2008
DOI: 10.1016/j.autneu.2008.09.001
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Interactions of carotid sinus or aortic input with emetic signals from gastric afferents and vestibular system

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Cited by 3 publications
(7 citation statements)
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“…In humans and preclinical models with an emetic reflex, application of gastric stretch or toxins to the gastric lumen produce nausea and emesis (Blackshaw et al 1987; Ladabaum et al 1998; Araya et al 2001; Olivares et al 2001; Hu et al 2007; Uchino et al 2008). Preclinical research using intragastric CuSO 4 (a mucosal irritant) has provided significant insights into this GI pathway: 1) CuSO 4 stimulates release of 5-HT from enteroendocrine cells in ferrets; 2) intragastric CuSO 4 increases vagal afferent activity in ferrets; 3) abdominal vagotomy markedly inhibits intragastric CuSO 4 -induced emesis in dogs, ferrets, and musk shrews; and, 4) systemic antagonism of 5-HT 4 receptors blocks CuSO 4 -induced emesis in dogs, ferrets, and musk shrews (Bhandari and Andrews 1991; Makale and King 1992; Fukui et al 1994; Endo et al 1995; Reynolds et al 1995; Hu et al 2007).…”
Section: What Is the Role Of Gastrointestinal Vagal Afferent Fibers Imentioning
confidence: 99%
“…In humans and preclinical models with an emetic reflex, application of gastric stretch or toxins to the gastric lumen produce nausea and emesis (Blackshaw et al 1987; Ladabaum et al 1998; Araya et al 2001; Olivares et al 2001; Hu et al 2007; Uchino et al 2008). Preclinical research using intragastric CuSO 4 (a mucosal irritant) has provided significant insights into this GI pathway: 1) CuSO 4 stimulates release of 5-HT from enteroendocrine cells in ferrets; 2) intragastric CuSO 4 increases vagal afferent activity in ferrets; 3) abdominal vagotomy markedly inhibits intragastric CuSO 4 -induced emesis in dogs, ferrets, and musk shrews; and, 4) systemic antagonism of 5-HT 4 receptors blocks CuSO 4 -induced emesis in dogs, ferrets, and musk shrews (Bhandari and Andrews 1991; Makale and King 1992; Fukui et al 1994; Endo et al 1995; Reynolds et al 1995; Hu et al 2007).…”
Section: What Is the Role Of Gastrointestinal Vagal Afferent Fibers Imentioning
confidence: 99%
“…The primary goal of this project was to assess the detailed physiological effects of GES on gastric distension‐induced emesis using an established emetic test system: an in vivo musk shrew preparation . We tested the effects of GES pulse duration (0.3, 1, 5, and 10 ms), current amplitude (0.5, 1, and 2 mA), pulse frequency (8, 15, 30, and 60 Hz), and electrode placement (antrum, body, and fundus).…”
Section: Discussionmentioning
confidence: 99%
“…Firstly, we used a limited range of stimulation parameters, with inclusion of only 0.5–2 mA #bib8–60 Hz, and 0.3–10 ms pulse duration. Secondly, we used only one emetic stimulus, vagal, and there are at least three additional routes for emetic stimulation: vestibular, area postrema, and forebrain (review). Excessive gastric distension can also provide nociceptive input to the spinal cord; and thus, is not a purely vagal stimulus.…”
Section: Discussionmentioning
confidence: 99%
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