Fasting Motor Pattern Research Articles

Peripheral apelin-13 administration inhibits gastrointestinal motor functions in rats: The role of cholecystokinin through CCK1 receptor-mediated pathway

Apelin is the endogenous ligand of the G protein-coupled receptor APJ. The APJ receptor is widely expressed in gastrointestinal (GI) tissues including stomach and small intestine. Apelin administration was shown to induce the release of cholecystokinin (CCK) which is a well-known alimentary hormone with its inhibitory actions on GI motor functions through CCK1 receptors on vagal afferent fibers. We investigated whether; (i) peripherally injected apelin-13 alters GI motor functions, (ii) apelin-induced changes are mediated by APJ receptor or CCK1 receptor and (iii) vagal afferents are involved in inhibitory effects of apelin. Solid gastric emptying (GE) and colon transit (CT) were measured, whereas duodenal phase III-like contractions were recorded in rats administered with apelin-13 (300μg/kg, ip). CCK1 receptor antagonist lorglumide (10mg/kg, ip) or APJ receptor antagonist F13A (300μg/kg, ip) was administered 30min prior to the apelin-13 injections. Vagal afferent denervation was achieved by systemic administration of vanilloid receptor agonist capsaicin (125mg/kg, sc). Apelin-13 administration significantly (p<0.01) increased the CCK level in portal venous plasma samples. Compared with vehicle-treated rats, apelin-13 significantly delayed both GE (p<0.001) and CT (p<0.01). Pretreatment of lorglumide or F13A completely abolished the apelin-13-induced inhibitory effects on GE and CT, moreover, apelin-13 was found ineffective in rats underwent afferent denervation. F13A administration alone significantly accelerated the basal CT. Apelin-13 noticeably disturbed the duodenal fasting motor pattern by impairing phase III-like contractions while increasing the amplitudes of phase II contractions which were prevented by pretreatment of lorglumide and capsaicin. Compared with vehicle-treated rats, lorglumide and capsaicin significantly (p<0.05) reduced the apelin-13-induced increases in phase II motility index. Peripherally administered apelin-13 inhibits GI motor functions through CCK-dependent pathway which appears to be mediated by CCK1 receptors on vagal afferents. Peripheral apelin might contribute to the motility changes occurred in postprandial period.

Antroduodenal motility and small bowel transit during continuous intraduodenal or intragastric administration of enteral nutrition.

Gastrointestinal intolerance is observed more frequently during intraduodenal (ID) tube feeding than during intragastric (IG) feeding, possibly because it evokes a stronger gastrointestinal response and accelerates small bowel transit. We have investigated whether the accelerated small bowel transit during ID feeding results from alterations in antroduodenal motility pattern. The effect of IG and ID infusion of a polymeric diet (Nutrison, 125 kcal h-1) on antroduodenal motility, small bowel transit time (SBTT) and gastrointestinal hormone release was studied in nine healthy subjects. These subjects were studied on three occasions for 6 h during fasting, continuous IG or ID feeding. Phase III recurrence time was significantly prolonged during IG feeding compared with fasting (240 +/- 51 vs. 136 +/- 24 min; P < 0.05). None of the subjects had recurrence of phase III during ID feeding; the fed motor pattern remained present. Parameters of fed motility (mean amplitude and motility index) were not significantly different between IG and ID feeding, although the frequency of antral and duodenal contractions was lower during ID than during IG feeding. SBTT was significantly accelerated during ID compared with IG feeding and with fasting (58 +/- 8 vs. 73 +/- 9 and 83 +/- 10 min respectively; P < 0.05). Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels were significantly higher during ID than during IG feeding. Peptide YY (PYY) levels were significantly higher during ID than during fasting, but not during IG feeding During intraduodenal feeding, a fed motility pattern is preserved, whereas during intragastric feeding transition from a fed to a fasting motor pattern is observed in over 50% of the subjects. These differences may be related to augmented hormone release during intraduodenal feeding.

Stress-induced changes in the gastrointestinal motor system.

Several autonomic, hormonal, behavioural and neuropeptidergic bodily responses to stressful stimuli have been described over the past few decades. Both animal models and human paradigms have been explored. It is acknowledged that stress modulates gastrointestinal (GI) motility through central mechanisms including corticotropin-releasing-factor. This process requires the integrity of autonomic neural pathways. It has become evident that the effects of stress on GI motility vary according to the stressful stimulus, its intensity, the animal species under study and the time course of the study. Recent evidence suggests that chronic or possibly permanent changes develop in enteric smooth muscle properties in response to stress. In animals, the most consistent findings include retardation of gastric emptying in response to various stressors; acceleration of gastric emptying upon cold stress, presumably through the secretion of brain thyroglobulin-hormone; acceleration of intestinal transit; and stimulation of colonic transit and fecal output. In humans, the cold water immersion test has been associated with an inhibition of gastric emptying, while labyrinthine stimulation induces the transition from postprandial to fasting motor patterns in the stomach and the small bowel. Psychological stress has been shown to induce a reduction in the number and amplitude of intestinal migrating motor complexes and to neither affect nor stimulate colonic motility. These various responses to stress are presumably attributed to the preferential activation of specific neuronal pathways under the influence of a given stimulus or its intensity. The significance of these findings and the directions of further studies are discussed.

Small bowel transit of a bran meal residue in humans: sieving of solids from liquids and response to feeding

Background—Ileal motor patterns are adapted to the propulsion of viscous meal residue, such as bran, which accumulates in the distal ileum postprandially.Aims—To examine the effects of a second liquid/solid meal...

Canine small bowel motor patterns and contractions are not neurally regulated during enteric nutrient infusion.

The aims of this study were to determine the effects of duodenal and jejunoileal nutrient infusions on small intestinal motor patterns and intestinal contractions in neurally intact and neurally isolated small bowel. Fifteen dogs were prepared with duodenal and jejunal infusion and manometry catheters and a diverting jejunal cannula. Ten of the dogs underwent in situ neural isolation of the jejunoileum. A mixed nutrient meal (0.5 kcal/ml) was infused into the duodenum or jejunum at 3 ml/min for 5 h. Control experiments involved infusion of a balanced salt solution. Manometric data collected on-line to a microcomputer were analyzed for direction, distance, and velocity of spread of single pressure waves (SPW) and clustered contractions. Isolated duodenal and jejunoileal nutrient infusions inhibited the fasting motor pattern in neurally intact and neurally isolated small bowel. Motor activity (motility index) increased slightly during nutrient infusion within groups, but there were few differences between groups. Neither neural isolation nor nutrient infusion had a consistent effect on spread of SPW or migration of clustered contractions. Isolated duodenal and jejunoileal nutrient infusions in the dog inhibit fasting motor patterns and increase motor activity slightly but have little effect on characteristics of individual and clustered contractions. Extrinsic innervation to the jejunoileum or intrinsic neural continuity of the jejunum with the duodenum had little effect on single or grouped contractions. Although the changes in motor activity demonstrated in this study appear small, alterations in intestinal transit and absorption may still occur and may be of importance physiologically.

Characteristics of fasting and fed myoelectric activity in rat small intestine: evaluation by computer analysis

Evaluation of gastrointestinal myoelectric activity has been limited by the assessment techniques and the complexity of the recorded myoelectric signal. Commonly, myoelectric activity is evaluated as motor patterns, which only gives a semiquantitative measure of myoelectric events within the bowel wall. Using myoelectric recordings from the proximal small intestine in rats, a computerized system for acquisition, storage, display and calculation of characteristics for the myoelectric activity was developed. The software was tested in myoelectric recordings from nine rats in fasting and fed states. All migrating myoelectric complexes (MMCs) during fasting and fed myoelectric patterns were recognized in both digital and analog recordings. Reproduction of myoelectric recordings by the computerized system was indistinguishable from that of the analog system. Employing an appropriate cut-off trigger level and a high sampling frequency, spike potentials were recorded in the proximal jejunum with 0.4 (0.3-0.5) spikes 10 s-1 during phase 1 of MMC, 19.5 (15.1-23.9) (P < 0.001) during phase 2, and 103.8 (97.2-110.5) (P < 0.001) during phase 3. In fasted state, MMCs were most frequent in the proximal jejunum whereas fewer were found in the duodenum and distal jejunum. To achieve stable values for MMC cycle length at least four MMCs had to be calculated. After feeding in phase 1, the myoelectric activity increased to 23.8 (13.6-33.9) spikes 10 s-1 (P < 0.001), whereafter the spiking activity decreased over a period of 2 h until a fasting motor pattern was resumed. It is concluded that computerized technology enables evaluation not only of myoelectric patterns, but also of spiking activity per time unit, i.e. the intensity of myoelectric activity in the gut.

Postnatal change in inhibitory regulation of intestinal motor activity in human and canine neonates.

Motor activity was recorded in 19 preterm infants three times during the first postnatal month. There was a paucity of small intestinal motor quiescence during fasting in the first postnatal week; however, its duration significantly increased with postnatal age (p < 0.03). Although fasting motor patterns changed with postnatal age, motor responses to feeding were present within the first few days of life. Motor activity was also recorded weekly in 11 newborn dogs for 6 wk. Intestinal motor quiescence was also absent during fasting for the first postnatal week but it significantly increased with postnatal age (p < 0.002). As in the human preterm infant, a motor response to feeding was present within the first few days of life. Plasma concentrations of gastrin and peptide YY during fasting were low in the preterm human and canine neonate during the first postnatal week but plasma concentrations of both peptides increased with postnatal age. Although plasma concentrations of gastrin were low during fasting for the first postnatal week, plasma concentrations of gastrin increased significantly postprandially compared with fasting (p < 0.05). We conclude that motor quiescence during fasting becomes a more prominent feature of newborn intestinal motor function postnatally. In addition the release of two peptides that regulate motor patterns also change postnatally. Thus, postnatal changes in motor patterns and peptide release change in a parallel fashion in human preterm neonates and canine neonates.(ABSTRACT TRUNCATED AT 250 WORDS)

Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?

The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.

Duodenal nutrients inhibit canine jejunal fasting motor patterns through a hormonal mechanism

Ingestion of a meal converts the fasting motor pattern, the migrating motor complex (MMC), to a fed pattern of motility. The role of specific anatomic gut regions involved in these changing patterns of motility and the neurohormonal factors which mediate these changes, however, are unknown. Our aim was to determine the neurohormonal mechanisms by which nutrients within the duodenal lumen alter proximal jejunal motility. Fifteen dogs were prepared with a gastric cannula, duodenal infusion catheter, duodenal and proximal jejunal manometry catheters, and a totally diverting cannula in the most proximal portion of the jejunum. Ten of the dogs also underwent complete in situ neural isolation of the entire jejunoileum. Experiments were performed in the fasting state with no infusion (0 ml/min) and during a 5-hr duodenal infusion (3 ml/min) of either a nonnutrient electrolyte solution or a mixed nutrient solution while diverting distal duodenal chyme from the jejunum. During sham infusion (0 ml/min), the MMC was present in neurally intact dogs (group 1) and dogs with neurally isolated jejunoileum (group 2). Nonnutrient infusion did not inhibit or consistently alter the MMC in either group. Nutrient infusion limited to the duodenum inhibited the MMC in both duodenum and jejunum in dogs with neurally intact and neurally isolated jejunoileum. Latency of onset of the fed pattern in the duodenum and jejunum did not differ between groups. We conclude that postprandial inhibition of the MMC in the jejunum is mediated, in part, by a hormonal mechanism induced by duodenal lumenal nutrients.

Effects of intraduodenal and intravenous fat infusion on small bowel motility in humans. A comparative study of medium- and long-chain triglycerides

Objective: To test the effects of medium-chain triglycerides (MCT) and long-chain triglycerides (LCT), given intraduodenally or intravenously to healthy volunteers, on small bowel motility. Design: Two groups comprized of eight volunteers were studied. The 5-h fat infusion always began 30 min after a phase III. In study 1, volunteers received at random either 50 g LCT or MCT intraduodenally. In study 2, they received 500 ml of an emulsion of either LCT only or 50% LCT/50% MCT intravenously. Manometric recording continued from the beginning of fat delivery until the recurrence of a phase III after fat administration ceased. Results: In study 1, LCTs reduced phases III and I, while intraduodenal MCTs did not effect the fasting motor pattern of the small bowel. In study 2, phase III was recorded in all volunteers with both intravenous infusions. The percentage of time in phase III was greater with MCT than with the LCT infusion but the percentage of time in phases I and II remained the same with both types of intravenous fat. Conclusions: The effects of lipids on small bowel motor activity in humans depends on two parameters: the type of lipid and the route of administration.

Fasting and postprandial gastrointestinal motility in ulcer and non-ulcer dyspepsia.

This study aimed to compare fasting and postprandial gastrointestinal motor patterns in patients with ulcer and non-ulcer dyspepsia. Forty five subjects were studied: 10 with uncomplicated gastric ulcer, eight with uncomplicated duodenal ulcer, 18 with chronic idiopathic dyspepsia, and nine healthy asymptomatic controls. Gastrointestinal fasting and postprandial motor patterns were recorded using a low compliance perfusion technique. The interdigestive antral cumulative motility index, computed for 30 minutes before the appearance of duodenal activity fronts, and the number of activity fronts with an antral component were significantly less in patients with ulcers and those with non-ulcer dyspepsia compared with asymptomatic controls. The patient groups also had a reduced antral motor response to a solid-liquid test meal compared with healthy controls. Intestinal motor abnormalities (bursts of non-propagated phasic pressure activity and discrete clustered contractions) were recorded in a minority of patients, all with associated irritable bowel symptoms. In conclusion, antral hypomotility is a frequent but nonspecific motor abnormality in dyspepsia; abnormal motor patterns of the small bowel are less frequent and seem to be confined to patients with concomitant irritable bowel syndrome.

Gastrointestinal correlates of the development of hunger in man

Experiments were carried out on ten healthy male volunteers to investigate the relationship between the return of hunger after a meal and gastric emptying, blood glucose levels and small intestinal motor patterns. There was a significant correlation between the postprandial increase in hunger ratings and the time for 90% of the meal to empty ( r = 0.75, p < 0.02): hunger ratings started to increase in three subjects when over 40% of the food still remained in the stomach, and they continued to increase in all subjects even when the meal had ceased to empty from the stomach. These results suggest the reduction of gastric distension may have a permissive role in the development of hunger after a meal. The increase in hunger was not related to any consistent change in plasma glucose concentration. Finally, the postprandial onset of a fasting motor pattern (phase-III-like activity) always occurred when the stomach had emptied more than 80% of its contents and after hunger had increased. Our data are compatible with the hypothesis that the return of hunger is directly related to a decline in the exposure of the upper small intestine to nutrient stimuli, but could be modulated by gastric distension.

A model of jejunoileal in vivo neural isolation of the entire jejunoileum: Transplantation and the effects on intestinal motility

The effects of intestinal transplantation on enteric physiology have not been well studied. Our aim was to determine the effect of jejunoileal transplantation on patterns of small intestinal motility. To avoid confounding effects of immune rejection or immunosuppression, we developed a model of autotransplantation in which all tissue connections to the entire jejunoileum were transected at the base of the mesentery except for the superior mesenteric artery and vein which were stripped meticulously of investing adventitia. After 3 weeks, motility was studied in eight dogs with intestinal electrodes during fasting, after meals of 50 and 500 g of liver, and during intravenous infusions of pentagastrin and cholecystokinin. During fasting, the characteristic interdigestive migrating motor complex (MMC) was present in both the innervated duodenum and the “autotransplanted” jejunoileum; however, temporal coordination between the two regions was abolished. Feeding 50 g of liver abolished the MMC in the duodenum, but not in the jejunoileum; in contrast, 500 g of liver interrupted the MMC in both regions. Exogenous pentagastrin and cholecystokinin inhibited the MMC for the duration of the infusions. These findings suggest that extrinsic nerves and/or intrinsic (enteric) myoneural continuity do not initiate fasting motor patterns in the jejunoileum but do regulate the temporal coordination of motor patterns between segments of small intestine. Postprandial inhibition of the MMC is only in part mediated by neural factors. After transplantation, motility is abnormal; the overall effects on enteric physiology remain unknown.

Effect of feeding on motor activity of Canine Stomach

The motor response of the canine stomach to test meals of varied nutrient content and physical state, administered either orally or intraduodenally, was studied. Oral feeding abolished regular contractions in the proximal stomach. There was a simultaneous fall in the proximal gastric baseline force, which slowly recovered to the preprandial level, at which time regular contractions returned. The magnitude and duration of these events varied with the type of meal, as did the distal gastric response, which was characterized by abolition of the fasting motor pattern and establishment of continuous low-amplitude contractions. Duodenal feeding of a nutrient, but not nonnutrient, meal abolished fasting motor activity in both proximal and distal stomach but did not induce either a fall in proximal gastric baseline force or distal gastric contractions. These results suggest that stimulation of duodenal as well as gastric receptors is required to elicit the normal prandial response of both proximal and distal stomach.

Total duodenectomy: Effect on canine gastrointestinal motility

Motor activity of the upper gastrointestinal tract undergoes a cyclic pattern during fasting called the migrating motor complex (MMC). The role of the duodenum in controlling this cyclic activity was studied in the dog. Five dogs served as controls. In four other dogs, the entire duodenum and the proximal 20 cm of jejunum were resected. The ostia of the bile duct and pancreatic duct were preserved as “mucosal buttons” and reimplanted in situ into the jejunum after gastrojejunostomy. All dogs had manometry catheters placed into the stomach and serosal electrodes implanted onto the small intestine to monitor gastrointestinal motility. All control dogs showed the characteristic MMC in the stomach and small intestine, the period being 112 ± 16 min (mean ± SEM). After total duodenectomy, an irregular, noncyclic pattern of contractions occurred in the stomach in two of the four dogs during fasting. The other two dogs had a cyclic pattern of gastric motility; however, the overall characteristics of these cyclic patterns of gastric motility differed from that of controls. A variable proportion of the phases of cyclic gastric activity did not fit the criterion for temporal coordination with the jejunum as defined from study of control dogs. In contrast, jejunal motility in all four dogs after total duodenectomy continued to exhibit the characteristic MMC, but the period of the cycle (58 ± 7 min) was shorter than in controls ( P < 0.05). “Ectopic” jejunal activity fronts with no preceding gastric contractions were frequent. After total duodenectomy, plasma concentration of motilin remained lower than normal and showed no cyclic variation with the jejunal MMC. After total duodenectomy, feeding interrupted the fasting motor pattern of the stomach as in controls, but did not disrupt the MMC in the jejunum. We concluded that the duodenum has an important role in initiating cyclic gastric motor activity and in coordinating motor activity between the stomach and the small intestine.

Disordered small intestinal motility: a rational basis for toddlers' diarrhoea.

Toddler diarrhoea is the commonest cause of chronic diarrhoea without failure to thrive in childhood, but its pathogenesis remains obscure. We have studied upper small intestinal motility in three groups of children (control group 1 - children with no intestinal pathology undergoing duodenal intubation, n = 6; control group 2 - children with gastrointestinal pathology other than toddler diarrhoea, n = 11; control group 3 - children with toddler diarrhoea, n = 8). We studied fasting motor patterns and the response of the migrating motor complex to intravenous cholecystokinin and an intraduodenal bolus of 5% dextrose. The characteristics of the migrating motor complex in the three groups did not differ but their response to dextrose did. Intraduodenal dextrose disrupted the migrating motor complex in four out of four children in group 1; seven out of nine children in group 2; and nil of eight children with toddler diarrhoea in group 3. We suggest that this failure of intestinal motor response may play a major role in the pathogenesis of the diarrhoea in this condition.

Hormonal control of the gastric motor response to feeding: cross-perfusion of an isolated stomach using a conscious donor dog.

AbstractThe purpose of this study was to determine the hormonal response of the gastric motor activity to a meal. A conscious donor dog was used to perfuse an isolated canine stomach placed in a chamber, using a pump‐oxygenator system for recirculation. Strain gauge transducers were used to record the motility of the isolated stomach. The donor dog was fed during the perfusion. An hour after the meal, the fed dog was replaced by a second fasted donor dog. Fasted motor activity in both the proximal and distal stomach was characterized by high‐amplitude contractions occurring in bursts every 10 minutes. After feeding, there was complete abolition of high‐amplitude contractions in the distal stomach in all 7 experiments. The proximal high‐amplitude contractions were abolished in 5 experiments, but were still present in 2, although the contractile pattern was irregular. When the fed dog was replaced by a fasted dog, characteristic fasting motor patterns were resumed in the isolated stomach. There was a delay of up to 17 minutes in the onset of both the postprandial changes in motility and the reappearance of fasted motor patterns. The changes in the motility pattern of the isolated stomach after feeding the donor dog point to a hormonal response.

Effects of pentagastrin on electrical activity of small intestine of the dog.

Effects of pentagastrin on electrical activity of small intestine of the dog.