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Biomedical subjects

L M Akkermans

Publications and source records attributed to L M Akkermans.

At least 55 records · Page 3Linked to original sources

Function of the proximal stomach after Nissen fundoplication.

BACKGROUND: After Nissen fundoplication patients frequently report upper abdominal (dyspeptic) symptoms. Theoretically, these symptoms may be the result of changes in function of the proximal stomach as induced by fundoplication. METHODS: In this case-control study the response of the proximal stomach to both distension by an air-filled bag and a liquid meal were evaluated with the use of a barostat. In 12 patients after fundoplication and 12 healthy volunteers (age- and sex-matched) perception of symptoms was evaluated during both bag distension and liquid meal stimulus. RESULTS: The minimal distending pressure required to overcome the intra-abdominal pressure was significantly different between patients and controls (mean(s.e.m.) 9.34(0.26) versus 6.73(0.43) mmHg; P < 0.001). There was no difference between groups in either the fasted state, volume-pressure curve (compliance) or total symptom score. After ingestion of the liquid meal the adaptive relaxation in the fundoplication group was significantly less than that in controls (mean(s.e.m.) 150(29.2) versus 244(34.8) ml; P = 0.04). CONCLUSION: This study showed that after Nissen fundoplication compliance of the proximal stomach is no different from that in healthy volunteers. Postprandial relaxation of the proximal stomach is decreased and this abnormality may be involved in the pathogenesis of reported dyspeptic symptoms.

Adult↗

The role of interdigestive small bowel motility in the regulation of gut microflora, bacterial overgrowth, and bacterial translocation in rats.

OBJECTIVE: To clarify the role of the migrating motor complex (MMC) in the regulation of small intestinal microflora and bacterial translocation. SUMMARY BACKGROUND DATA: The intestinal microflora may serve as a source of infectious microorganisms. Failure of regulatory mechanisms of the intestinal flora could therefore play an important role in the pathogenesis of gut-derived infections. METHODS: Rats were fitted with small intestinal myoelectrodes. MMCs were measured on a control day and 3 consecutive days during continuous administration of morphine or placebo. Mesenteric lymph nodes, liver, spleen, peripheral blood, duodenum, and ileum samples were cultured quantitatively. RESULTS: The mean MMC cycle length in placebo-treated animals was 15.1+/-0.5 minutes. MMCs were completely disrupted after morphine treatment. Total bacterial growth in the duodenum was 7.27+/-0.34 10log colony-forming units (CFU)/g with placebo and 8.28+/-0.27 CFU/g with morphine. In placebo-treated animals, the mean MMC cycle length the day before culturing correlated with total bacterial growth in the duodenum. Translocation incidences to the mesenteric lymph nodes, liver, spleen, and blood were 0/8, 1/8, 0/8, and 0/8 with placebo and 7/8, 6/8, 5/8, and 0/8 with morphine. The overall translocation incidence was 1/8 in placebo-treated animals and 8/8 in morphine-treated animals. CONCLUSIONS: The MMC is an important mechanism controlling bacterial growth in the upper small bowel. Its disruption with morphine promotes duodenal bacterial overgrowth and bacterial translocation.

Animals↗

Gastrointestinal motility and gastric tube feeding in mechanically ventilated patients.

OBJECTIVE: To determine the fasted and fed gastrointestinal motility characteristics that are possibly responsible for gastric retention in mechanically ventilated patients. DESIGN: Prospective, case series. SETTING: Surgical intensive care unit of a university hospital. PATIENTS: Seven patients who required mechanical ventilation for thoracic or combined thoracic-neurologic injuries and nine healthy volunteers. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Antroduodenal manometry was performed during fasting and gastric feeding with a polymeric diet in patients during mechanical ventilation, weaning, and after detubation. Gastric retention volumes were determined during gastric tube feeding. Motility data were compared with recordings from nine healthy volunteers. During the fasting state, under sedation and morphine, the migrating motor complex in patients was significantly (p < .001) shortened: median 32.0 vs. 101.0 mins in healthy volunteers. During gastric tube feeding, the motility pattern did not convert to a normal postprandial pattern until morphine was discontinued. An interdigestive or mixed interdigestive-postprandial pattern was seen during gastric tube feeding in most patients during morphine administration. Most (94%) of the activity fronts during gastric feeding started in the duodenum. Gastric retention percentages during gastric tube feeding were negatively correlated (r2=.44; p < .01) with antral motor activity. CONCLUSIONS: These data suggest that morphine administration affects antroduodenal motility in mechanically ventilated patients. The gastrointestinal motor pattern involved in impaired gastric emptying in morphine-treated patients is characterized by antral hypomotility and persisting duodenal activity fronts during continuous intragastric feeding. The observed motility patterns suggest that early administration of enteral feeding might be more effective into the duodenum or jejunum than into the stomach of mechanically ventilated patients.

Adult↗

Circulating gastrointestinal hormone abnormalities in patients with severe idiopathic constipation.

OBJECTIVE: This study aimed to determine if there is an abnormality of circulating gastrointestinal hormones in patients with severe idiopathic constipation. METHODS: Twelve patients, all female (median age 34 yr) and 12 healthy controls (eight female, median age 32 yr) were studied. A radioisotope-labeled solid/liquid meal was ingested, and the serum hormone response, as well as the relationship between serum hormones and rates of gastric emptying and small intestinal transit, were studied for 180 min postprandially. RESULTS: Somatostatin levels were higher in patients with constipation (basal level, controls vs patients, 31 vs 57 pmol/L, p < 0.05, median values; peak level, 48 vs 60, p < 0.05). Patients showed a significantly lower somatostatin integrated incremental meal response (2182 vs 104, p < 0.05). No correlation was found between the somatostatin levels and rates of upper gastrointestinal transit in patients. Pancreatic glucagon was significantly decreased (p=0.04). Enteroglucagon levels were significantly lower (p > 0.05) in patients between 30 and 60 min after the meal. The peak found after the meal in normal subjects was absent. Basal levels of pancreatic glucagon correlated with small bowel transit by two different measures: head of meal (r=0.69, p=0.03) and cecal filling at the time of 50% gastric emptying (r=0.84, p=0.002). No significant differences between the two groups could be found for basal and peak levels at different times and integrated incremental response to the meal for insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), gastrin, pancreatic polypeptide (PP), motilin, neurotensin, and peptide tyrosine tyrosine (PYY). CONCLUSION: Patients with severe idiopathic constipation have specific abnormalities of circulating gut hormones that most likely play a role in gastrointestinal motility and that may be of pathophysiological significance.

Acute Disease↗

Responses to gastric distension in functional dyspepsia.

BACKGROUND: Studies have shown that an altered visceral perception threshold plays a role in the pathogenesis of upper gastrointestinal tract symptoms in dyspeptic patients. However, it is not clear whether the compliance and adaptive relaxation of the proximal stomach contribute to the symptoms. AIMS: To investigate whether abnormal relaxation or adaptation of the proximal stomach during the interdigestive state and the postprandial phase could explain the symptoms of functional dyspepsia. SUBJECTS: Twelve volunteers and 12 patients with dysmotility-like functional dyspepsia were included in the study. METHODS: An electronic barostat was used to investigate adaptation to distension of the proximal stomach and accommodation in response to a liquid meal. Dyspeptic symptoms during distension and accommodation were assessed. RESULTS: When the subjects were in the fasting state, the pressure-volume curve showed slightly higher compliance in the dyspeptic patients (p < 0.05). Patients not only had a higher score for nausea, bloating, and pain but also the increase in nausea and pain scores with intragastric pressure was higher than in volunteers (p < 0.05). The increase in intragastric bag volume in response to a meal was significantly lower in patients (p < 0.05). Both bloating and pain significantly increased in the patients (p < 0.05), but not in the healthy volunteers. CONCLUSIONS: Patients with functional dyspepsia show slightly higher compliance to mechanical distension. Their visceral perception of mechanical stress is enhanced. In contrast with the balloon distension, relaxation after a meal was less. Therefore the postprandial symptoms cannot be explained fully by greater global tension in the stomach wall, as assessed by the barostat technique. Visceral hypersensitivity plays a major role in the pathogenesis of the symptoms.

Adult↗

Motilin induces gall bladder emptying and antral contractions in the fasted state in humans.

BACKGROUND: Animal studies have shown that motilin affects gall bladder motility. In humans, no effect has been shown, but erythromycin, a motilin receptor agonist, induces gall bladder emptying. AIMS: To explore the effect of increasing doses of exogenous motilin on gall bladder volume and antral contractility in the fasted state in humans. METHODS: After an overnight fast, eight healthy men received increasing intravenous doses of Leu13-motilin (KW-5139) or 0.9% NaCl in a double blind, randomised fashion. Gall bladder volume and antral contraction frequency were determined by ultrasonography. RESULTS: Infusion of motilin increased plasma motilin levels. Motilin induced a reduction in gall bladder volume of 8.0 (5.0)%, 17.1 (5.0)%, 18.5 (4.7)%, and 16.1 (4.9)% of baseline volume at the end of infusion of 2, 4, 8, and 16 pmol/kg/min respectively, compared with mean stable gall bladder volumes during placebo infusion (p < 0.05). Antral contraction frequency increased during motilin infusion, but not during placebo infusion (p < 0.05). CONCLUSIONS: Exogenous motilin reducted fasting gall bladder volume and increased antral contractions. After reaching maximal reduction, the gall bladder volume did not decrease further during continuous motilin infusion at higher doses and stayed at the same reduced volume. The degree of gall bladder volume reduction during motilin infusion mimicked gall bladder emptying preceding antral phase III activity of the migrating motor complex in humans. This study indicates that motilin may play a physiological role in the regulation of gall bladder emptying in the fasted state.

Adult↗

Effects of long-term oral L-arginine on esophageal motility and gallbladder dynamics in healthy humans.

Inhibitory nitrergic neurons are known to play a role in the regulation of motility patterns of the distal esophagus, the lower esophageal sphincter (LES), and the gallbladder. Our study aim was to investigate the effects of "long-term" (i.e., prolonged) oral intake of L-arginine (L-Arg), the endogenous source for nitric oxide (NO) synthesis, on postprandial LES pressure (LESP), esophageal motility, gastroesophageal reflux, and gallbladder motility. L-Arg (30 g/day) or glycine (placebo; 13 g/day; isosmolar) was given orally to 10 healthy male volunteers for 8 days, according to a randomized, crossover design. Twenty-four-hour urinary nitrite/nitrate excretion was measured to indicate NO synthesis. Basal early postprandial LESP was lower after L-Arg ingestion (2.2 kPa) than after glycine ingestion (2.7 kPa) (P < 0.05). L-Arg abolished the physiological late postprandial rise in LESP. Transient LES relaxations were longer lasting after L-Arg ingestion (P < 0.02). Esophageal motility and reflux were not affected (not significant). Fasting and residual gallbladder volumes were greater after L-Arg ingestion (P < 0.05). Urinary nitrite/nitrate excretion was higher after L-Arg intake (P < 0.05). In conclusion, long-term oral L-Arg suppresses late postprandial LESP increase, prolongs transient LES relaxations, and increases fasting and residual gallbladder volumes. These effects may be mediated by increased NO synthesis.

Adult↗

Migrating motor complex cycle duration is determined by gastric or duodenal origin of phase III.

The migrating motor complex (MMC) shows large variations within an individual and between individuals. This study aimed to investigate, with respect to this variability, the importance of gastric or duodenal origin of phase III activity. Interdigestive 6- to 10-h stationary antroduodenal motility recordings of 19 healthy male subjects were analyzed for MMC cycle durations and duration of phases I, II, and III, all with respect to the place of origin of each phase III. Data are given for the duodenal recording site as means +/- SE. Mean MMC cycle duration was 117.3 +/- 13.9 min, regardless of the place of origin of phase III. Seventy-two phase III cycles were observed in total, 35 and 37 starting in the "antrum" and duodenum, respectively. After a phase III of "antral" origin, MMC cycle duration was 156.1 +/- 11.0 min, significantly longer than MMC cycle duration following a phase III of duodenal origin, 80.5 +/- 10.7 min (P < 0.001). Phase III duration was longer when of "antral" origin than when starting in the duodenum (7.6 +/- 0.4 and 5.3 +/- 0.4 min, respectively; P < 0.001). MMC cycle duration and duration of phases I, II, and III depend on the place of origin of phase III ("antral" or duodenal) and on the origin of the preceding phase III. This factor explains part of the MMC variability observed within individuals. Mean MMC cycle duration in healthy subjects or patients should therefore also include information on the origin of phase III.

Adult↗

CCKA and CCKB receptor subtypes both mediate the effects of CCK-8 on myenteric neurons in the guinea-pig ileum.

The effects of cholecystokinin (CCK-8) on myenteric S neurons were investigated by intracellular recording techniques, with the aim to determine the CCK receptor subtypes involved. CCK-8 (1-1000 nM) evoked concentration-dependent long-lasting excitatory responses in 45 of 54 neurons. CCK receptor antagonists were applied to 15 neurons in which CCK-8 evoked an excitatory response. In 5 of these neurons, application of the CCKA antagonist L-364,718 (100-500 nM) antagonized the action of CCK-8 and the CCKB antagonist L-365,260 (500 nM) had no effect. L-365,260 (100-500 nM) antagonized the CCK-8 induced response in 5 neurons, on which L-364,718 had no effect. In the other 5 neurons each antagonist (500 nM) partly inhibited the CCK-8 evoked excitation and application of both antagonists (500 nM) caused a complete blockade of the response to CCK-8. The selective CCKB receptor agonist CCK-8NS had similar excitatory effects as CCK-8, but only on the neurons in which CCK-8 evoked effects were antagonized by L-365,260. The results demonstrate that the excitatory effects of CCK-8 are mediated by both CCKA and CCKB receptor subtypes. Further, the results indicate that some neurons possess exclusively the CCKA or the CCKB receptor subtype, but others possess both subtypes.

Action Potentials↗

Evidence for a role of cholecystokinin as neurotransmitter in the guinea-pig enteric nervous system.

Intracellular recordings were made of neurons in the myenteric plexus of the guinea-pig distal ileum. Slow excitatory postsynaptic potentials (sEPSPs) were evoked by electrical stimulation of an interganglionic fibre tract. The effect of cholecystokinin (CCK) receptor antagonists on the sEPSPs was investigated in 11 neurons. Application of the CCK receptor antagonists L-364,718 and L-365,260 (each 250 nM) markedly attenuated the sEPSPs in five of 11 neurons. The amplitude of the sEPSP reduced from 15 +/- 3 to 7 +/- 2 mV and the change in membrane resistance during the sEPSP was reduced from 28 +/- 9 to 11 +/- 8 MS. In six of 11 neurons the CCK antagonists had no effect on the sEPSPs. The results provide evidence that neurally released CCK is involved in the mediation of sEPSPs in some enteric neurons.

Animals↗

Disrupted bile flow affects interdigestive small bowel motility in rats.

BACKGROUND: The role of bile flow in the regulation of small bowel motility and the migrating myoelectric complex (MMC) is unclear. We aimed to study the effects of biliary diversion or obstruction on the MMC in a newly developed rat model. METHODS: In rats, myoelectrodes were implanted in the jejunum, and the proximal common bile duct (CBD) was cannulated and exteriorized at the head, enabling us to manipulate biliary flow without influencing pancreatic flow and without the need of anesthesia or additional surgery. Group A were controls without CBD cannulas. Biliary circulation was exteriorized but kept intact in group B; bile was diverted externally in group C; and the CBD was obstructed in group D. MMCs were recorded in unrestrained conditions by jejunal electromyography before and after biliary diversion or obstruction. Spontaneous recanalization of the CBD was monitored by measurement of serum bilirubin and by cholangiography. RESULTS: Exteriorization of the CBD without interruption of bile flow did not affect MMC duration (group A, 17.3 +/- 0.3 minutes [mean +/- SEM]; group B, 16.5 +/- 0.6 minutes). MMCs disappeared temporarily after CBD obstruction but not after biliary diversion. MMCs of increased duration were seen after 1 day in rats with biliary diversion or CBD obstruction (group C, 26.1 +/- 4.4 minutes; group D, 36.3 +/- 4.8 minutes [p < 0.05]). MMCs after biliary diversion or obstruction were characterized by an increased duration of phase II-like activity and decreased duration of phase I activity. CONCLUSIONS: We conclude that MMCs disappear temporarily early after CBD obstruction, but MMCs of increased duration are seen after 1 day of biliary diversion or obstruction. Thus disrupted bile flow affects interdigestive small bowel motility in rats.

Animals↗

Behavioural and intestinal responses to novelty in rats selected for diverging reactivity in the open field test.

There are indications that the severity of functional gastrointestinal disturbances in humans is linked to individual coping styles. In rodents, the open field test can be used to assess individual differences in behavioural responsivity to novel challenges. Two groups of Wistar rats were selected for high (HA) and low (LA) locomotor activity in a novel open field and fitted with electrodes on the proximal colon. During subsequent exposure to a novel box, a smaller locomotor activation in LA was accompanied by a greater increase in colonic spike burst activity compared to HA rats, even though this novel stressful challenge did not result in a clear defecation response in either group. In contrast, no marked behavioural differences between HA and LA were seen in the shock prod paradigm. Although detection of divergent behavioural responsivity in HA and LA rats may depend on stimulus quality or intensity, combined use of behavioural selection and intestinal motility recording in freely moving rats may offer a model to study individual vulnerability to stress-related disturbances of intestinal function.

Action Potentials↗

Barostat review.

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Digestive System Physiological Phenomena↗

Prospective, randomized trial on the effect of cyclic versus continuous enteral nutrition on postoperative gastric function after pylorus-preserving pancreatoduodenectomy.

OBJECTIVE: The effect of a cyclic versus a continuous enteral feeding protocol on postoperative delayed gastric emptying, start of normal diet, and hospital stay was assessed in patients undergoing pylorus-preserving pancreatoduodenectomy (PPPD). SUMMARY BACKGROUND DATA: Delayed gastric emptying occurs in approximately 30% of patients after PPPD and causes prolonged hospital stay. Enteral nutrition through a catheter jejunostomy is used to provide postoperative nutritional support. Enteral infusion of fats and proteins activates neurohumoral feedback mechanisms and therefore can potentially impair gastric emptying and prolong postoperative gastroparesis. METHODS: From September 1995 to December 1996, 72 consecutive patients underwent PPPD at the Academic Medical Center, Amsterdam. Fifty-seven patients were included and randomized for either continuous (CON) jejunal nutrition (0-24 hr; 1500 kCal/24 hr) or cyclic (CYC) enteral nutrition (6-24 hr; 1125 kCal/18 hr). Both groups had an equal caloric load of 1 kCal/min. The following parameters were assessed: days of nasogastric intubation, days of enteral nutrition, days until normal diet was tolerated orally, and hospital stay. On postoperative day 10, plasma cholecystokinin (CCK) levels were measured during both feeding protocols. RESULTS: Nasogastric intubation was 9.1 days in the CON group (n = 30) and 6.7 days in the CYC group (n = 27) (not statistically significant). First day of normal diet was earlier for the CYC group (15.7 vs. 12.2 days, p < 0.05). Hospital stay was shorter in the CYC group (21.4 vs. 17.5 days, p < 0.05). CCK levels were lower in CYC patients, before and after feeding, compared with CON patients (p < 0.05). CONCLUSIONS: Cyclic enteral feeding after PPPD is associated with a shorter period of enteral nutrition, a faster return to a normal diet, and a shorter hospital stay. Continuously high CCK levels could be a cause of prolonged time until normal diet is tolerated in patients on continuous enteral nutrition. Cyclic enteral nutrition is therefore the feeding regimen of choice in patients after PPPD.

Adult↗

Gastrointestinal motor mechanisms in hyperglycaemia induced delayed gastric emptying in type I diabetes mellitus.

BACKGROUND: Hyperglycaemia delays gastric emptying, both in healthy controls and in patients with diabetes mellitus. The effect of hyperglycaemia on antroduodenal motility in diabetes has not yet been studied. AIM: To investigate the gastrointestinal motor mechanisms involved in the hyperglycaemia induced retardation of gastric emptying in patients with type I diabetes mellitus and autonomic neuropathy. In eight diabetic patients antroduodenal manometry was performed simultaneously with scintigraphic measurement of emptying of a mixed solid-liquid meal, during euglycaemia (5-8 mmol/l glucose) and hyperglycaemia (16-19 mmol/l glucose), on separate days, in random order. RESULTS: Hyperglycaemia decreased the cumulative antral motility index from 38.3 (range 24.2-47.6) to 30.8 (range 17.3-38.1) (p = 0.025) and reduced the number of antral pressure waves propagated over > or = 4.5 cm (p = 0.04). Duodenal phase III-like activity was seen irrespective of the glycaemic state (in three patients during euglycaemia and in four patients during hyperglycaemia). Hyperglycaemia significantly affected gastric emptying of the solid meal: it prolonged the lag phase from 20.0 minutes to 28.5 minutes (P = 0.02), increased the 50% emptying time from 73.5 minutes to 104.5 minutes (p = 0.03), and increased the percentage of isotope remaining in the stomach after 120 minutes from 33.5% to 46.5% (p = 0.02). The cumulative antral motility index was correlated with the 50% emptying time (r = 0.75, p = 0.02) during euglycaemia, but not during hyperglycaemia (r = 0.28, P = 0.31). Liquid emptying was not influenced by the blood glucose concentration. CONCLUSIONS: Hyperglycaemia reduces postprandial antral contractile activity and its organisation in patients with type I diabetes and autonomic neuropathy. These changes in antroduodenal motility are likely to constitute the mechanism through which gastric emptying of solids is delayed during high blood glucose concentrations in these diabetic patients.

Adult↗

The effect of octreotide on gastric emptying at a dosage used to prevent complications after pancreatic surgery: a randomised, placebo controlled study in volunteers.

BACKGROUND: Octreotide is used in many centres to prevent complications after pancreatic surgery. Delayed gastric emptying is a another complication occurring in around 30% of patients after pancreatoduodenectomy (PD) and causes prolonged hospital stay. The influence of octreotide on this complication is doubtful. AIMS: To assess the effect of octreotide, at the clinical dosage used after pancreatic surgery, on gastric emptying in healthy volunteers. SUBJECTS AND METHODS: Eight healthy male volunteers (mean age 22.5 years) participated in this double blind, placebo controlled study. On day 1 subjects received 100 micrograms of octreotide or placebo subcutaneously, three times daily and on day 2, one hour after the fourth injection, gastric emptying, postprandial cholecystokinin (CCK) release, and mouth to caecum transit time (MCTT) were measured. This protocol was repeated after one week, in a crossover design. On the test day subjects received a liquid test meal (1.57 MJ/300 ml) and gastric emptying measurements were performed with applied potential tomography, an non-invasive, validated technique which measures gastric emptying through impedance differences. From the gastric emptying curves, lag time, t50, and postlag emptying rate were measured. MCTT was measured using the hydrogen breath test. RESULTS: Lag time decreased from 29.6 (6.3) (mean (SEM)) to 12.2 (4.6) minutes (p < 0.05) during octretide treatment; t50 decreased from 87.8 (12.0) to 47.5 (8.2) minutes (p < 0.02) and there was a trend towards an increased postlag emptying rate (0.8 to 1.6% per minute; p = 0.07). MCTT increased from 150 (12.7) to 229 (17.9) minutes during octreotide treatment (p < 0.01). Octreotide suppressed postprandial CCK release (p < 0.05). CONCLUSIONS: MCTT was delayed by octreotide, suggesting impairment of small bowl treatment. Octreotide administered at the clinical dosage for pancreatic surgery accelerates gastric emptying, mainly by shortening the lag time. Suppression of postprandial CCK release may be involved in this process. Octreotide administration is therefore not a contributing factor in the pathogenesis of delayed postoperative gastric emptying after PD and might even play a role in preventing this complication.

Adult↗

Effects of the inflammatory mediator prostaglandin E2 on myenteric neurons in guinea pig ileum.

The effects of the inflammatory mediator prostaglandin E2 (PGE2) on myenteric neurons were investigated by intracellular recordings in a conventional plexus preparation. Bath application of PGE2 (1-1,000 nM) evoked a concentration-dependent and reversible slow depolarization and an augmentation of excitability in 23 of 26 AH and 12 of 13 S neurons. The amplitude of the slow depolarization ranged from 4 +/- 1 mV at 1 nM to 13 +/- 3 mV at 1 microM in S and AH neurons. In AH neurons, PGE2 evoked an increase in membrane resistance and a reduction of afterhyperpolarization. In S neurons, PGE2 evoked either an increase or a decrease in membrane resistance. PGE2 slightly reduced the amplitude of electrically evoked fast excitatory postsynaptic potentials and had no effect on slow excitatory postsynaptic potentials. Moreover, PGE2 evoked bursts of fast excitatory postsynaptic potentials and action potentials in S neurons, indicative of cyclical neural activity in the myenteric plexus. It is concluded that the inflammatory mediator PGE2 can act as an excitatory neuromodulator of gastrointestinal motility through direct action on neurons in the myenteric plexus.

Animals↗