al, 1990; Uchino et al, 2006). Interestingly, studies in mice, a species that does not vomit, have demonstrated that emesis was accompanied by tachycardia in contrast to bradycardia observed in shrews.…”

Section: Role Of Vagal Neurocircuitry In Nausea and Vomitingmentioning

confidence: 99%

“…However, the bradycardia observed in shrews was blocked by vagotomy, suggesting that it was due to baroreceptor activation. In contrast to the shrew, the baroreflex in mice and rats during emesis does not appear to be as sensitive (Uchino et al, 2006). These observations are consistent with findings on human subjects, which have demonstrated that during parabolic flight, subjects that vomited had an increased baroreflex responsiveness, whereas those that did not vomit displayed no changes (Schlegel et al, 2001).…”

Section: Role Of Vagal Neurocircuitry In Nausea and Vomitingmentioning

confidence: 99%

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The role of vagal neurocircuits in the regulation of nausea and vomiting

Babic

Browning

2014

European Journal of Pharmacology

183

143

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Nausea and vomiting are among the most frequently occurring symptoms observed by clinicians. While advances have been made in understanding both the physiological as well as the neurophysiological pathways involved in nausea and vomiting, the final common pathway(s) for emesis have yet to be defined. Regardless of the difficulties in elucidating the precise neurocircuitry involved in nausea and vomiting, it has been accepted for over a century that the locus for these neurocircuits encompasses several structures within the medullary reticular formation of the hindbrain and that the role of vagal neurocircuits in particular are of critical importance. The afferent vagus nerve is responsible for relaying a vast amount of sensory information from thoracic and abdominal organs to the central nervous system. Neurons within the nucleus of the tractus solitarius not only receive these peripheral sensory inputs but have direct or indirect connections with several other hindbrain, midbrain and forebrain structures responsible for the co-ordination of the multiple organ systems. The efferent vagus nerve relays the integrated and co-ordinated output response to several peripheral organs responsible for emesis. The important role of both sensory and motor vagus nerves, and the available nature of peripheral vagal afferent and efferent nerve terminals, provides extensive and readily accessible targets for the development of drugs to combat nausea and vomiting.

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Section: Role Of Vagal Neurocircuitry In Nausea and Vomitingmentioning

confidence: 99%

Section: Role Of Vagal Neurocircuitry In Nausea and Vomitingmentioning

confidence: 99%

Section: Role Of Vagal Neurocircuitry In Nausea and Vomitingmentioning

confidence: 99%

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The role of vagal neurocircuits in the regulation of nausea and vomiting

Babic

Browning

2014

European Journal of Pharmacology

183

143

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“…It is unknown what determines these variable temporal patterns; certainly the type (e.g., chemotherapy versus a motion stimulus) and amount of stimulation play a role but it might also be related to the propensity of other neural systems to adjust the tone of emetic circuitry. For example, cardiovascular inputs from carotid baro-and chemoreceptors modulate the emetic response (Uchino, Kuwahara, Ebukuro, & Tsubone, 2006). Early work also suggested the existence of brainstem circuits containing opioid receptors that modulate emetic pathways (Rudd & Naylor, 1995).…”

Section: Neurobiology Of Nausea and Vomitingmentioning

confidence: 99%

Why is the neurobiology of nausea and vomiting so important?

2008

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Nausea and vomiting are important as biological systems for drug side effects, disease co-morbidities, and defenses against food poisoning. Vomiting can serve the function of emptying a noxious chemical from the gut, and nausea appears to play a role in a conditioned response to avoid ingestion of offending substances. The sensory pathways for nausea and vomiting, such as gut and vestibular inputs, are generally defined but the problem of determining the brain's final common pathway and central pattern generator for nausea and vomiting is largely unsolved. A neurophysiological analysis of brain pathways provides an opportunity to more closely determine the neurobiology of nausea and vomiting and its prodromal signs (e.g., cold sweating, salivation).

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“…Mechanical stimulation of the digestive tract from pharynx to small intestine by distension or obstruction can induce nausea and vomiting 35 . Excessive distension of the gut induces pain via serosal stretch receptors whose output passes via sympathetic neurones to the central nervous system; it also activates both vagus and splanchnic nerves and induces retching accompanied by cardiovascular and respiratory responses with a short latency and high success rates 36 . The stimuli arising from the stomach and small intestine are important in the aetiology of upper GI symptoms and disordered gastric motility 37,38 .…”

Section: Discussionmentioning

confidence: 99%

Intestinal electrical stimulation improves delayed gastric emptying and vomiting induced by duodenal distension in dogs

Chen

2007

Neurogastroenterology Motil

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The aim of this study was to investigate the effects of short-pulse intestinal electrical stimulation (IES) on duodenal distention-induced delayed gastric emptying and vomiting in dogs and its possible mechanisms. The study was performed in 12 dogs with jejunal electrodes and a duodenal cannula in three separate experiments to investigate the effects of IES on duodenal distension (DD)-induced delayed gastric emptying and discomfort signs, vagal efferent activity, and jejunal tone. We found that: (i) IES significantly accelerated gastric emptying of liquid delayed by distension (18.05 +/- 4.06%vs. 7.18 +/- 1.99%, P = 0.036 at 60 min). (ii) IES significantly reduced vomiting and discomfort/pain induced by distension. The average signs score was 15.33 +/- 1.37 during distension which decreased to 6.50 +/- 0.91 (P = 0.0002) with IES. (iii) IES did not change vagal afferent activity, which was assessed by the spectral analysis of the heart rate variability. (iv) IES decreased jejunal tone. In conclusion, IES with parameters commonly used in gastric electrical stimulation for nausea and vomiting associated with gastroparesis improves DD-induced delayed gastric emptying and prevents DD-induced vomiting and discomfort signs. Further studies are warranted to investigate the therapeutic potential of IES for gastrointestinal symptoms associated with disturbances in motility and sensory function in small intestine.

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Modulation of emetic response by carotid baro- and chemoreceptor activations

Cited by 14 publications

References 61 publications

The role of vagal neurocircuits in the regulation of nausea and vomiting

The role of vagal neurocircuits in the regulation of nausea and vomiting

Why is the neurobiology of nausea and vomiting so important?

Intestinal electrical stimulation improves delayed gastric emptying and vomiting induced by duodenal distension in dogs

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