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Journal articles on the topic 'Gastric emptying'

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Published: 4 June 2021
Last updated: 21 February 2023

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1

Jin, H. O., K. Y. Lee, T. M. Chang, W. Y. Chey, and A. Dubois. "Secretin: a physiological regulator of gastric emptying and acid output in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 4 (October 1, 1994): G702—G708. http://dx.doi.org/10.1152/ajpgi.1994.267.4.g702.

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Secretin has been known to inhibit gastric acid secretion in several species. However, the physiological role of secretin on the postprandial acid output and gastric emptying in an intact stomach remains controversial. In the present study, we reinvestigated the role of secretin in physiological dose range and endogenous secretin on gastric acid secretion and emptying in the stomach without influencing intragastric luminal pH in dogs. In seven conscious dogs with gastric cannulas, a 4% amino acid meal was administered intragastrically, and three different doses of secretin and an antisecretin serum were infused intravenously in each dog on separate days. Gastric emptying and net acid output were measured using a dye dilution technique, and plasma secretin and gastrin were determined by specific radioimmunoassays. After the meal, gastric emptying was exponential: acid output peaked at 25 min, and plasma concentrations of gastrin and secretin peaked at 15 and 60 min, respectively. Intravenous infusion of secretin at 1.25, 2.5, and 5.0 pmol.kg-1.h-1 dose dependently increased plasma levels of the peptide and suppressed postprandial plasma gastrin response and gastric acid output and emptying of the meal. Immunoneutralization of circulating secretin with a rabbit antisecretin serum abolished the postprandial rise of plasma secretin and significantly increased plasma gastrin, and augmented gastric emptying as well as acid output. It is concluded that, in dogs, secretin plays a physiological role in the regulation of gastric emptying and acid output after a liquid amino acid meal and that these effects may be mediated in part by suppression of the release of gastrin.
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2

Shillabeer, G., and J. S. Davison. "Proglumide, a cholecystokinin antagonist, increases gastric emptying in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 2 (February 1, 1987): R353—R360. http://dx.doi.org/10.1152/ajpregu.1987.252.2.r353.

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Injection of cholecystokinin (CCK) reduces food intake and delays gastric emptying. We have previously shown that endogenous CCK also reduces food intake. This may be achieved by a delay in gastric emptying. We investigated the role of CCK in gastric emptying by inhibiting the actions of CCK released by a meal, using a CCK antagonist, proglumide. We postulated that inhibition of CCK should induce an increase in gastric emptying. Gastric emptying was determined in rats by a marker dilution technique using direct gastric intubation. Proglumide (150 mg/kg) significantly accelerated emptying of liquid food by 12.8% (P less than 0.005, n = 12) when injected intraperitoneally following a food preload. Proglumide injected before feeding was ineffective. Oral proglumide, which inhibited gastrin-stimulated acid secretion, was also ineffective. We concluded that proglumide increased gastric emptying by acting on a factor released by the preload, and since proglumide is a specific antagonist, this factor was probably CCK. Therefore CCK may play a physiological role in the regulation of gastric emptying.
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3

MITCHELL, J. B., D. L. COSTILL, J. A. HOUMARD, W. J. FINK, R. A. ROBERGS, and J. A. DAVIS. "Gastric emptying." Medicine & Science in Sports & Exercise 21, no. 3 (June 1989): 269???274. http://dx.doi.org/10.1249/00005768-198906000-00007.

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4

Perkins, Alan C., Peter Hay, and Maura Corsetti. "Gastric emptying." Nuclear Medicine Communications 41, no. 6 (June 2020): 497–98. http://dx.doi.org/10.1097/mnm.0000000000001195.

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5

Wheeler-Usher, Donna H., Lee A. Wanke, and Marc J. Bayer. "Gastric Emptying." Medical Toxicology 1, no. 2 (April 1986): 142–53. http://dx.doi.org/10.1007/bf03259833.

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6

Tonoy, M. O., N. Katz, J. D. Hcironimus, and T. Smith. "GASTRIC EMPTYING." Clinical Nuclear Medicine 17, no. 3 (March 1992): 255. http://dx.doi.org/10.1097/00003072-199203000-00041.

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7

KATZ, NEIL, MORAKINYO O. TONEY, JAMES D. HEIRONIMUS, and THOMAS E. SMITH. "Gastric Emptying." Clinical Nuclear Medicine 19, no. 5 (May 1994): 396–400. http://dx.doi.org/10.1097/00003072-199405000-00004.

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8

Szarka, Lawrence A., and Michael Camilleri. "Gastric Emptying." Clinical Gastroenterology and Hepatology 7, no. 8 (August 2009): 823–27. http://dx.doi.org/10.1016/j.cgh.2009.04.011.

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9

Boltin, Doron, Ibrahim Zvidi, Adam Steinmetz, Hanna Bernstine, David Groshar, Yuval Nardi, Mona Boaz, Yaron Niv, and Ram Dickman. "Vomiting and Dysphagia Predict Delayed Gastric Emptying in Diabetic and Nondiabetic Subjects." Journal of Diabetes Research 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/294032.

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Background.Gastroparesis is a heterogeneous disorder most often idiopathic, diabetic, or postsurgical in nature. The demographic and clinical predictors of gastroparesis in Israeli patients are poorly defined.Methods.During the study period we identified all adult patients who were referred to gastric emptying scintigraphy (GES) for the evaluation of dyspeptic symptoms. Of those, 193 patients who were referred to GES from our institution were retrospectively identified (76 (39%) males, mean age60.2±15.6years). Subjects were grouped according to gastric half-emptying times (gastricT1/2). Demographic and clinical data were extracted from electronic medical records or by a phone interview.Key Results.Gastric emptying half-times were normal (gastricT1/20–99 min) in 101 patients, abnormal (gastricT1/2100–299 min) in 67 patients, and grossly abnormal (gastricT1/2≥300 min) in 25 patients. Vomiting and dysphagia, but neither early satiety nor bloating, correlated with delayed gastric emptying. Diabetes was associated with grossly abnormal gastricT1/2. Idiopathic gastroparesis was associated with a younger age at GES. No correlation was observed between gastricT1/2values and gender, smoking,H. pyloriinfection, HBA1C, or microvascular complication of diabetes.Conclusions Inferences.Vomiting and dysphagia are predictive of delayed gastric emptying in both diabetic and nondiabetic subjects. Diabetes is associated with more severe gastroparesis.
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10

Muenzing, W., K. Tatsch, and R. Linke. "Is normal gastric emptying a predictor of normal gastric function?" Nuklearmedizin 44, no. 03 (2005): 81–85. http://dx.doi.org/10.1055/s-0038-1625690.

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Summary Aim: Impaired gastric emptying is common in many disorders. Assuming that gastric disorders primarily affect gastric peristalsis, which secondarily results in impaired emptying, the aim of our study was to evaluate whether quantitative analysis of gastric peristalsis might be a more sensitive parameter than gastric emptying to demonstrate functional gastric impairment. Patients, methods: Gastric emptying was determined scintigraphically in 141 adult (age: 18–78 years) patients (long-term Type 1 diabetes mellitus, 82 cases; systemic sclerosis, 31 cases; atrophic gastritis, 28 cases) and 20 healthy age-matched controls after ingestion of a semiliquid test meal. In addition, gastric peristalsis was evaluated by Fourier analysis of condensed images. Results: Compared to the control persons emptying was delayed in 75/141 patients, regular in 63/141 patients, and accelerated in 3/141 patients. As expected, 81% of patients with delayed emptying presented with diminished gastric contraction amplitudes. However, independent of the aetiology of the underlying disorder, 40/63 patients with regular emptying also exhibited reduced peristalsis. Conclusion: Normal gastric emptying does not predict normal gastric function. This assumption is supported by the presence of reduced amplitudes in subgroups of patients with various disorders and normal emptying. Our results suggest that the amplitude of gastric contractions may represent a more sensitive parameter for the detection of gastric dysfunction than does gastric emptying.
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11

Vijayvargiya, Priya, Sina Jameie-Oskooei, Michael Camilleri, Victor Chedid, Patricia J. Erwin, and Mohammad Hassan Murad. "Association between delayed gastric emptying and upper gastrointestinal symptoms: a systematic review and meta-analysis." Gut 68, no. 5 (June 2, 2018): 804–13. http://dx.doi.org/10.1136/gutjnl-2018-316405.

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BackgroundThe relationship between delayed gastric emptying and upper GI symptoms (UGI Sx) is controversial.ObjectiveTo assess association between gastric emptying and UGI Sx, independent of treatment.DesignWe performed a systematic review and meta-analysis of the literature from 2007 to 2017, review of references and additional papers identified by content expert. We included studies evaluating the association between gastric emptying and nausea, vomiting, early satiety/postprandial fullness, abdominal pain and bloating. Covariate analyses included optimal gastric emptying test method, gastric emptying type (breath test or scintigraphy) and patient category. Meta-regression compared the differences based on type of gastric emptying tests.ResultsSystematic review included 92 gastric emptying studies (26 breath test, 62 scintigraphy, 1 ultrasound and 3 wireless motility capsule); 25 of these studies provided quantitative data for meta-analysis (15 scintigraphy studies enrolling 4056 participants and 10 breath test studies enrolling 2231 participants). Meta-regression demonstrated a significant difference between optimal and suboptimal gastric emptying test methods when comparing delayed gastric emptying with nausea and vomiting. On evaluating studies using optimal gastric emptying test methodology, there were significant associations between gastric emptying and nausea (OR 1.6, 95% CI 1.4 to 1.8), vomiting (OR 2.0, 95% CI 1.6 to 2.7), abdominal pain (OR 1.5, 95% CI 1.0 to 2.2) and early satiety/fullness (OR 1.8, 95% CI 1.2 to 2.6) for patients with UGI Sx; gastric emptying and early satiety/fullness in patients with diabetes; gastric emptying and nausea in patients with gastroparesis.ConclusionsThe systematic review and meta-analysis supports an association between optimally measured delayed gastric emptying and UGI Sx.
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12

Choi, Kyoung Moo, Jin Zhu, Gary J. Stoltz, Steven Vernino, Michael Camilleri, Joseph H. Szurszewski, Simon J. Gibbons, and Gianrico Farrugia. "Determination of gastric emptying in nonobese diabetic mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 5 (November 2007): G1039—G1045. http://dx.doi.org/10.1152/ajpgi.00317.2007.

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Animal studies on diabetic gastroparesis are limited by inability to follow gastric emptying changes in the same mouse. The study aim was to validate a nonlethal gastric emptying method in nonobese diabetic (NOD) LtJ mice, a model of type 1 diabetes, and study sequential changes with age and early diabetic status. The reliability and responsiveness of a [13C]octanoic acid breath test in NOD LtJ mice was tested, and the test was used to measure solid gastric emptying in NOD LtJ mice and nonobese diabetes resistant (NOR) LtJ mice. The 13C breath test produced results similar to postmortem recovery of a meal. Bethanechol accelerated gastric emptying [control: 92 ± 9 min; bethanechol: 53 ± 3 min, mean half emptying time ( T1/2) ± SE], and atropine slowed gastric emptying (control: 92 ± 9 min; atropine: 184 ± 31 min, mean T1/2 ± SE). Normal gastric emptying ( T1/2) in nondiabetic NOD LtJ mice (8–12 wk) was 91 ± 2 min. Aging had differing effects on gastric emptying in NOD LtJ and NOR LtJ mice. Onset of diabetes was accompanied by accelerated gastric emptying during weeks 1–2 of diabetes. Gastric emptying returned to normal by weeks 3–5 with no delay. The [13C]octanoic acid breath test accurately measures gastric emptying in NOD LtJ mice, is useful to study the time course of changes in gastric emptying in diabetic NOD LtJ mice, and is able to detect acceleration in gastric emptying early in diabetes. Opposing changes in gastric emptying between NOD LtJ and NOR LtJ mice suggest that NOR LtJ mice are not good controls for the study of gastric emptying in NOD LtJ mice.
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13

Schwartz, G. J., G. Berkow, P. R. McHugh, and T. H. Moran. "Gastric branch vagotomy blocks nutrient and cholecystokinin-induced suppression of gastric emptying." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 3 (March 1, 1993): R630—R637. http://dx.doi.org/10.1152/ajpregu.1993.264.3.r630.

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A role for the vagus nerve in the emptying of intragastric nutrients and the gastric inhibitory actions of the brain-gut peptide cholecystokinin (CCK) has been proposed. To directly assess the role of the gastric vagal branches in these actions, we compared the emptying of 5-ml nutrient and nonnutrient gastric loads in male rats in which both branches of the gastric vagus nerves were cut (GVX, n = 7) with emptying in surgical control (n = 8) rats. Gastric emptying of saline was also examined in both groups after intraperitoneal administration of 8 micrograms/kg CCK. In control rats, high osmolarity, low pH, and caloric density all significantly decreased gastric emptying compared with the emptying of physiological saline. In addition, fat (oleic acid) and protein (peptone) loads emptied significantly more slowly than isocaloric carbohydrate (glucose) loads. Gastric branch vagotomy completely blocked the suppression of emptying produced by fat, protein, carbohydrate, and acid loads. In addition, GVX attenuated the ability of hyperosmotic nutrient and nonnutrient loads to inhibit emptying to the same degree, irrespective of their caloric content. Finally, in intact rats, CCK significantly inhibited the emptying of physiological saline, and gastric vagotomy abolished this suppression. Taken together, these results are consistent with the proposals that 1) the controlled emptying of caloric, hyperosmotic, and acidic solutions is dependent on gastric vagal branches, and 2) exogenous CCK relies on an intact vagal pathway in the control of gastric emptying.
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14

Nakade, Yukiomi, Daisuke Tsuchida, Hiroyuki Fukuda, Masahiro Iwa, Theodore N. Pappas, and Toku Takahashi. "Restraint stress delays solid gastric emptying via a central CRF and peripheral sympathetic neuron in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 2 (February 2005): R427—R432. http://dx.doi.org/10.1152/ajpregu.00499.2004.

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Central corticotropin-releasing factor (CRF) delays gastric emptying through the autonomic nervous system. CRF plays an important role in mediating delayed gastric emptying induced by stress. However, it is not clear whether a sympathetic or parasympathetic pathway is involved in the mechanism of central CRF-induced inhibition of solid gastric emptying. The purpose of this study was to investigate whether 1) CRF inhibits solid gastric emptying via a peripheral sympathetic pathway and 2) stress-induced inhibition of solid gastric emptying is mediated via a central CRF and peripheral sympathetic pathways. Using male Sprague-Dawley rats, CRF was injected intracisternally with or without various adrenergic-blocking agents. To investigate whether central CRF-induced inhibition of solid gastric emptying is mediated via a peripheral sympathetic pathway, rats underwent celiac ganglionectomy 1 wk before the gastric emptying study. After solid meal ingestion (90 min), gastric emptying was calculated. To investigate the role of endogenous CRF in stress-induced delayed gastric emptying, a CRF type2receptor antagonist, astressin2-B, was intracisternally administered. Rats were subjected to a restraint stress immediately after the feeding. Intracisternal injection of CRF (0.1–1.0 μg) dose-dependently inhibited solid gastric emptying. The inhibitory effect of CRF on solid gastric emptying was significantly blocked by guanethidine, propranolol, and celiac ganglionectomy but not by phentolamine. Restraint stress significantly delayed solid gastric emptying, which was improved by astressin2-B, guanethidine, and celiac ganglionectomy. Our research suggests that restraint stress inhibits solid gastric emptying via a central CRF type2receptor and peripheral sympathetic neural pathway in rats.
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15

Sallam, Hanaa S., Hermes M. Oliveira, Suhuan Liu, and Jiande D. Z. Chen. "Mechanisms of burn-induced impairment in gastric slow waves and emptying in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 1 (July 2010): R298—R305. http://dx.doi.org/10.1152/ajpregu.00135.2010.

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Delayed gastric emptying is common following severe large cutaneous burns; however, the mechanisms of burn-induced delayed gastric emptying remain unknown. The aim of this study was to explore the possible involvement of hyperglycemia and cyclooxygenase-2 receptors in the burn-induced gastric dysrhythmias. Gastric slow waves and gastric emptying were assessed in rats 6 h following sham or burn injury. Animals were randomized to one sham-burn and seven burn groups: untreated; two groups of saline treated (control); insulin treated (5 IU/kg); cyclooxygenase-2 inhibitor treated (10 mg/kg); ghrelin treated (2 nmol/rat); and gastric electrical stimulation treated. It was found that 1) severe burn injury impaired gastric slow waves postprandially and delayed gastric emptying; 2) the impairment in gastric slow waves included a decrease in the slow-wave frequency and in the percentage of normal slow waves, and an increase in the percentage of bradygastria ( P = 0.001, 0.01, and 0.01, respectively vs. preburn values). None of the gastric slow-wave parameters was significantly correlated with gastric emptying; 3) cyclooxygenase-2 inhibitor normalized burn-induced delayed gastric emptying ( P = 0.3 vs. sham-burn), but not gastric dysrhythmias ( P < 0.002 vs. sham), whereas insulin normalized both gastric emptying ( P = 0.4 vs. sham-burn) and gastric dysrhythmias ( P = 0.3 vs. sham-burn); 4) both gastric electrical stimulation and ghrelin accelerated burn-induced delayed gastric emptying ( P = 0.002 and 0.04, respectively, vs. untreated burn). In conclusion, hyperglycemia alters gastric slow-wave activity and delayed gastric emptying, while cyclooxygenase-2 inhibition delays gastric emptying without altering gastric slow-wave activity.
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16

Pappas, T., H. T. Debas, J. H. Walsh, J. Rivier, and Y. Tache. "Calcitonin gene-related peptide-induced selective inhibition of gastric acid secretion in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 1 (January 1, 1986): G127—G133. http://dx.doi.org/10.1152/ajpgi.1986.250.1.g127.

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Calcitonin gene-related peptide (CGRP) is a 37-residue peptide recently characterized in the brain and found in high concentrations in the gut, particularly in the stomach and pancreas. The effects of intravenous infusion of human and rat CGRP (260 pmol . kg-1 . h-1) on gastric secretion and emptying and pancreatic exocrine secretion were studied in conscious dogs. CGRP inhibited by 60-75% gastric acid secretion stimulated by a meal, sham feeding, or step doses of bombesin but did not modify acid response to step doses of histamine or bethanechol. The inhibitory effect of CGRP is not due to blockage of postprandial or bombesin-stimulated gastrin release. CGRP did not influence basal or meal-stimulated pancreatic exocrine secretion or the rate of gastric emptying of a saline meal. These results indicate that CGRP is a potent and selective inhibitor of gastrin-mediated acid secretion in dogs and, under these conditions, did not alter other gastrointestinal functions such as gastric emptying or pancreatic exocrine secretion.
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17

Corvilain, B., M. Abramowicz, F. Fery, A. Schoutens, M. Verlinden, E. Balasse, and M. Horowitz. "Effect of short-term starvation on gastric emptying in humans: relationship to oral glucose tolerance." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 4 (October 1, 1995): G512—G517. http://dx.doi.org/10.1152/ajpgi.1995.269.4.g512.

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To evaluate the effects of short-term starvation on gastric emptying in normal and obese subjects, the relationship between gastric emptying and oral glucose tolerance, and the mechanisms responsible for the delay in the systemic appearance of oral glucose observed after short-term fasting, we determined the effects of a 4-day fast on 1) gastric emptying and oral glucose tolerance in normal subjects and 2) gastric emptying in obese patients. Gastric emptying of 75 g glucose (320 ml) labeled with 99mTc colloid was measured in 12 healthy volunteers and 11 obese subjects after 12-h and 4-day fasts. In seven other obese subjects, the effect of a 4-day fast on gastric emptying of 320 ml normal saline was quantified. Gastric emptying of glucose was slower after the 4-day than after the overnight fast in both normal (P > 0.02) and obese (P < 0.001) subjects, with no difference between the two groups. In normal subjects, the rate of gastric emptying was related directly to the rise in plasma glucose at 30 min (r = 0.60; P < 0.05) but inversely to the plasma glucose at 180 min (r = -0.64; P < 0.02). In the obese subjects, gastric emptying of saline was not affected by fasting. These observations indicate that 1) gastric emptying of glucose is retarded by a 4-day fast, 2) the changes in gastric emptying reported in obesity may reflect different patterns of prior nutrient intake, and 3) delay in gastric emptying accounts for the slower systemic appearance of glucose after fasting.
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18

Lenz, H. J. "CNS regulation of gastric and autonomic functions in dogs by gastrin-releasing peptide." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 3 (September 1, 1988): G298—G303. http://dx.doi.org/10.1152/ajpgi.1988.255.3.g298.

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The central nervous system effects of canine gastrin-releasing peptide (GRP) were studied on gastric acid secretion, emptying, blood flow, and the autonomic nervous system in conscious dogs. GRP injected into the third cerebral ventricle significantly (P less than 0.01) increased plasma epinephrine but not norepinephrine concentrations. GRP (0.1-1.0 nmol/kg) significantly decreased gastric acid secretion stimulated by an 8% peptone meal, delayed gastric emptying of the liquid peptone meal, and increased left gastric artery flow. Ganglionic blockade, truncal vagotomy, or adrenalectomy did not abolish the inhibitory effect of GRP on gastric acid secretion. However, ganglionic blockade or vagotomy abolished the GRP-induced inhibition of gastric emptying, and ganglionic blockade or adrenalectomy abolished the GRP-induced increases in left gastric artery flow and plasma epinephrine concentrations. An intravenous infusion of epinephrine that produced similar plasma concentrations of epinephrine that were observed after cerebroventricular injection of GRP mimicked the increase in left gastric artery flow induced by GRP. It is concluded that 1) GRP acts within the central nervous system to activate the sympathoadrenal axis, 2) GRP inhibits gastric emptying of a liquid meal by a vagally dependent mechanism and enhances left gastric artery flow by the release of epinephrine from the adrenal medulla, and 3) the pathway(s) that mediate the GRP-induced inhibition of gastric acid in the dog remain unknown.
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19

Dickson, J. A., and S. Nour. "Gastric motility and gastric emptying." Archives of Disease in Childhood - Fetal and Neonatal Edition 72, no. 3 (May 1, 1995): F212. http://dx.doi.org/10.1136/fn.72.3.f212-b.

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20

Wittebol, P., H. J. T. M. Haarman, A. Hoekstra, A. J. P. M. Smout, and L. M. A. Akkermans. "Gastric Emptying after Gastric Surgery." Digestive Surgery 5, no. 3 (1988): 160–66. http://dx.doi.org/10.1159/000171854.

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21

Farrell, Mary Beth. "Gastric Emptying Scintigraphy." Journal of Nuclear Medicine Technology 47, no. 2 (June 2019): 111–19. http://dx.doi.org/10.2967/jnmt.117.227892.

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22

McCallum, Richard W. "Gastric emptying disorders." Postgraduate Medicine 81, no. 3 (February 15, 1987): 67–76. http://dx.doi.org/10.1080/00325481.1987.11699726.

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23

Pathikonda, Murali, Priyanka Sachdeva, Nidhi Malhotra, Robert S. Fisher, Alan H. Maurer, and Henry P. Parkman. "Gastric Emptying Scintigraphy." Journal of Clinical Gastroenterology 46, no. 3 (March 2012): 209–15. http://dx.doi.org/10.1097/mcg.0b013e31822f3ad2.

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24

&NA;. "Understanding Gastric Emptying." Journal of Pediatric Gastroenterology and Nutrition 4, no. 1 (February 1985): 1–3. http://dx.doi.org/10.1097/00005176-198502000-00001.

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25

Abell, Thomas L., Gervais Tougas, Ying Chen, Amar Al-Juburi, Anil Minocha, and Warren Starkebaum. "RAPID GASTRIC EMPTYING." American Journal of Gastroenterology 99 (October 2004): S41. http://dx.doi.org/10.14309/00000434-200410001-00123.

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26

Gin, T. "Postpartum gastric emptying." Anaesthesia 48, no. 9 (September 1993): 821. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07603.x.

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27

Whitehead, E., and G. O'Sullivan. "Postpartum gastric emptying." Anaesthesia 48, no. 9 (September 1993): 821–22. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07604.x.

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28

Davis, Joseph H. "Gastric Emptying Time." American Journal of Forensic Medicine and Pathology 10, no. 3 (September 1989): 271–72. http://dx.doi.org/10.1097/00000433-198909000-00048.

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29

Su, Bailey, Zachary Callahan, Kristine M. Kuchta, Pierce Paterakos, and Michael Ujiki. "Delayed Gastric Emptying." Journal of the American College of Surgeons 229, no. 4 (October 2019): S20. http://dx.doi.org/10.1016/j.jamcollsurg.2019.08.058.

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30

McCallum, Richard W., and Robert Lange. "Gastric emptying abnormalities." Digestive Diseases and Sciences 31, no. 11 (November 1986): 1277. http://dx.doi.org/10.1007/bf01296533.

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31

Shafer, R. B., A. S. Levine, J. M. Marlette, and J. E. Morley. "Do calories, osmolality, or calcium determine gastric emptying?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 4 (April 1, 1985): R479—R483. http://dx.doi.org/10.1152/ajpregu.1985.248.4.r479.

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To determine whether calories, osmolality, or calcium mediate gastric emptying we employed a standardized radioactive meal in 10 normal human volunteers. A variety of simple and complex sugars, medium-chain fatty acid (MCFA), pectin, and gluten were dissolved in water and ingested with the test meal. The studies were also performed with calcium chloride, EDTA, and an equimolar combination of these chemicals. Results of gastric emptying showed that incremental glucose produced an increase in emptying time with a tendency for emptying time to show a proportionally greater delay with increasing glucose concentrations. Fructose and polyhexose had similar effects to glucose. Pentoses (xylose and arabanose) markedly prolonged gastric emptying when compared with the same amount of glucose. The effect of sucrose and gluten on gastric emptying did not significantly differ from controls. Twenty-five grams MCFA had an effect similar to 50 g glucose. Pectin, a complex carbohydrate, produced a varied effect in different individuals. There was no obvious relationship between osmolality and gastric emptying. Calcium chloride and EDTA prolonged gastric emptying, but the equimolar combination gave values similar to controls. Our findings suggest 1) calories nor osmolality alone determine gastric emptying, 2) both calcium and calcium chelation with EDTA prolong gastric emptying, and 3) a specific food does not necessarily produce the same effect on gastric emptying in different individuals.
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32

Wang, Xiao Jing, Duane D. Burton, Margaret Breen-Lyles, and Michael Camilleri. "Gastric accommodation influences proximal gastric and total gastric emptying in concurrent measurements conducted in healthy volunteers." American Journal of Physiology-Gastrointestinal and Liver Physiology 320, no. 5 (May 1, 2021): G759—G767. http://dx.doi.org/10.1152/ajpgi.00008.2021.

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In vivo human studies evaluated concurrently the volume of the stomach during fasting and after a solid and liquid meal using a new SPECT-based method. Although fasting gastric volumes did not impact the rates of gastric emptying, both postprandial and accommodation volumes of the whole and proximal stomach were significantly correlated with gastric emptying. Larger stomach volumes were associated with slower gastric emptying.
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33

Dubois, A., and D. O. Castell. "Histamine H2-receptor involvement in the regulation of gastric emptying." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 2 (February 1, 1986): G244—G247. http://dx.doi.org/10.1152/ajpgi.1986.250.2.g244.

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The effect of cimetidine on gastric emptying and gastric secretion was evaluated in eight chair-adapted rhesus monkeys. A dye-dilution technique was used to simultaneously determine gastric emptying, gastric secretion of water and hydrogen ion (H+), and intragastric volume and H+ concentration. A continuous intravenous infusion of either saline (control) or cimetidine (4 mg X kg-1 X h-1) was administered during a 40-min fasting steady state and following intragastric instillation of 100 ml of water. During fasting, administration of cimetidine abolished H+ secretion and significantly decreased fractional emptying rate and water secretion (P less than 0.05). After the water load, cimetidine also suppressed H+ secretion and reduced fractional emptying and water secretion compared with control (P less than 0.05). Increasing HCl concentration of the test solution to 50 mM significantly decreased fractional emptying both during saline and further suppressed emptying during cimetidine infusion (P less than 0.05). In conclusion, cimetidine significantly decreased gastric emptying during fasting and following a liquid load. Restoring intragastric acidity to physiological levels removed the effect of gastric acid suppression on emptying and unmasked the full potential for cimetidine to decrease gastric emptying, possibily through an effect on gastric smooth muscle.
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34

Covasa, Mihai, and Robert C. Ritter. "Adaptation to high-fat diet reduces inhibition of gastric emptying by CCK and intestinal oleate." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 1 (January 1, 2000): R166—R170. http://dx.doi.org/10.1152/ajpregu.2000.278.1.r166.

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Rats maintained on low-fat (LF) or high-fat (HF) diets were fitted with gastric cannulas and duodenal catheters. Intraperitoneal injection of 0.250–2.0 μg/kg cholecystokinin (CCK) significantly inhibited gastric emptying of a 5-ml NaCl load in LF rats by 26.2–55.1% compared with emptying after vehicle injection. By contrast, CCK-induced inhibition of gastric emptying was significantly less in HF rats given the same CCK doses (10.0–31.7% inhibition over the same CCK dose range). A 20-min intraduodenal infusion of oleate (0.03 or 0.06 kcal/ml) also resulted in significant inhibition of gastric emptying in LF rats (24 and 89%, respectively). Oleate-induced inhibition of gastric emptying was significantly attenuated in rats maintained on the HF diet (2 and 56%, respectively). Unlike CCK injections or oleate infusion, intraduodenal maltotriose infusion inhibited gastric emptying to a similar degree in LF and HF rats (77 and 78%, respectively). These results indicate that feeding HF diets diminishes the enterogastric inhibition of gastric emptying by intestinal oleate and diminishes the ability of CCK to inhibit gastric emptying.
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35

Moran, Timothy H., James B. Wirth, Gary J. Schwartz, and Paul R. McHugh. "Interactions between gastric volume and duodenal nutrients in the control of liquid gastric emptying." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 4 (April 1, 1999): R997—R1002. http://dx.doi.org/10.1152/ajpregu.1999.276.4.r997.

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We examined the relationships between gastric volume and duodenal glucose load in the regulation of gastric emptying in adult male rhesus monkeys. Intragastric glucose loads (0.125 g/ml) of volumes ranging from 150 to 375 ml empty from the stomach at the same rate from 20 to 120 min. However, to achieve these equivalent emptying rates, progressively larger volumes were emptied in the initial 20 min with increasing gastric volume. Duodenal glucose infusions dose dependently inhibited the 10-min emptying of various volumes of intragastric saline. Although increasing gastric volume resulted in increased emptying, duodenal glucose right-shifted the relationship between initial gastric volume and volume emptied. These data demonstrate that liquid nutrient gastric emptying represents an interaction between gastric volume and nutrient-induced duodenal feedback. For controlled duodenal caloric delivery rates to be established, sufficient nutrient emptying must occur to increase the magnitude of duodenal feedback to withhold a given gastric volume.
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36

Ott, Linda, Byron Young, Reneé Phillips, Craig McClain, Linas Adams, Robert Dempsey, Phillip Tibbs, and U. Yun Ryo. "Altered gastric emptying in the head-injured patient: relationship to feeding intolerance." Journal of Neurosurgery 74, no. 5 (May 1991): 738–42. http://dx.doi.org/10.3171/jns.1991.74.5.0738.

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✓ Most patients with moderate to severe head injury initially do not tolerate enteral feedings postinjury. This intolerance is more prolonged than that found in patients suffering other types of trauma. The authors prospectively evaluated 12 patients with moderate to severe head injury (Glasgow Coma Scale score between 4 and 10) throughout their hospitalization for liquid gastric emptying as a possible mechanism for intolerance to enteral feeding. During Week 1, the majority of patients displayed a delay in gastric emptying. Patients also displayed an abnormal biphasic response (gastric emptying faster than normal during the early stage but prolonged later). By Week 2, many patients still had delayed and abnormal biphasic responses to gastric emptying. By Week 3, an improvement was observed with the majority of patients exhibiting rapid gastric emptying, but delays and abnormal biphasic responses were still seen. Patients who initially had rapid or normal gastric emptying tolerated full-strength full-rate feedings significantly earlier compared with those who experienced delayed gastric emptying (8.5 ± 0.5 days vs. 13.7 ± 3.2 days, p < 0.001). All patients tolerated full-strength full-rate feedings by Day 16 postinjury (range 7 to 16 days) except the two patients who displayed delayed gastric emptying for prolonged periods of time (mean 25 days). This is the first study to longitudinally evaluate gastric emptying following head injury. The authors suggest that patients with moderate to severe head injury often experience alterations in gastric emptying which may affect their ability to tolerate enteral feedings.
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37

Kaplan, Joel M., William H. Siemers, Ulrika Smedh, Gary J. Schwartz, and Harvey J. Grill. "Gastric branch vagotomy and gastric emptying during and after intragastric infusion of glucose." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 5 (November 1, 1997): R1786—R1792. http://dx.doi.org/10.1152/ajpregu.1997.273.5.r1786.

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The effect of gastric branch vagotomy (GVX) on the gastric emptying of glucose was evaluated during two phases of emptying control: as the stomach fills and in the postload period. GVX and control rats received a series of intragastric glucose infusions (1.0 ml/min) through indwelling gastric fistulas. In experiment 1, gastric samples were withdrawn either immediately after the offset of 9- or 18-min infusions of 12.5% glucose or at various times up to 36 min postinfusion. In experiment 2, samples were withdrawn either immediately or 30 min after termination of 12-min infusions of 12.5 or 25% glucose. After gastric fill, glucose solute emptying rate was stable over time, not influenced by concentration doubling, and, surprisingly, not affected by GVX. During gastric fill, solute emptying rate doubled with concentration in both GVX and control rats. For each concentration, however, glucose emptied during fill at almost twice the rate in GVX compared with control rats. This accelerated emptying of glucose during fill in GVX rats is consistent with a gastric vagal contribution to inhibitory mechanisms (e.g., receptive relaxation) that operate as the stomach fills under normal conditions. The absence of a GVX effect on emptying after fill suggests either that gastric branch vagal efferents play little role in feedback inhibitory control of glucose emptying under normal conditions or that other systems compensate for the function previously served by vagal gastric branch efferents. Further work is required to address the possible role of the gastric vagus in feedback control of gastric emptying when nutritive fluids other than glucose are delivered.
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38

Lorenz, D. N. "Gastric emptying of milk in rat pups." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 6 (June 1, 1985): R732—R738. http://dx.doi.org/10.1152/ajpregu.1985.248.6.r732.

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Gastric emptying of rat's milk in rat pups was investigated using two experimental procedures. In the first experiment pups were matched for age, body weight, and gastric contents after ingesting mother's milk in the natural suckling situation. Then the pups were placed in one of three different environmental conditions for the test period. They were killed at 0, 2, or 4 h, and their gastric contents were weighed. The results revealed a very consistent gastric emptying process across ages, regardless of the presence or absence of the dam or moderate alterations in the environment. Gastric volume appeared to be the only factor affecting the rate of gastric emptying. In the second experiment gastric emptying was investigated in fasted pups after intubation with one of several volumes of rat's milk. Pups were killed at 0, 1, 2, or 4 h after gavage, and their gastric contents were weighed. The results indicate that the rate of gastric emptying is directly related to the immediate gastric volume. The emptying process is described as exponential, but the distribution of halftime values indicates the kinetics are not strictly first order. The volume-related effect on gastric emptying rate also correlated highly with the volume-related suppression of ingestion reported in a previous study. A model of gastric emptying is proposed for infant mammals.
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39

Conover, K. L., S. M. Collins, and H. P. Weingarten. "A comparison of cholecystokinin-induced changes in gastric emptying and feeding in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 1 (July 1, 1988): R21—R26. http://dx.doi.org/10.1152/ajpregu.1988.255.1.r21.

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We have compared the abilities of the cholecystokinin octapeptide (CCK-8) to delay gastric emptying and to influence feeding under similar experimental conditions in the rat. The effect of CCK-8 on gastric emptying was assessed in 6-h-deprived rats receiving 10-ml intragastric test loads of 0.15 M saline or 15% (wt/vol) sucrose. Analysis of half-emptying times indicated that intraperitoneal administration of CCK-8 in doses of 1.4-22.4 micrograms/kg produced a dose-dependent retardation of emptying of both saline and nutrient. Lower doses of CCK-8, 0.01 and 0.1 micrograms/kg, had no effect on gastric emptying. The effect of CCK-8 on feeding was assessed in normally feeding rats tested under the same experimental conditions used in the gastric emptying studies. Doses of CCK-8 capable of retarding gastric emptying also suppressed eating in a dose-dependent manner. These findings provide necessary correlational support for the hypothesis that the satiety produced by CCK-8 may be mediated by inhibition of gastric emptying. However, a further quantitative analysis of the correspondence of the gastric emptying and feeding effects of CCK-8 suggest that retardation of emptying cannot account entirely for the satiety effect of the peptide.
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40

Barquist, E., M. Zinner, J. Rivier, and Y. Tache. "Abdominal surgery-induced delayed gastric emptying in rats: role of CRF and sensory neurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 4 (April 1, 1992): G616—G620. http://dx.doi.org/10.1152/ajpgi.1992.262.4.g616.

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The role of peripheral corticotropin-releasing factor (CRF) and afferent pathways in mediating abdominal surgery-induced delayed gastric emptying was investigated using an intravenous injection of the competitive CRF antagonist alpha-helical CRF9-41 and capsaicin pretreatment in adult fasted rats. Gastric emptying of a non-caloric solution was measured by the phenol red method. Intravenous CRF (0.13 nmol) inhibited by 65% gastric emptying. CRF effect was completely reversed by simultaneous intravenous injection of alpha-helical CRF9-41 (13 nmol). Abdominal surgery under enflurane anesthesia inhibited gastric emptying by 60% measured 3 h postoperatively. Enflurane anesthesia alone had no effect on gastric emptying 3 h after exposure. Abdominal surgery-induced delay of gastric emptying was reversed by 46, 60, and 100% by capsaicin pretreatment (125 mg/kg, -3 wk), intravenous injection of alpha-helical CRF9-41 (13 nmol), and combined pretreatments with capsaicin and CRF antagonist, respectively. Capsaicin and alpha-helical CRF9-41 given alone or in combination did not influence gastric emptying. These results indicate that peripheral CRF receptors along with capsaicin-sensitive afferent neurons contribute to somatovisceral stress (abdominal surgery)-induced delayed gastric emptying.
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41

Coulie, B., J. Tack, B. Maes, B. Geypens, M. De Roo, and J. Janssens. "Sumatriptan, a selective 5-HT1 receptor agonist, induces a lag phase for gastric emptying of liquids in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 4 (April 1, 1997): G902—G908. http://dx.doi.org/10.1152/ajpgi.1997.272.4.g902.

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Sumatriptan, a 5-hydroxytryptamine1 (5-HT1) receptor agonist at enteric neuronal 5-HT receptors, causes a relaxation of the gastric fundus and inhibition of antral contractile activity. The present study examined the effect of sumatriptan on gastric emptying of solids and liquids in humans. In eight healthy subjects the gastric emptying rate for liquids and solids was measured using the carbon-labeled glycine and octanoic acid breath test after subcutaneous administration of placebo or sumatriptan. Sumatriptan increased the gastric half-emptying time of liquids (P < 0.0005) and induced a prolonged lag phase for liquids (P < 0.0005) in all subjects. Sumatriptan increased gastric half-emptying time (P < 0.005) and the lag phase of solids (P < 0.05) in all subjects. In two healthy subjects gastric emptying of liquids and solids after subcutaneous administration of sumatriptan was studied by radioscintigraphy. Radioscintigraphy confirmed the delayed emptying and the prolonged lag phases after sumatriptan. In conclusion, sumatriptan delays gastric emptying of solids and liquids in healthy subjects. Moreover, sumatriptan induces a lag phase for liquids. The mechanism by which sumatriptan alters gastric emptying remains to be studied.
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42

Perano, Shiree J., Chris K. Rayner, Stamatiki Kritas, Michael Horowitz, Kim Donaghue, Christine Mpundu-Kaambwa, Lynne Giles, and Jenny J. Couper. "Gastric Emptying Is More Rapid in Adolescents With Type 1 Diabetes and Impacts on Postprandial Glycemia." Journal of Clinical Endocrinology & Metabolism 100, no. 6 (June 1, 2015): 2248–53. http://dx.doi.org/10.1210/jc.2015-1055.

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Context: Gastric emptying is a critical determinant of postprandial glycemic control in health and type 1 diabetes. There are few studies that assess the relationship between gastric emptying and postprandial glycaemia in adolescents with type 1 diabetes. Objective: The objectives of the study were to quantify gastric emptying in adolescents with type 1 diabetes and examine its relationship to postprandial glycaemia and autonomic function. Design: This was a case-control study. Gastric half-emptying time of a solid meal was measured by a 13C-octanoate breath test. Cardio-autonomic function was measured by heart rate variability. Chronic and postprandial gastrointestinal symptoms were evaluated by questionnaire and visual analog scales. Blood glucose concentrations were monitored frequently during the study. Setting: The study was conducted at a tertiary pediatric hospital in South Australia. Participants: Thirty adolescents (aged 15 ± 2.5 y) with type 1 diabetes and age- and sex-matched controls (gastric emptying, n = 20; heart rate variability, n = 135) participated in the study. Main Outcome: Gastric half-emptying time was the main outcome in the study. Results: Gastric emptying was more rapid in subjects with type 1 diabetes than controls [median half emptying time 78 (interquartile range 61–99) vs 109 (interquartile range 71–124) min, P = .02]. The postprandial rise in blood glucose at 60 minutes was strongly related to gastric half-emptying time (R = −0.65, P = .0001). Gastric emptying was slower in subjects with fasting hyperglycemia but was not related to heart rate variability. Nausea, bloating, and anxiety were related to fasting glycemia (P = .03). Conclusion: Rapid gastric emptying is a major determinant of postprandial glycemia in adolescents with type 1 diabetes. This observation has significant implications for therapy.
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43

Burton, Duane D., H. Jae Kim, Michael Camilleri, Debra A. Stephens, Brian P. Mullan, Michael K. O’Connor, and Nicholas J. Talley. "Relationship of gastric emptying and volume changes after a solid meal in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 2 (August 2005): G261—G266. http://dx.doi.org/10.1152/ajpgi.00052.2005.

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Noninvasive imaging has been developed to measure gastric volumes. The relationship between gastric emptying and volume postprandially is unclear. The aims were to 1) develop a 3-dimensional (3D) single photon emission-computed tomography (SPECT) method to simultaneously measure gastric volume and emptying postprandially, 2) describe the course of gastric volume change during emptying of the meal, and 3) assess a 3D method measuring gastric emptying. In 30 healthy volunteers, we used 111In-planar and 99mTc-SPECT imaging to estimate gastric emptying and volume after a radiolabeled meal. A customized analysis program of SPECT imaging assessed gastric emptying. A Bland-Altman plot assessed the performance of the new SPECT analysis compared with planar analysis. Gastric volume postprandially exceeds the fasting volume plus meal volume. The course of volume change and gastric emptying differ over time. Higher differences in volumes exist relative to fasting plus residual meal volumes at 15 min (median 763 vs. 568 ml, respectively, P < 0.001), 1 h (median 632 vs. 524 ml, P < 0.001), and 2 h (median 518 vs. 428 ml, P < 0.02), in contrast to similar volumes at 3 h (median 320 vs. 314 ml, P = 0.85). Analysis of SPECT imaging accurately measures gastric emptying compared with planar imaging with median differences of 1% (IQR −2.25 to 2.0) at 1 h, 1% (−3.25 to 2.25) at 2 h, and −2.5% (−4 to 0) at 3 h. Gastric volume exceeds meal volume during the first 2 postprandial hours, and simultaneous measurements of gastric volume and emptying can be achieved with a novel 3D SPECT method.
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44

Hegar, Badriul, and Yvan Vandenplas. "Electrogastrography in Delayed Gastric Emptying." Paediatrica Indonesiana 38, no. 9-10 (July 11, 2017): 181. http://dx.doi.org/10.14238/pi38.9-10.1998.181-92.

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Disorders of gastric motility are generally manifested by an abnormal rate of gastric emptying. The emptying process of the stomach is very complex, and knowledge is limited to the observation that gastric emptying rate is a highly variable phenomenon, and that delayed gastric emptying is frequently the case. The advances in the knowledge of the physiology of gastric muscle and enteric nerves, and the recognition of the patterns of organization of smooth muscle contractions gave a new input to the study of gastric motility. The gastric emptying can be monitored in various ways, such as manometry, scintigraphy, or electrogastrography (EGG). Recently, EGG has received more attention. There is correlation between the EGG signal obtained from body surface electrodes and signals obtained directly from electrodes locates in the gastric muscle (serosal records). Some studies showed an association between EGG-findings and gastric motility disorders, and indicate that EGG is a reliable, non-invasive, useful method to detect gastric myoelectric activity.
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45

Tominaga, K., T. Kido, M. Ochi, C. Sadakane, A. Mase, H. Okazaki, H. Yamagami, et al. "The Traditional Japanese Medicine Rikkunshito Promotes Gastric Emptying via the Antagonistic Action of the 5-HT3Receptor Pathway in Rats." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–8. http://dx.doi.org/10.1093/ecam/nep173.

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The traditional Japanese medicine rikkunshito ameliorates the nitric oxide-associated delay in gastric emptying. Whether rikkunshito affects gastric motility associated with 5-hydroxytryptamine (serotonin: 5-HT) receptors or dopamine receptors is unknown. We examined the effects of rikkunshito on the delay in gastric emptying induced by 5-HT or dopamine using the phenol red method in male Wistar rats. 5-HT (0.01–1.0 mg kg−1, i.p.) dose dependently delayed gastric emptying, similar to the effect of the 5-HT3receptor agonist 1-(3-chlorophenyl) biguanide (0.01–1.0 mg kg−1, i.p.). Dopamine also dose dependently delayed gastric emptying. The 5-HT3receptor antagonist ondansetron (0.04–4.0 mg kg−1) and rikkunshito (125–500 mg kg−1) significantly suppressed the delay in gastric emptying caused by 5-HT or 1-(3-chlorophenyl) biguanide. Hesperidin (the most active ingredient in rikkunshito) suppressed the 5-HT-induced delayed gastric emptying in a dose-dependent manner, the maximum effect of which was similar to that of ondansetron (0.4 mg kg−1). The improvement obtained by rikkunshito or ondansetron in delaying gastric emptying was completely blocked by pretreatment with atropine. Rikkunshito appears to improve delay in gastric emptying via the antagonistic action of the 5-HT3receptor pathway.
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46

Yin, Jieyun, and Jiande D. Z. Chen. "Electroacupuncture improves rectal distension-induced delay in solid gastric emptying in dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 2 (August 2011): R465—R472. http://dx.doi.org/10.1152/ajpregu.00271.2010.

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The aim of this study was to investigate the effects and mechanisms of electroacupuncture (EA) on rectal distension (RD)-induced delay in solid gastric emptying in dogs. Gastric emptying of solids was assessed in 12 dogs chronically implanted with a duodenal cannula by collecting samples at different time points from the cannula and measuring the dried weights of the samples. Bethanechol and atropine were used to qualitatively validate the method. In separate experiments, gastric emptying of solids was measured in a number of sessions: control, RD, RD + sham-EA, RD + EA of 6 mA, RD + EA of 3 mA, and RD + EA + naloxone. The method of gastric emptying by collecting and drying gastric chyme from the duodenal cannula was found to be accurate and reliable. Using the method, we found gastric emptying to be accelerated with bethanechol (70.01 ± 8.10% vs. 82.61 ± 4.15%, P = 0.04, vs. control) and delayed with atropine (4.31 ± 1.57%, P < 0.001, vs. control). RD substantially and significantly delayed gastric emptying. EA, but not sham-EA, attenuated delayed gastric emptying induced by RD (sham-EA: 48.79 ± 9.47% vs. EA: 74.28 ± 5.96%, P < 0.01). The effect was more potent with EA of 6 mA than EA of 3 mA and blocked by naloxone. EA is able to attenuate RD-induced delay in gastric emptying of solids, and this ameliorating effect may be mediated via the opioid pathway. EA may have a therapeutic potential for treating delayed gastric emptying attributed to lower gut distension.
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47

Gregory, P. C., M. Mcfadyen, and D. V. Rayner. "Pattern of gastric emptying in the pig: Relation to feeding." British Journal of Nutrition 64, no. 1 (July 1990): 45–58. http://dx.doi.org/10.1079/bjn19900008.

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The aims of the present study were to compare the gastric emptying of dry matter (DM) and liquids during the feeding period with that following meal consumption, to clarify the relationship between feeding and gastric emptying, and to investigate how gastric emptying changes in growing animals. The studies were performed in pigs fitted with a gastric cannula and fed on a normal finely ground solid diet mixed with water containing CrEDTA as liquid marker. Gastric emptying was measured using a gastric evacuation technique. It was observed that between 0.75 and 6 h after feeding the total amounts emptied increased, but the proportion of the meal emptied fell, with increase in meal size; emptying of both DM and liquids with large and small meals followed and exponential pattern. In contrast, while the animals were feeding, there was linear and rapid emptying of both DM and liquids following a very short (approximately 2 min) lag phase before emptying began. The rate of emptying increased linearly with body-;weight (by 0.55 g DM/min and by 0.24 ml/min per kg body-weight over the range 58–200 kg) such that the emptying of digestible energy per kg metabolic body-weight (W0.75) was roughly maintained (between 2.9 and 3.2 kJ/min per kg W0.75). This suggests that the rate of emptying may be linked in some way with the metabolic requirements of the body. The biphasic pattern of gastric emptying observed is probably the intrinsic pattern of emptying of a meal which does not require breakdown of particles before emptying can occur.
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48

Parkman, H. P., J.-L. C. Urbain, L. C. Knight, K. L. Brown, D. M. Trate, M. A. Miller, A. H. Maurer, and R. S. Fisher. "Effect of gastric acid suppressants on human gastric motility." Gut 42, no. 2 (February 1, 1998): 243–50. http://dx.doi.org/10.1136/gut.42.2.243.

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Background—The effect of histamine H2receptor antagonists on gastric emptying is controversial.Aims—To determine the effects of ranitidine, famotidine, and omeprazole on gastric motility and emptying.Patients and methods—Fifteen normal subjects underwent simultaneous antroduodenal manometry, electrogastrography (EGG), and gastric emptying with dynamic antral scintigraphy (DAS). After 30 minutes of fasting manometry and EGG recording, subjects received either intravenous saline, ranitidine, or famotidine, followed by another 30 minutes recording and then three hours of postprandial recording after ingestion of a radiolabelled meal. Images were obtained every 10–15 minutes for three hours to measure gastric emptying and assess antral contractility. Similar testing was performed after omeprazole 20 mg daily for one week.Results—Fasting antral phase III migrating motor complexes (MMCs) were more common after ranitidine (9/15 subjects, 60%), famotidine (12/15, 80%), and omeprazole (8/12, 67%) compared with placebo (4/14, 29%; p<0.05). Postprandially, ranitidine, famotidine, and omeprazole slowed gastric emptying, increased the amplitude of DAS contractions, increased the EGG power, and increased the antral manometric motility index.Conclusions—Suppression of gastric acid secretion with therapeutic doses of gastric acid suppressants is associated with delayed gastric emptying but increased antral motility.
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49

Jehangir, Asad, and Henry P. Parkman. "Role of Gastric Emptying in Symptoms of Gastroparesis." Gastrointestinal Disorders 1, no. 4 (November 19, 2019): 391–402. http://dx.doi.org/10.3390/gidisord1040032.

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The symptoms of gastroparesis, such as nausea, vomiting, postprandial fullness, early satiety and abdominal pain, frequently impair the quality of life of the affected individuals. The diagnosis of gastroparesis is made after structural etiologies are ruled out and an assessment of gastric function shows delayed gastric emptying. The role of the delay in gastric emptying in the pathogenesis of symptoms of gastroparesis has been debated, with some studies suggesting an association between delayed gastric emptying and the upper gastrointestinal symptoms, while others do not. The recent literature supports the importance of using reliable methods to assess gastric emptying, as delay in gastric emptying measured on a reliable test (4-h scintigraphy or breath test) is associated with the severity of upper gastrointestinal symptoms. In addition to measuring total gastric emptying, evaluation of regional gastric retention in the proximal and distal stomach and whole gut transit to assess small intestinal and colonic transit may provide additional useful information in patients with more generalized symptoms of gastrointestinal dysmotility.
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50

van der Velde, P., I. Koslowsky, and H. S. Koopmans. "Measurement of gastric emptying during and between meal intake in free-feeding Lewis rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 2 (February 1, 1999): R597—R605. http://dx.doi.org/10.1152/ajpregu.1999.276.2.r597.

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A new scintigraphic measurement technique is described that allows accurate assessment of gastric emptying in between as well as during a number of successive meals. Measurements were made every minute of food intake, gastric nutrient filling, and gastric emptying over a 6 h, 40 min period in conscious, free-feeding, loosely restrained rats. Before receiving access to the food, the animals had been deprived for a period of 31 h. Over the full duration of the experiment, an average rate of gastric emptying of 2.46 ± 0.18 (SE) kcal/h was established. During most meals, however, the gastric emptying rate was increased so that an average of 26.9 ± 2.7% of the ingested calories was emptied while the animals were feeding, with an average emptying rate of 0.15 ± 0.014 kcal/min or 8.88 ± 0.84 kcal/h. This transient increase in the rate of gastric emptying was followed by a subsequent slowing of gastric emptying after meal termination; in the 10-min postmeal interval, an average emptying rate of 0.96 ± 0.12 kcal/h was found. Despite these fluctuations during and immediately after meals, a relatively constant rate of caloric emptying is maintained over longer periods. There were no differences between the emptying rate during the first meal when the gastrointestinal tract was still empty, compared with later meals when the gastrointestinal tract had been filled with food. The emptying rate during the 10-min postmeal interval, however, was significantly reduced during later meals. The results suggest that gastric emptying is controlled by different mechanisms during and after the ingestion of food and that these mechanisms remain in effect at various degrees of gastrointestinal filling.
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