Interdigestive Myoelectric Complex Research Articles

Extrinsic ghrelin in the paraventricular nucleus increases small intestinal motility in rats by activating central growth hormone secretagogue and enteric cholinergic receptors

Background/ObjectivesGhrelin is a brain-gut peptide that regulates gastrointestinal (GI) motility. We hypothesized that the excitatory effect of ghrelin on the paraventricular nucleus (PVN) increases GI motility by activating the central growth hormone secretagogue receptor (GHSR) and central neuropeptide Y (NPY) signaling pathways, leading to increased enteric cholinergic activity. MethodsThirty-six male Sprague Dawley rats were maintained on duodenal catheterization and PVN cannulation. Small intestinal transit (SIT) was observed and rats were divided as follows: experimental animals received ghrelin injections in the PVN (0.03, 0.08, or 0.24nM); 1nM GHSR antagonist D-Lys3-GHRP6 alone; 1nM D-Lys3-GHRP6 before ghrelin injection in the PVN, respectively. Electrophysiologic parameters of the interdigestive myoelectric complex (IMC) were examined by administration of 0.24nM ghrelin in the PVN after small intestinal electrode implantation and PVN cannulation. GI cholinergic pathway activation was analyzed after intravenous atropine administration. The involvement of central NPY signaling was evaluated by injecting an anti-NPY immunoglobulin (IgG) in the PVN. Neuronal expression of c-Fos in the brain and GI tract was examined using immunohistochemistry. ResultsInjection of ghrelin in the PVN dose-dependently accelerated SIT, and this excitatory effect was competitively inhibited by a GHSR antagonist. The excitatory effect of ghrelin on IMC activity was diminished by GHSR antagonism and NPY neutralization, as well as by blockade of peripheral muscarinic acetylcholine receptors. Extrinsic ghrelin significantly upregulated c-Fos expression in the PVN and other central nuclei, as well as in the enteric nervous plexuses of the stomach, duodenum, and proximal colon. The ghrelin-induced upregulation of central and enteric c-Fos expression was also dependent on central GHSR activation. ConclusionsGhrelin positively regulates GI motility by exciting both central and enteric neurons, including those of the PVN, by activating GHSR and NPY pathways, and peripheral muscarinic acetylcholine receptors.

Uremic anorexia and gastrointestinal motility dysfunction correlate with the changes of ghrelin system in hypothalamus

Ghrelin can act as a signal for meal initiation and play a role in the regulation of gastrointestinal (GI) motility via hypothalamic circuit. This study investigated the correlation between changes of hypothalamic ghrelin system and GI motility dysfunction and anorexia in rats with chronic renal failure (CRF). Sprague-Dawley (SD) rats (male/female 1:1, 180 ± 20 g) were randomly classified into a CRF group and control group (n = 8 per group). 5/6 nephrectomy was used to construct the CRF model. When plasma creatinine concentration (PCr) and blood urea nitrogen (BUN) in the CRF group were twice higher than the normal, food intake (g/24 h) and gastrointestinal interdigestive myoelectric complex (IMC) were detected. Then all rats were killed for assessment of the mRNA expression of ghrelin and growth hormone secretagogue receptor (GHS-R) in hypothalamus using reverse transcription-polymerase chain reaction. Analysis of variance, Student-Newman-Keuls-q-test and Correlation Analysis were used to do statistical analysis. P < 0.05 was considered as statistically significant. Compared to the control group, the CRF group was obviously decreased in the food intake (g/24 h), the phase III duration and amplitude and the ghrelin and GHS-R expression in the hypothalamus (P < 0.05). There was a positive correlation between them (P < 0.05). Changes of ghrelin and GHS-R in the hypothalamus correlate with gastrointestinal motility dysfunction and anorexia in rats with CRF.

Effects of Chronic Renal Failure on Gastrointestinal Motility: A Study on the Changes of Gastric Emptying, Small Intestinal Transit, Interdigestive Myoelectric Complex, and Fecal Water Content

Background: Gastrointestinal (GI) dysfunction may lead to malnutrition in patients with chronic renal failure (CRF). This study investigated the effects of CRF on GI motility. Methods: Forty-eight Sprague Dawley rats (180 ± 20 g) were randomly classified into CRF group and sham-operated (Sham) group, and each group was further assigned for gastric emptying (GE), small intestinal transit (SIT), interdigestive myoelectric complex (IMC), and fecal water content (FWC) experiments (6 CRF and 6 Sham rats per experiment). The CRF model was established by 5/6 nephrectomy. The body weight (BT), GE, SIT, IMC, and FWC of the rats were observed. ANOVA and Student–Newman–Keuls q-test were utilized to do statistical analysis. Results: The BT of the rats in the two groups had no statistical difference before surgery. But in the ninth week after surgery, the CRF rats (230 ± 20 g) weighed less than the Sham rats (260 ± 15 g) (p < 0.05). The GE rate and SIT rate in CRF rats were significantly lower than that of Sham rats (GE 33.08 ± 7.50 vs. 53.37 ± 9.78%; SIT 42.92 ± 8.96 vs. 58.67 ± 9.12%) (p < 0.05). Compared with the IMC of the Sham rats, the CRF rats showed obvious alterations in (a) IMC cycle; (b) phase II and phase III duration; and (c) phase III cycling frequency, amplitude, and percentage (p < 0.05). FWC of the CRF rats increased significantly (p < 0.05). Conclusion: The GI motility of the CRF rats is obviously impaired. This finding may indicate that the effects of CRF on GI motility might be relatively prevalent.

48 The effect of electrical acupuncture points on fasting and postprandial gastroduodenal myoelectric activities and brain gut peptide release in rats

Fasting interdigestive myoelectric complex (IMC) and postprandial gastroduodenal myoelectric activities are regulated by motilin and leptin, respectively (L. Zhou 2005). This study is to observe whether electrical acupuncture points could increase fasting gastroduodenal IMC and postprandial activities, as well as increase the release of motilin and leptin.Methods: Bipolar platinum electrodes were implanted on the serosa of antrum and duodenum in 10 conscious Wistar rats to record IMC and postprandial digestive myoelectric activities. We acupunctured Points Zusanli (S‐36), Tianshu (S‐25), and Liangmen (S‐21) during phase I of IMC (Frequency 20~100 Hz, Strengthen 12~16 mA, period 90 min) and compared with non‐specific electric stimulation (sham acupuncture) group. Serum motilin and leptin level was measured by RIA.Results: (1) Acupuncture points could shorten markedly phase I of antroduodenal IMC and increase the period of phase III (P &lt; 0.01). Acupuncture points also increased the number of spike burst of antral and duodenal slow wave by (121.24 ± 20.0)% and (97.34 ± 15.20)% (compared with control group, P &lt; 0.01). In postprandial period, acupuncture points could increase the number of spike burst of antral and duodenal slow wave by (142.52 ± 23.50)% and (102.48 ± 13.25)% (compared with control group, P &lt; 0.01). (2) When acupuncture points increased the number of spike burst of IMC in fasting state, serum motilin concentration also increased, which was (74.56 ± 8.20)% more than control group (P &lt; 0.01). When acupuncture points with meal, serum leptin concentration increased with myoelectric activity, which was (139.84 ± 20.25)% more than control group (P &lt; 0.01). There was no change of motilin and leptin concentration in non‐specific electric stimulation group. (3) Cutting off subphrenic vagus nerves could totally block the effect of acupuncture points on antroduodenal myoelectric activities and release of motilin and leptin.Conclusions: Acupuncture points could effectively increase fasting and postprandial antroduodenal myoelectric activities. This effect is mediated by motilin and leptin, respectively.

Effects of surface gastric pacing on gastric myoelectrical activity and plasma motilin in a canine model of gastric motility disorders

To investigate the effects of surface gastric pacing on gastric myoelectrical activity and plasma motilin concentration in a canine model of gastric motility disorders. Ten healthy mongrel dogs were divided into two groups: an experimental group of six dogs and control group of four dogs. The model of gastric motility disorders was established in the experimental group with truncal vagotomy combined with injection of glucagon. Gastric serosal myoelectrical activity was recorded with a four-channel computer analysis device. Plasma motilin concentration was measured with a radioimmunoassay (RIA) kit. Surface gastric pacing at 1.1-1.2-fold the intrinsic slow-wave frequency superimposed with a series of high frequency pulses (10-30 Hz) was performed for 45 min daily for 1 month in the conscious dogs. The basic electrical rhythm (BER) amplitude (2.32 +/- 0.35 mV) and propagation velocity (4.06 +/- 0.40 cm/s) of the dogs with bilateral truncal vagotomy in the fed state decreased more significantly than those of the controls (4.25 +/- 0.12 mV, 6.92 +/- 0.24 cm/s) (P < 0.03). After long-term surface gastric pacing, the BER amplitude (3.97 +/- 0.19 mV) and propagation velocity (5.57 +/- 0.48 cm/s) was increased significantly compared with before pacing (P < 0.05). Postprandial gastric dysrhythmias were provoked by large doses of glucagon; the percentage of regular slow waves of the dogs with vagotomy was markedly reduced from 67.4 +/- 6.2% at baseline to 10.0 +/- 6.7% (P < 0.001), and that of the control was also decreased from 87.1 +/- 6.9% to 35.0 +/- 11.0% (P < 0.01), but the entrainment of gastric slow waves was 100% by means of gastric pacing at optimal parameters. There was a significant increase in the plasma concentration of motilin at the phase III of the interdigestive myoelectrical complex (IMC III) in the dogs with bilateral truncal vagotomy (baseline vs vagotomy, 184.29 +/- 9.81 pg/mL vs 242.09 +/- 17.22 pg/mL; P< 0.01). However, the plasma motilin concentration (212.55 +/- 11.20 pg/mL; P < 0.02) was decreased significantly after long-term gastric pacing. Before gastric pacing the plasma motilin concentration showed an equally negative correlation with the BER amplitude, and propagation velocity in the dogs with vagotomy in the fed state (r = -0.473, r = -0.807, P < 0.04), but after long-term gastric pacing, the plasma motilin concentration showed an equally positive correlation with the BER amplitude and propagation velocity (r = 0.523, r = 0.896, P < 0.02). Surface gastric pacing with optimal pacing parameters is able to entrain completely propagated slow waves, improve the parameters of gastric myoelectrical activity and normalize gastric dysrhythmias induced by a pharmacological agent. Surface gastric pacing might be useful in the treatment of gastric dysrhythmia. The gastric myoelectrical activity correlated well with the plasma motilin concentration before and after pacing, which suggests that motilin could modulate the effect of gastric pacing through alteration of the gastric myoelectrical parameters.

Effects of gastric pacing on gastric emptying and plasma motilin.

To investigate the effects of gastric pacing on gastric emptying and plasma motilin level in a canine model of gastric motility disorders and the correlation between gastric emptying and plasma motilin level. Ten healthy Mongrel dogs were divided into: experimental group of six dogs and control group of four dogs. A model of gastric motility disorders was established in the experimental group undergone truncal vagotomy combined with injection of glucagon. Gastric half-emptying time (GEt(1/2)) was monitored with single photon emission computerized tomography (SPECT), and the half-solid test meal was labeled with an isotope-(99m)Tc sulfur colloid. Plasma motilin concentration was measured with radioimmunoassay (RIA) kit. Surface gastric pacing at 1.1-1.2 times the intrinsic slow-wave frequency and a superimposed series of high frequency pulses (10-30 Hz) was performed for 45 min daily for a month in conscious dogs. After surgery, GEt(1/2) in dogs undergone truncal vagotomy was increased significantly from 56.35+/-2.99 min to 79.42+/-1.91 min (P<0.001), but surface gastric pacing markedly accelerated gastric emptying and significantly decreased GEt(1/2) to 64.94+/-1.75 min (P<0.001) in animals undergone vagotomy. There was a significant increase of plasma level of motilin at the phase of IMCIII (interdigestive myoelectrical complex, IMCIII) in the dogs undergone bilateral truncal vagotomy (baseline vs vagotomy, 184.29+/-9.81 pg/ml vs 242.09+/-17.22 pg/ml; P<0.01). But plasma motilin concentration (212.55+/-11.20 pg/ml; P<0.02) was decreased significantly after a long-term treatment with gastric pacing. Before gastric pacing, GEt(1/2) and plasma motilin concentration of the dogs undergone vagotomy showed a positive correlation (r=0.867, P<0.01), but after a long-term gastric pacing, GEt(1/2) and motilin level showed a negative correlation (r=-0.733, P<0.04). Surface gastric pacing with optimal pacing parameters can improve gastric emptying parameters and significantly accelerate gastric emptying and can resume or alter motor function in a canine model of motility disorders. Gastric emptying is correlated well with plasma motilin level before and after pacing, which suggests that motilin can modulate the mechanism of gastric pacing by altering gastric motility.

Interaction of luminal enterotoxin and low dose systemic endotoxin on small intestinal motility, secretion and permeability in the rat

We evaluated small intestinal motility, secretion, and mucosal permeability in fasted Sprague–Dawley rats following administration of luminal Escherichia coli heatstable enterotoxin (500 ng ml −1) alone or in combination with intravenous endotoxin (100 μg kg −1). Systemic endotoxin alone, or in combination with enterotoxin, caused a disruption of the regular interdigestive myoelectric complex as well as induction of spike bursts and diarrhea. Enterotoxin alone produced only minimal effects on intestinal myoelectric activity. Exposure of the intestine to systemic endotoxin and luminal enterotoxin in combination, led to a 2-fold increase in intestinal secretion in comparison with controls. This effect was significantly greater than the increase observed with enterotoxin (64±51%, P<0.05) or endotoxin alone (39±34%, P<0.001). Significant increase in intestinal permeability to luminal Evans blue was observed in intestinal loops exposed to systemic endotoxin (76±79%, P<0.05), but not to enterotoxin. Our data suggests that the secretory effects of luminal enterotoxin on the small intestine can be further augmented by endotoxin administered intravenously, which also results in increased intestinal mucosal permeability and a diarrheogenic motility pattern.

Gastrointestinal peptide hormones during postoperative ileus. Effect of octreotide.

The hypothesis was that postoperative ileus might be caused by a disturbed balance between the motor-stimulating hormones, motilin and substance P, and the motor-inhibitory hormone, vasoactive intestinal polypeptide, and that octreotide might prevent this disturbance and so ameliorate the ileus. In 15 conscious dogs with chronic gastrointestinal electrodes, electrical activity was recorded and blood was drawn for radioimmunoassay of motilin, substance P, and vasoactive intestinal peptide (VIP) during fasting and after a liquid meal. Ileus was then induced by celiotomy and intestinal abrasion. During and after operation, five dogs received 154 mM NaCl only, five dogs octreotide, 0.19 micrograms/kg/hr, and five octreotide, 0.83 micrograms/kg/hr. Plasma levels of motilin, substance P, and VIP were changed little by operation, but cyclical increases in plasma motilin, which occurred preoperatively during phase III of the interdigestive myoelectric complex, were completely abolished postoperatively during ileus, as was the complex itself. Octreotide ameliorated the ileus and restored the cyclic increases in motilin found in health, nor did it alter plasma substance P and VIP. In conclusion, octreotide ameliorates postoperative ileus, but it does not do so by increasing plasma motilin or substance P or decreasing plasma VIP.

Effects of buprenorphine on gastrointestinal interdigestive myo-electric complex in dogs

The effect of buprenorphine on the interdigestive myoelectric complex (IMC) was studied by gastrointestinal electromyogram in 3 mature mongrel dogs. The electromyograms were used to study the IMC cycle and total elapsed time (TET). Buprenorphine had very strong hyperkinetic action on the gastrointestinal tract at doses of 1 and 2 micrograms/kg which revealed phasic contraction, but since this action disappeared when atropine was administered. The phasic contraction originated in the upper jejunum just under the ligament of Treitz and then showed a migration pattern of J-->D and J-->I in 11 out of 23 cases (47.8%), D-->J-->I in nine cases (39.1%), J-->D-->J-->I in one case and no response in two cases. TET (min) showed a mean value of 90.3 +/- 11.2 (n = 23), which was not significantly different from the controls (106.1 +/- 14.3) (n = 24), but tended to be longer (0.1 > p > 0.05). After administration of buprenorphine at a dose of 20 micrograms/kg, phasic contraction migrated to ileum, which was disappeared an interval of 6-7 hours until next IMC. At low doses of buprenorphine were administered after a meal, the postprandial pattern was restored and converted to fasted pattern only one IMC cycle. Buprenorphine is partial agonist for the mu receptor. Ahmad et al. (1989) reported that alpha 2 adrenergic receptor and opiate receptors (mainly mu) were presented in submucosal plexus. In concludes that alpha 2 adrenergic activity and other humoral factors seems to take an important role for the initiation of phasic contraction and to control maintenance of IMC cycle.

Studies of Small Intestinal Myoelectrical Activity and Intraluminal Pressure Changes in the Unrestrained Conscious Rat

Our aim was to develop and validate a methodology to permit chronic recordings of small intestinal intraluminal pressure changes in the conscious rat and thereby to study regional variations in motor activity. A low‐flow (0.014 cc/min) perfusion system permitted reliable intraluminal pressure recordings at four sites along the small intestine from unrestrained animals. Comparison of overall patterns of fasted and fed motor activity and the various parameters of the migrating motor complex (MMC) from these recordings with those obtained from another group of animals prepared with serosal electrodes provided similar results in the proximal small intestine (MMC frequency 3.4 ± 0.5 vs. 3.9 ± 0.3 cycles/h, phase II duration 3.8 ± 0.7 vs. 4.7 ± 0.4 min, and phase III duration 4.0 ± 0.2 vs. 3.5 ± 0.2 min for duodenal catheters vs. electrodes, all NS). However, the distal deal phase II was considerably shorter in catheter than electrode recordings (6.0 ± 0.8 vs. 15.7 ± 2.4 min, p &lt; 0.0001). Both methodologies confirmed significant regional variations in small intestinal motor parameters: the incidence of interdigestive myoelectrical complex (IDMEC) cycles was lower and phase II of the IDMEC was considerably prolonged in the distal Hewn. In summary, a system to permit chronic recordings of small intestinal intraluminal pressure has been developed and validated by comparison to myoelectrical recordings. Motor specialization was evident in the rat distal ileum.

Motor and Absorptive Function of the Canine Intestine Following Serosal Patching: The Effects of a Lateral Enterotomy on Small Intestinal Myoelectrical Activity

We studied the effects of serosal patching of a 4 x 15-cm, full-thickness, jejunal defect on absorptive function and fasting and postprandial myoelectrical activity in 5 patched and 5 control animals over a 3-month period. While fat and D-xylose absorption were similar in both groups, serum albumin was significantly depressed (2.96 +/- 0.24 g/dL preop vs 2.29 +/- 0.23 g/dL postop, p less than .05) and stool moisture content was elevated following patching (54 +/- 4% vs 67 +/- 9%, p less than .05). Neither the generation of the various phases of the interdigestive myoelectrical complex (IDMEC), the development of postprandial myoelectrical activity, or colonic myoelectrical patterns were impaired in the patched animals. The normal gradients of slow wave frequency, phase III propagation velocity, and onset of the fed pattern were similar in control and patched animals. However, jejunal slow wave frequency (cpm, control vs patch: 18.6 +/- 0.6 vs 19.5 +/- 0.6, p less than .05) and IDMEC frequency (0.36 +/- 0.25 vs 0.56 +/- 0.32, p less than .05) were greater and the IDMEC period shorter (109.6 +/- 27.8 vs 88 +/- 35.7, p less than .05) in the patch animals. In vitro studies demonstrated similar absorptive function in intact mucosa and neomucosa. We conclude that the technique of serosal patching is associated with impaired absorption in vivo. While this may be related, in part, to the minor motility changes observed, other factors such as hormonal changes may also be important.

Disruption of canine jejunal interdigestive myoelectrical activity by artificial ileocolonic sphincter. Studies of intestinal motor response to surgically fashioned sphincter substitute.

We studied the effects of an ileocolonic sphincter substitute on canine small intestine motor activity. Recordings of fasting and postprandial myoelectrical activity were performed in three groups of animals in whom the following procedures had been performed: (1) electrode placement alone, intestinal continuity undisturbed (controls); (2) ileocolonic sphincter substitute fashioned in mid-jejunum; and (3) transection and reanastomosis at a similar location in mid-jejunum. Transection alone resulted in a decrease in slow-wave frequency, a shortening of the period of the interdigestive myoelectrical complex (IDMEC) and a prolongation of phase III of the IDMEC in the jejunum distal to the site of transection. The IDMEC period was also shorter at proximal electrode sites, but the incidence of IDMEC phase III complexes was similar on either side of the transection. However, in those animals in whom a sphincter substitute had been fashioned at the site of the transection, the incidence of IDMEC phase III complexes was significantly suppressed in the proximal intestine; IDMEC phase III frequency per hour (mean +/- SD transection vs sphincter substitute) was 0.59 +/- 0.20 vs 0.23 +/- 0.24, P less than 0.002; 0.61 +/- 0.24 vs 0.28 +/- 0.30, P less than 0.006; 0.61 +/- 0.24 vs 0.29 +/- 0.30, P = 0.008, at electrodes 10, 35, and 85 cm proximal to the sphincter substitute, respectively. In addition, the sphincter-substitute animals alone demonstrated, during fasting, recurrent propagated bursts of spike clusters and occasional prolonged spike bursts in electrodes proximal to the sphincter substitute.(ABSTRACT TRUNCATED AT 250 WORDS)

Interdigestive myoelectric complex in germ-free rats.

The effect of intestinal bacteria on the interdigestive myoelectric complex (IDMEC) was studied by recordings of the electrical activity of the proximal and distal small bowel in fasting germ-free (n = 6), gnotobiotic (n = 7), and conventional (n = 6) rats in vivo. Germ-free and gnotobiotic rats were operated and studied in germ-free or gnotobiotic conditions. The IDMEC period (mean +/- SD) in the proximal and distal small bowel was significantly longer in germ-free rats (20 +/- 2 min and 102 +/- 14 min) as compared to conventional rats (13 +/- 1 min and 58 +/- 5 min). Association of germ-free rats with a limited flora (gnotobiotic rats) decreased the IDMEC period significantly (15 +/- 1.5 min and 75 +/- 14 min). The migration velocity of the IDMEC was inversely related to the IDMEC period. These observations confirm previous data suggesting that the interdigestive motor complex has a role in the homeostasis of the bacterial content of the small bowel.

遊離空腸による咽頭食道再建例における移植空腸自律運動の経時的変化とえん下障害

Manometric studies were carried out for thirteen cases of pharyngoesophageal reconstruction with free transplantation of jejunal segments in order to evaluate intermittent dysphagia during the early postoperative period. The following results were obtained.1. Dysphagia was observed when transplanted jejunum made spontaneous continuous contractions, and it disappeared after the contractions were subsided.2. Continuous waves were observed for 13.0% of the testing period with the duration of 3.6±3.5 minutes. The average value of the maximum pressure for the continuous waves were 109.7±72.5cm H2O. The average rate of the wave was 10.9±1.8 times per minute in interdigestive period.3. The shorter the postoperative period was, the shorter the duration of continuous waves was in operated cases.4. The continuous jejunal waves after swallowing were observed more frequently for the cases whose postoperative periods were within two months than for other cases. The waves were thought to be a disadvantage for oral intake.5. Almost all of the continuous jejunai waves after 5 months of postoperative periods were similar to normal interdigestive jejunal strong contractions (interdigestive myo-electric complex; IMEC).From these results and the facts that interdigestive myo-electric complex (IMEC) is not triggered by swallowing and that they disappear immediately after feeding, it is suggested that dysphagia or nasal regurgitation observed in the early postoperative period for the cases of free jejunal transplantation is related to irregular jejunal movements which is different from normal IMEC.

Variations in plasma motilin, somatostatin, and pancreatic polypeptide concentrations and the interdigestive myoelectric complex in dog.

We have looked at the plasma concentrations of motilin, pancreatic polypeptide (PP), and somatostatin (STS) during the various phases of the interdigestive motor complex (IDMC) in dogs. As expected, motilin cyclical increase was always associated with the phase III of the IDMC. Statistical analysis of PP variations revealed a significant rise 10 min before duodenal phase III; however, in individual animals, this relationship was inconsistent. Although a dose-related increase in PP blood levels was induced by administration of synthetic canine motilin (0-200 ng kg-1 iv), fasting plasma levels of PP were not correlated with the concentrations of circulating endogenous motilin. After truncal vagotomy, while motilin release and the intestinal motility pattern remained unaltered, the phase III associated cyclical increases of PP disappeared. Infusion of physiological amounts of PP (1 microgram kg-1 h-1 for 3 h) mimicking the postprandial release failed to reproduce a fed pattern type of intestinal motility and of motilin secretion. No statistical correlation could be established between STS plasma levels and the motor activity of the intestine. STS plasma levels were not correlated with circulating concentrations of motilin and the exogenous administration of physiological doses of synthetic canine motilin failed to modify STS plasma levels. Morphine (200 micrograms kg-1 iv) stimulated only the release of motilin. These data suggest that the role played by circulating concentrations of PP and STS in the control of the IDMC in dog is at most minimal.

Contractile patterns and transit of fluid in canine terminal ileum.

Earlier recordings of intraluminal pressure from the terminal ileum and across the ileocolonic sphincter of dogs revealed, in addition to the usual interdigestive and digestive patterns, pressure waves that appeared to have propulsive potential. One of these, which we designated as a "prolonged propagated contraction" (PPC), was a wave of high amplitude; it had a duration much longer than the ileal slow wave and migrated rapidly through the ileum, often into the proximal colon. The other pattern was one of "discrete clustered contractions" (DCC); these were propagated bursts of rhythmic phasic waves, distinct from phase III of the interdigestive myoelectric complex. These migrated through the ileum more rapidly than did phase III. Our aims were to record the electrical and mechanical equivalents of these pressure events using only extraluminal sensors and to evaluate the capacity of these contractions to propel fluids. PPCs and DCCs were recorded by extraluminal strain gauges, and flow was assessed by recovery of a nonabsorbable marker. Phase III of the migrating motor complex propelled fluid through the ileum, but in addition DCCs and, especially, PPCs were able to empty the ileum. These latter contractions have similarities to the ileal "peristaltic rush" described by others, and we believe these waves are an important force for ileal emptying.

Motilin and the vagus in dogs.

The aim of this work was to determine the influence of the vagus on the circulating levels of immunoreactive (IR) motilin. Five mongrel dogs were equipped with chronically implanted electrodes in the small intestine to record the myoelectrical activity. The release of IR motilin during fasting, after a meal, and during an infusion of insulin was studied before and after truncal vagotomy at the diaphragmatic level. When tested at least two weeks after the operation, the motility pattern of the small intestine and the secretion of IR motilin remained unaltered by vagal section. Cyclic increases in IR motilin associated with phase III's of the interdigestive myoelectric complexes were still observed after vagotomy (maximum levels of IR motilin: 250 +/- 37 versus 239 +/- 19 fmol X mL-1, not significant), and they were still abolished by feeding or by insulin. However, an inhibitory influence can probably be mediated by the vagus since, in normal animals, vagal stimulation by a "modified sham feeding" (tease feeding or presentation of food) at the beginning of a period of phase III activity promptly interrupted this part of the complex and decreased significantly the release of IR motilin by about 20%. The release of motilin is not chronically altered by distal vagotomy in dogs.

Gastric influences on canine small intestinal myoelectric activity.

The aim was to determine whether the canine stomach modulates interdigestive and digestive small intestinal myoelectric activity. In four conscious dogs with electrodes implanted chronically on the duodenum and jejunum, enteric myoelectric activity was recorded during fasting and after feeding a 200-g liver meal. The dogs then underwent total gastrectomy and esophagoduodenostomy, after which they were restudied. Gastrectomy did not alter the pattern of the enteric interdigestive myoelectric complexes; the occurrence, period, duration of phase III, and consistency of distal propagation of enteric IMCs remained unchanged. Gastrectomy also preserved both the postcibal inhibition of the enteric IMCs and the postcibal induction of the fed myoelectric pattern in the small bowel. However, the onset of the fed pattern occurred more promptly after gastrectomy than before gastrectomy. We concluded that the pattern of canine duodenal and jejunal interdigestive myoelectric activity was largely independent of the stomach. The more rapid onset of the fed pattern with feeding postgastrectomy may relate to more rapid entry of chyme into the small intestine.

Myoelectric Activity and Intraluminal Pressure of the Canine Ileocolonic Sphincter

We constructed ileocolonic loops of distal ileum, ileocolonic sphincter, and proximal colon in 5 dogs; neuromuscular continuity was maintained between loop and intact bowel by a bridge of tunica muscularis. To study ileocolonic sphincter function, we recorded myoelectric activity from subserosal electrodes and intraluminal pressures from perfused catheters and a sleeve sensor. Recordings included at least one interdigestive myoelectric complex and four postprandial hours. Ileal slow waves were recorded from the loop and the ileocolonic sphincter; most interdigestive myoelectric complexes were propagated to the ileocolonic sphincter. Intraluminal pressures at the ileocolonic sphincter fluctuated phasically (mean 12.5 cycles/min) for 72% of recording time during fasting and 81% postprandially. Tonic pressures at the ileocolonic sphincter were higher during fasting (31 +/- 18 cmH2O; p less than 0.05) than postprandially (24 +/- 20 cmH2O); moreover, tonic pressures fluctuated more during fasting than after food. Tonic elevations of pressure were prolonged (mean duration 28.5 min) concomitant with arrival of phase 3 of interdigestive myoelectric complexes at the ileocolonic sphincter. Thus the ileocolonic sphincter participates in both the myoelectric and motor components of the interdigestive cycle and exhibits an intense phasic and tonic response to phase 3. The association of tonic pressure and intense phasic contractions may serve to retard and segment ileal chyme. On the other hand, the presence of rapidly propagated phasic pressures in the region may provide the basis for propulsive function. In this way, these unique motor events will facilitate two distinct functions of the region, namely the alternate retarding and forward propulsion of chyme.

Stimulation of motilin release by bombesin in dogs.

Bombesin (BBS) was infused in conscious fasting dogs to document its effects on the release of motilin in the blood and on intestinal motility. When BBS was infused for 3 h (0.125 and 0.5 microgram X kg-1 X h-1), a specific pattern of myoelectric activity was induced: 1) the pacesetter potentials were increased in frequency but decreased in amplitude; 2) a moderate spike activity (weak phase II) was superimposed on this disorganized pacesetter activity, and activity fronts were abolished despite elevated motilin levels. A second experiment was performed in which motilin levels during BBS administration for a selected period of an interdigestive myoelectric complex (IDMC) could be compared with those obtained at a similar period of a preceding IDMC in which a saline solution had been infused. The motilin blood levels measured during BBS administration (0.25, 0.5, 1.0, and 2.0 micrograms X kg-1 X h-1 for 20 min each stepwise) were significantly higher than those obtained with saline. The administration of BBS synchronized with the IDMC was necessary to document its effect on motilin release, because when BBS was infused at an unknown period of the IDMC no rise of motilin levels over basal could be detected. Because of its contradictory effects on the release of motilin (stimulation of motilin release) and on the IDMC (inhibition of motilin effect), a physiological role of BBS as an endocrine regulator of motilin release is questionable. On the other hand, the possibility that BBS controls motilin release in a paracrine or neurocrine role cannot be excluded.