Inhibitory effect of ileal oleate on postprandial motility of the upper gut

1991 ◽  
Vol 261 (3) ◽  
pp. G458-G463 ◽  
Author(s):  
Z. Dreznik ◽  
D. Brocksmith ◽  
T. A. Meininger ◽  
N. J. Soper
Keyword(s):  
Oleic Acid ◽  
Gastric Emptying ◽  
Gamma Camera ◽  
Delayed Gastric Emptying ◽  
Early Period ◽  
Inhibitory Effect ◽  
Myoelectric Activity ◽  
Phenol Red ◽  
Mixed Meal ◽  
Postprandial Motility

To determine the effect of ileal oleate on postprandial gastrointestinal motility, duodenal and paired perfusion-aspiration ileal catheters and bipolar duodenal and jejunal electrodes were surgically implanted in five dogs. The ileum was perfused with either saline or an isotonic oleic acid emulsion at 2 ml/min. A 205-kcal mixed meal containing 120 ml liquid nutrient labeled with 111In-diethylenetriamine pentaacetic acid (DTPA) and solid food labeled with 99mTc was then administered orally. Gastric emptying was assessed by a gamma camera, myoelectric activity was continuously monitored, and duodenal-ileal transit of phenol red was determined over the ensuing 240 min. Ileal oleate reduced duodenal spikeburst frequency by 50% (P less than 0.05) and delayed gastric emptying of liquids and solids. Four hours after ingesting the meal, 62% of solids and 34% of liquids were retained in the stomach during oleic acid perfusion compared with 25 and 4%, respectively, when saline was perfused (P less than 0.05). Duodenal-ileal transit was markedly slowed by ileal perfusion with the oleic acid emulsion (P less than 0.001). Ileal oleate therefore exerted a profound inhibitory effect on proximal gut motility in the early period after ingestion of a mixed-nutrient meal in dogs.

scholarly journals Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

2006 ◽  
Vol 290 (3) ◽  
pp. G511-G518 ◽  
Author(s):  
József Czimmer ◽  
Mulugeta Million ◽  
Yvette Taché
Keyword(s):  
Gastric Emptying ◽  
Receptor Agonist ◽  
Inhibitory Action ◽  
Delayed Gastric Emptying ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Factor ◽  
Phenol Red ◽  
Sympathetic Blockade ◽  
Intracisternal Injection ◽  
Urocortin 1

We characterized the influence of the selective corticotropin-releasing factor 2 (CRF2) receptor agonist human urocortin 2 (Ucn 2), injected intracisternally, on gastric emptying and its mechanism of action compared with intracisternal CRF or urocortin (Ucn 1) in conscious rats. The methylcellulose phenol red solution was gavaged 20 min after peptide injection, and gastric emptying was measured 20 min later. The intracisternal injection of Ucn 2 (0.1 and 1 μg) and Ucn 1 (1 μg) decreased gastric emptying to 37.8 ± 6.9%, 23.1 ± 8.6%, and 21.6 ± 5.9%, respectively, compared with 58.4 ± 3.8% after intracisternal vehicle. At lower doses, Ucn 2 (0.03 μg) and Ucn 1 (0.1 μg) had no effect. The CRF2 antagonist astressin2-B (3 μg ic) antagonized intracisternal Ucn 2 (0.1 μg) and CRF (0.3 μg)-induced inhibition of gastric emptying. Vagotomy enhanced intracisternal Ucn 2 (0.1 or 1 μg)-induced inhibition of gastric emptying compared with sham-operated group, whereas it blocked intracisternal CRF (1 μg) inhibitory action (45.5 ± 8.4% vs. 9.7 ± 9.7%). Sympathetic blockade by bretylium prevented intracisternal and intracerebroventricular Ucn 2-induced delayed gastric emptying, whereas it did not influence intravenous Ucn 2-, intracisternal CRF-, and intracisternal Ucn 1-induced inhibition of gastric emptying. Prazosin abolished the intracisternal Ucn 2 inhibitory effect, whereas yohimbine and propranolol did not. None of the pretreatments modified basal gastric emptying. These data indicate that intracisternal Ucn 2 induced a central CRF2-mediated inhibition of gastric emptying involving sympathetic α1-adrenergic mechanisms independent from the vagus contrasting with the vagal-dependent inhibitory actions of CRF and Ucn 1.

scholarly journals Electrogastrography in Delayed Gastric Emptying

2017 ◽  
Vol 38 (9-10) ◽  
pp. 181
Author(s):  
Badriul Hegar ◽  
Yvan Vandenplas
Keyword(s):  
Gastric Emptying ◽  
Gastric Motility ◽  
Delayed Gastric Emptying ◽  
Myoelectric Activity ◽  
Gastric Emptying Rate ◽  
Gastric Myoelectric Activity ◽  
Enteric Nerves ◽  
Gastric Muscle ◽  
Abnormal Rate ◽  
Smooth Muscle Contractions

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.

scholarly journals Monitoring gastric myoelectric activity after pancreaticoduodenectomy for diet “readiness”

2018 ◽  
Vol 315 (5) ◽  
pp. G743-G751 ◽  
Author(s):  
Monica M. Dua ◽  
Anand Navalgund ◽  
Steve Axelrod ◽  
Lindsay Axelrod ◽  
Patrick J. Worth ◽  
...  
Keyword(s):  
At Risk ◽  
Gastric Emptying ◽  
Delayed Gastric Emptying ◽  
Oral Intake ◽  
Myoelectric Activity ◽  
Gastric Myoelectrical Activity ◽  
Myoelectrical Activity ◽  
Gastric Myoelectric Activity ◽  
Patients At Risk ◽  
Late Group

Postoperative delayed gastric emptying (DGE) is a frustrating complication of pancreaticoduodenectomy (PD). We studied whether monitoring of postoperative gastric motor activity using a novel wireless patch system can identify patients at risk for DGE. Patients ( n = 81) were prospectively studied since 2016; 75 patients total were analyzed for this study. After PD, battery-operated wireless patches (G-Tech Medical) that acquire gastrointestinal myoelectrical signals are placed on the abdomen and transmit data by Bluetooth. Patients were divided into early and late groups by diet tolerance of 7 days [enhanced recovery after surgery (ERAS) goal]. Subgroup analysis was done of patients included after ERAS initiation. The early and late groups had 50 and 25 patients, respectively, with a length of stay (LOS) of 7 and 11 days ( P < 0.05). Nasogastric insertion was required in 44% of the late group. Tolerance of food was noted by 6 versus 9 days in the early versus late group ( P < 0.05) with higher cumulative gastric myoelectrical activity. Diminished gastric myoelectrical activity accurately identified delayed tolerance to regular diet in a logistical regression analysis [area under the curve (AUC): 0.81; 95% confidence interval (CI), 0.74–0.92]. The gastric myoelectrical activity also identified a delayed LOS status with an AUC of 0.75 (95% CI, 0.67–0.88). This stomach signal continued to be predictive in 90% of the ERAS cohort, despite earlier oral intake. Measurement of gastric activity after PD can distinguish patients with shorter or longer times to diet. This noninvasive technology provides data to identify patients at risk for DGE and may guide the timing of oral intake by gastric “readiness.” NEW & NOTEWORTHY Limited clinical indicators exist after pancreaticoduodenectomy to allow prediction of delayed gastric emptying (DGE). This study introduces a novel, noninvasive, wireless patch system capable of accurately monitoring gastric myoelectric activity after surgery. This system can differentiate patients with longer or shorter times to a regular diet as well as provide objective data to identify patients at risk for DGE. This technology has the potential to individualize feeding regimens based on gastric activity patterns to improve outcomes.

scholarly journals The Traditional Japanese Medicine Rikkunshito Promotes Gastric Emptying via the Antagonistic Action of the 5-HT3Receptor Pathway in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
K. Tominaga ◽  
T. Kido ◽  
M. Ochi ◽  
C. Sadakane ◽  
A. Mase ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Receptor Agonist ◽  
Delayed Gastric Emptying ◽  
Maximum Effect ◽  
Phenol Red ◽  
Dependent Manner ◽  
Antagonistic Action ◽  
Traditional Japanese Medicine ◽  
Male Wistar Rats ◽  
Dose Dependent

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.

Mechanism of action of exenatide to reduce postprandial hyperglycemia in type 2 diabetes

2008 ◽  
Vol 294 (5) ◽  
pp. E846-E852 ◽  
Author(s):  
Antonio Cervera ◽  
Estela Wajcberg ◽  
Apiradee Sriwijitkamol ◽  
Marianella Fernandez ◽  
Pengou Zuo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Emptying ◽  
Delayed Gastric Emptying ◽  
Postprandial Hyperglycemia ◽  
Oral Glucose ◽  
Plasma Glucagon ◽  
Tracer Technique ◽  
Mixed Meal ◽  
Glucagon Suppression

We examined the contributions of insulin secretion, glucagon suppression, splanchnic and peripheral glucose metabolism, and delayed gastric emptying to the attenuation of postprandial hyperglycemia during intravenous exenatide administration. Twelve subjects with type 2 diabetes (3 F/9 M, 44 ± 2 yr, BMI 34 ± 4 kg/m2, Hb A1c 7.5 ± 1.5%) participated in three meal-tolerance tests performed with double tracer technique (iv [3-3H]glucose and oral [1-14C]glucose): 1) iv saline (CON), 2) iv exenatide (EXE), and 3) iv exenatide plus glucagon (E+G). Acetaminophen was given with the mixed meal (75 g glucose, 25 g fat, 20 g protein) to monitor gastric emptying. Plasma glucose, insulin, glucagon, acetaminophen concentrations and glucose specific activities were measured for 6 h post meal. Post-meal hyperglycemia was markedly reduced ( P < 0.01) in EXE (138 ± 16 mg/dl) and in E+G (165 ± 12) compared with CON (206 ± 15). Baseline plasma glucagon (∼90 pg/ml) decreased by ∼20% to 73 ± 4 pg/ml in EXE ( P < 0.01) and was not different from CON in E+G (81 ± 2). EGP was suppressed by exenatide [231 ± 9 to 108 ± 8 mg/min (54%) vs. 254 ± 29 to189 ± 27 mg/min (26%, P < 0.001, EXE vs. CON] and partially reversed by glucagon replacement [247 ± 15 to 173 ± 18 mg/min (31%)]. Oral glucose appearance was 39 ± 4 g in CON vs. 23 ± 6 g in EXE ( P < 0.001) and 15 ± 5 g in E+G, ( P < 0.01 vs. CON). The glucose retained within the splanchnic bed increased from ∼36g in CON to ∼52g in EXE and to ∼60g in E+G ( P < 0.001 vs. CON). Acetaminophen(AUC) was reduced by ∼80% in EXE vs. CON ( P < 0.01). We conclude that exenatide infusion attenuates postprandial hyperglycemia by decreasing EGP (by ∼50%) and by slowing gastric emptying.

Restraint stress delays solid gastric emptying via a central CRF and peripheral sympathetic neuron in rats

2005 ◽  
Vol 288 (2) ◽  
pp. R427-R432 ◽  
Author(s):  
Yukiomi Nakade ◽  
Daisuke Tsuchida ◽  
Hiroyuki Fukuda ◽  
Masahiro Iwa ◽  
Theodore N. Pappas ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Restraint Stress ◽  
Delayed Gastric Emptying ◽  
Sympathetic Neuron ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Solid Meal ◽  
Celiac Ganglionectomy ◽  
Meal Ingestion ◽  
Sympathetic Pathway

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.

scholarly journals Effect of standardizing the incision line on delayed gastric emptying after laparoscopic gastrectomy: A retrospective preliminary analysis

2020 ◽  
Author(s):  
Tomoya Tsukada ◽  
Masahide Kaji ◽  
Jun Kinoshita ◽  
Koichi Shimizu
Keyword(s):  
Gastric Emptying ◽  
Laparoscopic Gastrectomy ◽  
Delayed Gastric Emptying ◽  
Surgical Techniques ◽  
Early Period ◽  
Operation Time ◽  
Late Period ◽  
Billroth I ◽  
Billroth I Reconstruction ◽  
Perioperative Bleeding

Background: The use of totally laparoscopic surgery with Billroth-I reconstruction (delta-shaped anastomosis) has rapidly become widespread in recent years. However, we experienced delayed gastric emptying (DGE) in the early period after introduction of this technique. To the best of our knowledge, there are no report mentioned the incision line to prevent DGE in distal gastrectomy. In the present study, we standardized the surgical techniques, including the gastric incision line and compared the short-term results before and after standardization. Methods: A total of 86 patients were enrolled in this study. 28 procedures were performed in the early period and 58 procedures were performed in the late period, and the 2 groups were compared retrospectively. Results: The operation time decreased significantly after standardization from 288 min to 224 min (P &lt; 0.001). The median value of perioperative bleeding volume reduced from 22.5 mL to 12.5 mL (P =0.060). There were no postoperative complications related to the site of anastomosis in either group. 5 cases of DGE (17.8%) was noted in the early period, but only 2 cases (3.4%) in the late period (P =0.022). Conclusions: Standardization of the incision line after laparoscopic gastrectomy resulted in a decline in incidence of DGE.

Abdominal surgery-induced delayed gastric emptying in rats: role of CRF and sensory neurons

1992 ◽  
Vol 262 (4) ◽  
pp. G616-G620 ◽  
Author(s):  
E. Barquist ◽  
M. Zinner ◽  
J. Rivier ◽  
Y. Tache
Keyword(s):  
Gastric Emptying ◽  
Abdominal Surgery ◽  
Intravenous Injection ◽  
Delayed Gastric Emptying ◽  
Phenol Red ◽  
Afferent Neurons ◽  
Afferent Pathways ◽  
Enflurane Anesthesia ◽  
Fasted Rats

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.

Glucose-induced delay in fat absorption and in appearance of Stypven clot accelerator

1960 ◽  
Vol 199 (6) ◽  
pp. 1011-1014 ◽  
Author(s):  
John H. Tilden ◽  
Robert E. Shipley
Keyword(s):  
Small Intestine ◽  
Oleic Acid ◽  
Gastric Emptying ◽  
Intestinal Absorption ◽  
Delayed Gastric Emptying ◽  
Human Subjects ◽  
Peanut Oil ◽  
Fat Absorption ◽  
Glucose Feeding

When oleic-1-C14 acid was fed to dogs, the plasma isotope, lactescence and Stypven accelerator activity (AA) appeared simultaneously 2–4 hours after ingestion. When either peanut oil or labeled oleic acid was preceded, accompanied and followed by glucose feeding, the appearance of lactescence, AA and plasma isotope was again simultaneous but markedly delayed until 8–10 hours after fat ingestion. Serial roentgenograms of dogs given radiopaque (iodinated) peanut oil plus glucose showed that the delay in absorption of fat was not attributable to delayed gastric emptying. Although the appearance of fat in the small intestine was evident within 1–3 hours after ingestion, plasma lactescence and AA were not seen for 9–12 hours. The delay in intestinal absorption of orally ingested fat caused by glucose was also demonstrated in rats and in human subjects.

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