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Motor and myoelectric activity associated with vomiting, regurgitation, and nausea

Ivan M. Lang, Sushil K. Sarna

10.1002/cphy.cp060132

Source: Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Digestive Tract Motor and Myoelectric Activity Associated With Vomiting
1.1 Motor Events
1.2 Myoelectric Events
1.3 Independence From Retching and Vomitus Expulsion
1.4 Functions of Retrograde Giant Contraction
1.5 Neural Control
1.6 Neuropharmacology
2 Digestive Tract Motor Activity Associated With Regurgitation
3 Nausea and Prodromal Signs of Vomiting
3.1 Nausea
3.2 Prodromal Signs of Vomiting
4 Conclusions
Figure 1. Figure 1.

Consecutive radiographs of abdomen, thorax, and neck of a dog before, during, and after retching and vomitus expulsion. Prior to initiation of vomiting by apomorphine (1.5 mg/kg), 1.2‐kg dog was fed 50 g of finely ground meat with 10 g of contrast material. A: contrast material filled the stomach but was not displaced during prodromal signs of vomiting. B: 60 s later the first retch occurred, which propelled the gastric contents into lower third of esophagus as gastroesophageal junction widened. Time between each radiograph from B to G was 3–5 s. C: contrast material moved to cervical esophagus but expulsion to oral cavity did not occur. D: at end of the retch, contents of esophagus returned to the stomach as gastroesophageal junction remained dilated. E: next retch propelled gastric contents back into esophagus. F: esophagus became filled with contrast material, and expulsion to oral cavity occurred between F and G. G: after vomitus expulsion, dilated gastroesophageal junction and cardia remained filled with contrast material. H: 6 s later the stomach contour had not yet returned to control state.

From Hesse 58
Figure 2. Figure 2.

Radiograph of the stomach and esophagus of a woman in supine position during vomitus expulsion of barium. Cardia and gastroesophageal junction are elevated and dilated, forming a funnel between the stomach and esophagus.

From Lundsen and Holden 82
Figure 3. Figure 3.

Radiograph (top) and diagram (bottom) of gastroesophageal region of a dog with metal markers sewn on hiatus and gastroesophageal junction just prior to retching and vomiting. Six metal bars were sewn on upper surface of crura of the diaphragm, forming a ring around the esophageal hiatus. Four metal rings were sewn on seromuscular layer of cardia in a line around the circumference. Two metal triangles were sewn on submucosa of the most distal centimeter of esophagus after separation of the overlying seromuscular layer. This radiograph was taken 1 min after apomorphine administration (2 mg iv) but before onset of retching or vomitus expulsion. Markers of submucosa and cardia have risen in the thoracic cavity, but markers of the hiatus have not.

From Johnson and Laws 62
Figure 4. Figure 4.

Effect of vagotomy on apomorphine‐induced retching and gastric relaxation in unanesthetized decerebrate cat. Apomorphine increased gastric volume followed by retching, but only the change in gastric volume was blocked by bilateral cervical vagotomy. Therefore retching and vomiting are preceded by a long‐lasting gastric relaxation mediated by vagus nerves.

From Abrahamsson et al. 4
Figure 5. Figure 5.

Gastrointestinal motor correlates of vomiting in the dog. This emetic episode occurred spontaneously. Numbers in parentheses indicate position in gastrointestinal tract of strain‐gauge force transducers from the pylorus. Broken vertical line, time of first observation of gastrointestinal motor correlates of vomiting. Numbers on chart identify the 4 different motor responses comprising gastrointestinal motor correlates of vomiting: 1 and 1a, peri‐retrograde giant contraction (RGC) inhibitory period of small intestine; 2, RGC; 3, post‐RGC phasic contractions; and 4, post‐RGC inhibitory period.

From Lang et al. 71. Copyright 1986 by The American Gastroenterological Association
Figure 6. Figure 6.

Effect of supradiaphragmatic vagotomy on gastrointestinal motor correlates of vomiting activated by apomorphine. Vagotomy blocked gastrointestinal motor correlates of vomiting but not retching or vomitus expulsion.

From Lang et al. 71. Copyright 1986 by The American Gastroenterological Association
Figure 7. Figure 7.

Myoelectric responses associated with gastrointestinal motor correlates of vomiting. These responses occurred spontaneously and were not followed by retching or vomitus expulsion. Arrows, occurrences of the RGC potential (i.e., myoelectric correlate of RGC). Cycling of electrical control activity (ECA) in small intestine is disrupted before and after RGC potential. A, antrum; D, duodenum; and J‐I, jejunoileum.

From Lang et al. 70
Figure 8. Figure 8.

Changes in ECA frequency in association with spontaneous occurrences of gastrointestinal motor correlates of vomiting. ECA frequency of lower jejunum and ileum slows ∼4 cycles/min, and this slowing lasts longer at more distal sites. D, duodenum at 15 cm from pylorus; J‐I, jejunoileum at 75 ± 5 cm (J‐I1), 125 ± 5 cm (J‐I2), 165 ± 5 cm (J‐I3), 220 ± 5 cm (J‐I4), and 285 ± 10 cm (J‐I5) from pylorus.

From Lang et al. 70
Figure 9. Figure 9.

Simultaneous recording of myoelectric (E) and contractile (SG) activities of gastrointestinal tract from same sites during gastrointestinal motor correlates of vomiting activated by apomorphine. Hatched bars, period of ECA disruption; filled circles, initiation of ECA frequency slowing; and vertical arrows, occurrences of RGC potential at upstroke of RGC.

From Lang et al. 70
Figure 10. Figure 10.

Spontaneous occurrence of gastrointestinal motor correlates of vomiting without subsequent retching or vomitus expulsion. Broken vertical line, first observed occurrence of gastrointestinal motor correlates of vomiting.
Figure 11. Figure 11.

Recording of gastrointestinal motor correlates of vomiting simultaneously with radiographic observations of movement of intraluminal contrast material after apomorphine administration. Top: motor activity of stomach and duodenum recorded with strain‐gauge force transducers and diameter of pylorus measured with induction coil. Bottom: distribution of contrast material in stomach and small intestine. A, antrum; P, pylorus; B, duodenal bulb; D1, proximal duodenum; and D2, distal duodenum. Numbers of radiographic images (bottom) correspond with numbered time marks on chart recording (top) and indicate when each image was taken relative to RGC. RGC was observed to empty contents of upper small intestine into proximal stomach.

From Ehrlein 38. Reprinted from Scand. J. Gastroenterol, by permission of Norwegian University Press, Oslo
Figure 12. Figure 12.

Mechanisms involved in initiation of gastrointestinal motor correlates of vomiting. DA, dopaminergic receptor; CTZ, chemoreceptive trigger zone; EPG, emetic pattern generator; ACh, acetylcholine; OP, opioid receptor; 5‐HT, serotonergic receptor; CCK‐OP, cholecystokinin octapeptide; N, nicotinic receptor; M, muscarinic receptor; NANC, nonadrenergic‐noncholinergic receptor; RGC, retrograde giant contraction. Stimulation of receptors in CTZ or gastrointestinal mucosa activates the EPG, which consists of 2 functionally distinct parts that are activated sequentially and always in the same order. At low stimulus intensities, only gastrointestinal responses are activated; at high stimulus intensities, retching and vomitus expulsion occur and are always preceded by gastrointestinal responses. All gastrointestinal motor correlates of vomiting are mediated by vagus nerves. Neurotransmitters mediating responses at each level of neuraxis are depicted. Opioid receptor of EPG is inhibitory, and dotted line around EPG shows blood‐brain barrier.
Figure 13. Figure 13.

Changes in autonomic functions associated with nausea induced by caloric stimulation of vestibular apparatus in subject with gastric fistula. Nausea was accompanied by decreased skin resistance, increased heart rate, blanching of gastric mucosa, decreased gastric acid secretion, and decreased gastric contractile activity.

From Wolf 134


Figure 1.

Consecutive radiographs of abdomen, thorax, and neck of a dog before, during, and after retching and vomitus expulsion. Prior to initiation of vomiting by apomorphine (1.5 mg/kg), 1.2‐kg dog was fed 50 g of finely ground meat with 10 g of contrast material. A: contrast material filled the stomach but was not displaced during prodromal signs of vomiting. B: 60 s later the first retch occurred, which propelled the gastric contents into lower third of esophagus as gastroesophageal junction widened. Time between each radiograph from B to G was 3–5 s. C: contrast material moved to cervical esophagus but expulsion to oral cavity did not occur. D: at end of the retch, contents of esophagus returned to the stomach as gastroesophageal junction remained dilated. E: next retch propelled gastric contents back into esophagus. F: esophagus became filled with contrast material, and expulsion to oral cavity occurred between F and G. G: after vomitus expulsion, dilated gastroesophageal junction and cardia remained filled with contrast material. H: 6 s later the stomach contour had not yet returned to control state.

From Hesse 58


Figure 2.

Radiograph of the stomach and esophagus of a woman in supine position during vomitus expulsion of barium. Cardia and gastroesophageal junction are elevated and dilated, forming a funnel between the stomach and esophagus.

From Lundsen and Holden 82


Figure 3.

Radiograph (top) and diagram (bottom) of gastroesophageal region of a dog with metal markers sewn on hiatus and gastroesophageal junction just prior to retching and vomiting. Six metal bars were sewn on upper surface of crura of the diaphragm, forming a ring around the esophageal hiatus. Four metal rings were sewn on seromuscular layer of cardia in a line around the circumference. Two metal triangles were sewn on submucosa of the most distal centimeter of esophagus after separation of the overlying seromuscular layer. This radiograph was taken 1 min after apomorphine administration (2 mg iv) but before onset of retching or vomitus expulsion. Markers of submucosa and cardia have risen in the thoracic cavity, but markers of the hiatus have not.

From Johnson and Laws 62


Figure 4.

Effect of vagotomy on apomorphine‐induced retching and gastric relaxation in unanesthetized decerebrate cat. Apomorphine increased gastric volume followed by retching, but only the change in gastric volume was blocked by bilateral cervical vagotomy. Therefore retching and vomiting are preceded by a long‐lasting gastric relaxation mediated by vagus nerves.

From Abrahamsson et al. 4


Figure 5.

Gastrointestinal motor correlates of vomiting in the dog. This emetic episode occurred spontaneously. Numbers in parentheses indicate position in gastrointestinal tract of strain‐gauge force transducers from the pylorus. Broken vertical line, time of first observation of gastrointestinal motor correlates of vomiting. Numbers on chart identify the 4 different motor responses comprising gastrointestinal motor correlates of vomiting: 1 and 1a, peri‐retrograde giant contraction (RGC) inhibitory period of small intestine; 2, RGC; 3, post‐RGC phasic contractions; and 4, post‐RGC inhibitory period.

From Lang et al. 71. Copyright 1986 by The American Gastroenterological Association


Figure 6.

Effect of supradiaphragmatic vagotomy on gastrointestinal motor correlates of vomiting activated by apomorphine. Vagotomy blocked gastrointestinal motor correlates of vomiting but not retching or vomitus expulsion.

From Lang et al. 71. Copyright 1986 by The American Gastroenterological Association


Figure 7.

Myoelectric responses associated with gastrointestinal motor correlates of vomiting. These responses occurred spontaneously and were not followed by retching or vomitus expulsion. Arrows, occurrences of the RGC potential (i.e., myoelectric correlate of RGC). Cycling of electrical control activity (ECA) in small intestine is disrupted before and after RGC potential. A, antrum; D, duodenum; and J‐I, jejunoileum.

From Lang et al. 70


Figure 8.

Changes in ECA frequency in association with spontaneous occurrences of gastrointestinal motor correlates of vomiting. ECA frequency of lower jejunum and ileum slows ∼4 cycles/min, and this slowing lasts longer at more distal sites. D, duodenum at 15 cm from pylorus; J‐I, jejunoileum at 75 ± 5 cm (J‐I1), 125 ± 5 cm (J‐I2), 165 ± 5 cm (J‐I3), 220 ± 5 cm (J‐I4), and 285 ± 10 cm (J‐I5) from pylorus.

From Lang et al. 70


Figure 9.

Simultaneous recording of myoelectric (E) and contractile (SG) activities of gastrointestinal tract from same sites during gastrointestinal motor correlates of vomiting activated by apomorphine. Hatched bars, period of ECA disruption; filled circles, initiation of ECA frequency slowing; and vertical arrows, occurrences of RGC potential at upstroke of RGC.

From Lang et al. 70


Figure 10.

Spontaneous occurrence of gastrointestinal motor correlates of vomiting without subsequent retching or vomitus expulsion. Broken vertical line, first observed occurrence of gastrointestinal motor correlates of vomiting.



Figure 11.

Recording of gastrointestinal motor correlates of vomiting simultaneously with radiographic observations of movement of intraluminal contrast material after apomorphine administration. Top: motor activity of stomach and duodenum recorded with strain‐gauge force transducers and diameter of pylorus measured with induction coil. Bottom: distribution of contrast material in stomach and small intestine. A, antrum; P, pylorus; B, duodenal bulb; D1, proximal duodenum; and D2, distal duodenum. Numbers of radiographic images (bottom) correspond with numbered time marks on chart recording (top) and indicate when each image was taken relative to RGC. RGC was observed to empty contents of upper small intestine into proximal stomach.

From Ehrlein 38. Reprinted from Scand. J. Gastroenterol, by permission of Norwegian University Press, Oslo


Figure 12.

Mechanisms involved in initiation of gastrointestinal motor correlates of vomiting. DA, dopaminergic receptor; CTZ, chemoreceptive trigger zone; EPG, emetic pattern generator; ACh, acetylcholine; OP, opioid receptor; 5‐HT, serotonergic receptor; CCK‐OP, cholecystokinin octapeptide; N, nicotinic receptor; M, muscarinic receptor; NANC, nonadrenergic‐noncholinergic receptor; RGC, retrograde giant contraction. Stimulation of receptors in CTZ or gastrointestinal mucosa activates the EPG, which consists of 2 functionally distinct parts that are activated sequentially and always in the same order. At low stimulus intensities, only gastrointestinal responses are activated; at high stimulus intensities, retching and vomitus expulsion occur and are always preceded by gastrointestinal responses. All gastrointestinal motor correlates of vomiting are mediated by vagus nerves. Neurotransmitters mediating responses at each level of neuraxis are depicted. Opioid receptor of EPG is inhibitory, and dotted line around EPG shows blood‐brain barrier.



Figure 13.

Changes in autonomic functions associated with nausea induced by caloric stimulation of vestibular apparatus in subject with gastric fistula. Nausea was accompanied by decreased skin resistance, increased heart rate, blanching of gastric mucosa, decreased gastric acid secretion, and decreased gastric contractile activity.

From Wolf 134
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Article Title: Motor and myoelectric activity associated with vomiting, regurgitation, and nausea
 

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Ivan M. Lang, Sushil K. Sarna. Motor and myoelectric activity associated with vomiting, regurgitation, and nausea. Compr Physiol 2011, Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation: 1179-1198. First published in print 1989. doi: 10.1002/cphy.cp060132