Oral prostaglandin E analogues induce intestinal migrating motor complexes after a meal in dogs. Evidence for a central mechanism

The effects of oral, intravenous, and intracerebroventricular administration of synthetic derivatives of prostaglandins E1 (misoprostol) and E2 (enprostil) on postprandial gastrointestinal motility were investigated in dogs chronically fitted with strain gauge transducers on the antrum and the proximal and middle jejunum. Synthetic prostaglandin E analogues administered orally at a dose of 20-50 micrograms/kg 15 min before the meal did not modify the postprandial pattern of gastric contractions but suppressed the spontaneous postprandial irregular activity on the jejunum and induced a cyclic pattern of migrating motor complexes for 4-6 h after the meal. These postprandial migrating motor complexes induced by prostaglandin E were propagated between the two recording sites and had a period similar to that observed in the fasted state. However, the duration of phase 2 was significantly increased and the amplitude of the phase 3 decreased. This jejunal cyclic motor pattern was reproduced by administration of synthetic prostaglandin E derivatives either intravenously (4-10 micrograms/kg) 15 min before the meal or intracerebroventricularly (50 ng/kg) 1 h after the meal. The intestinal migrating motor complex activity observed after oral administration of synthetic prostaglandin E derivatives was abolished by the previous intracerebroventricular (40 micrograms/kg) but not intravenous (200 micrograms/kg) administration of SC-19220, a receptor antagonist of prostaglandin E. These results suggest that oral administration of synthetic prostaglandin E1 (misoprostol) or prostaglandin E2 (enprostil) analogues before a meal induces postprandial migrating motor complexes on the jejunum in dogs through a mechanism involving central prostaglandin receptors.     

Circadian rhythm of rectal motor complexes

PURPOSE: Prolonged rectal pressure recordings have revealed that the rectum exhibits typical bursts of regular pressure waves, also called rectal motor complexes. Although there is consensus regarding the characteristics of rectal motor complexes, their function is poorly understood. Furthermore, data regarding the circadian rhythm of these complexes are either lacking or conflicting. Therefore, we conducted a study to investigate the circadian rhythm of rectal motor complexes in fully ambulant subjects. Because a meal is a powerful and physiologic stimulus to elicit colonic pressure activity, we also studied the effect of a meal on these rectal motor complexes. METHODS: Prolonged ambulant anorectal pressure recordings were performed in 12 healthy volunteers (male:female ratio, 6:6; median age, 27 (range, 22–53) years). A total of 139 rectal motor complexes were observed in >300 hours of recording. RESULTS: All subjects exhibited rectal motor complexes during the daytime, whereas in five subjects, no rectal motor complexes were observed during sleep. The number of rectal motor complexes was significantly lower during sleep (diurnalvs. nocturnal, 8vs. 1 per subject,P<0.0001). Furthermore, the duration and peak amplitude of these nocturnal rectal motor complexes were significantly reduced. On the ambulant recordings, the subjects marked a total of 20 meals. During the first 2 hours after these meals, rectal motor complexes were noted in 65 percent of the cases. The postprandial frequency of rectal motor complexes was significantly higher than the overall frequency (2/hourvs. 0.4/hour,P=0.004). CONCLUSIONS: These findings suggest that sleep results in a reduction of rectal motor activity, whereas a meal provides a stimulus for increased rectal motor activity in fully ambulant subjects.     

A Normal Gastrointestinal Motility Excludes Chronic Intestinal Pseudoobstruction in Children

Gastrointestinal manometry has gained wide acceptance in the approach to patients with suspected enteric neuromuscular disorders. However, performing gastrointestinal manometry in these subjects without a previous exhaustive diagnostic evaluation is unjustified. Twelve children (median age: 7.0 years; range: 8 months–13 years), with clinical and x-ray features suggesting chronic intestinal pseudoobstruction, were referred to our unit for gastrointestinal manometry. The latter was performed with a perfused catheter for 5 hr in the fasting state and for 90 min after feeding. Data were compared with those recorded in eight age-matched controls. In all patients and controls, interdigestive motor complexes with propagated phases III were detected; a regular postprandial antroduodenal motor activity was also recorded. Patients and controls did not differ for fed antral and duodenal motility indexes, fed antroduodenal coordination, and length of duodenal phase III. Most of the patients showed short or prolonged bursts of nonpropagated activity in the fasting and/or fed states; in four cases fasting and/or fed sustained phasic activity was recorded. Manometric evidence of migrating motor complexes and postfeeding activity did not support the diagnosis of intestinal pseudoobstruction and suggested redirecting the diagnostic evaluation. Final diagnoses were: Munchausen syndrome-by-proxy (four cases), celiac disease (two cases), intestinal malrotation (two cases), Crohns disease (two cases), multiple food intolerance (one case), and congenital chloride-losing diarrhea (one case). It is concluded that in children with suspected chronic intestinal pseudoobstruction manometric evidence of migrating motor complexes and fed motor activity excludes an enteric neuromuscular disorder and suggests a reassessment of the diagnostic work-up. Furthermore, if gastrointestinal manometry shows migrating motor complexes and postfeeding motor activity, qualitative abnormalities of the manometric tracings do not indicate an underlying enteric neuromuscular disorder and must not be overemphasized. Patients referred for gastrointestinal manometry should previously undergo an extensive diagnostic investigation to exclude disorders mimicking chronic intestinal pseudoobstruction.     

Colonic myoelectrical activity in IBS painless diarrhoea.

Colonic myoelectrical activity was recorded during 24 hours in 23 patients with painless diarrhoea and compared with a control group of 10 healthy subjects without digestive functional disorders. Diurnal fasting activity showed no significant difference in the total long spike bursts activity (LSB lasting greater than 7 seconds), but short spike bursts activity (SSB, lasting less than 7 seconds) was significantly lower (p less than 0.05) in diarrhoeal patients. A striking difference was observed in colonic response to eating, with an increased number of migrating long spike bursts (MLSB: mass movements) during the first postprandial hour in diarrhoeal patients (p less than 0.001), while short spike bursts (segmental activity) were almost absent in the rectosigmoid area. A marked decrease in the retrograde LSB activity was also observed in eight patients. During the night (from 2200 h to 0600 h) the number of migrating long spike bursts was increased in the diarrhoea group, but almost absent in controls (p less than 0.001). This study shows that colonic motor activity was altered in painless diarrhoea. These disturbances were not limited to the decreased SSB activity in the sigmoid, but involved the whole colon, with lower SSB activity and abnormal increase of migrating long spike bursts activity (MLSB) in postprandial and nocturnal periods.     

Effect of irradiation on morphology and motility of canine small intestine

In addition to severe damage to the intestinal mucosa, there is evidence based on altered transit that irradiation affects intestinal motor function. A single dose of 938 cGy to the intestine of dogs consistently produced an acute intestinal radiation syndrome consisting of vomiting and diarrhea but was not lethal. In the fasting state, the migrating myoelectric complex was uniformly interrupted. After a meal, jejunal myoelectric activity analyzed by a computer program showed a progressive decline in the number, duration, and length of migration of spike bursts. There were occasionally bizarre motility patterns consisting of clusters of migrating spike bursts. Slow waves demonstrated irregular rhythm and nonuniform morphology. They occasionally migrated in an orad direction and at times were totally uncoupled. At 24 hr and four days after irradiation, the muscle and the neural plexus were nearly normal by light microscopy, but the mucosa exhibited severe necrosis. Therefore, irradiation produces profound functional abnormalities in intestinal muscle even though the morphology is minimally altered.This study was supported by Veterans Administration Medical Research Funds and NIH Digestive Disease Core Center grant AM 34986-01.     

Migrating myoelectric complex and jejunal slow-wave propagation after Roux gastrectomy in dogs

Roux-en-Y gastrectomy is associated with a high incidence of symptoms of gastric stasis. Retrograde propagation of jejunal electrical slow waves and spike bursts has been implicated in the Roux Y stasis syndrome. Since the fasted state may persist after feeding, this study examined the extent of retrograde slow-wave propagation in the fasted state, particularly during aboral migration of phase III. Six dogs underwent Roux gastrectomy and placement of bipolar electrodes along the Roux limb. Four normal dogs with electrodes acted as controls. Thirty-five migrating myoelectric complexes were recorded in Roux dogs and 13 in controls. In Roux dogs, the incidences of retrograde propagation of slow waves during the migrating myoelectric complex were phase I 56±13%, phase II 60±12% and phase III 58±14% (not significant). For controls, the incidences were 0%, 0%, and 1%, respectively (P<0.006 versus Roux dogs). In the Roux limb, retrograde propagation of slow waves, and hence spike bursts, occurs even during aboral migration of phase III. This abnormality may contribute to the Roux Y stasis syndrome.An abstract of this work has previously been presented at American Federation for Clinical Research Mid Western Section, October 31, 1990, at Chicago.Supported in part by a grant from the Veterans Administration and from the Department of Surgery, SUNY Health Science Center at Syracuse, Syracuse, New York.     

Daytime and night time motor activity of the small bowel after solid meals of different caloric value in humans.

BACKGROUND: Meals disrupt the interdigestive pattern of small bowel motor activity and convert it into the postprandial pattern. Previous studies have shown that duration of postprandial motor activity depends on the caloric value of a meal, but results from two recent human studies suggested that there is a caloric ceiling, above which an additional increase in the caloric load fails to prolong the postprandial period further. AIM: To investigate the hypothesis of a caloric ceiling by studying daytime motor activity of the human small bowel in response to five solid meals, covering a wide range of calories. METHODS: Eight healthy male volunteers underwent five separate, ambulatory small bowel manometry studies and had a total of 80 meals. For lunch, volunteers ate between one and five portions of a solid meal (220, 440, 660, 880, or 1100 kcal). Ten hours later and 30 minutes before they went to bed, they ate either two or four portions of the same meal (440 kcal or 880 kcal). Recordings were analysed visually for phase III of the migrating motor complex and a validated computer program calculated incidence and amplitude of contractions. RESULTS: Apart from two versus three portions (440 kcal v 660 kcal), postprandial motor activity was significantly prolonged by each 220 kcal increase in the caloric load of the lunch (168 (SEM 14), 305 (22), 298 (23), 368 (36), and 398 (38) min). Mean incidence of contractions was significantly different only between the two extremes tested: 220 kcal and 1100 kcal (2.9 (0.3) v 4.5 (0.6) min-1). Amplitude of contractions did not depend on meal size. Daytime and night time postprandial activity were not significantly different. This was true for duration of fed activity, as well as mean incidence and amplitude of contractions during the postprandial period. CONCLUSION: Caloric value of a meal regulates duration of the fed activity in the human small bowel over a wide range of calories, and-for caloric loads up to 1100 kcal-there is no maximum duration of postprandial motor activity. Furthermore the postprandial small bowel motor activity is very similar between daytime and night time.     

Is colonic electrical activity a similar phenomena to small-bowel electrical activity?

PURPOSE: This study was designed to investigate colonic spike bursts regarding 1) their migration behavior, 2) their pressure correlates, and 3) comparing colonic short spike bursts with spike bursts from migrating myoelectric complex from the small bowel. METHODS: Rectosigmoid electromyography and manometry were recorded simultaneously in seven normal volunteers and electromyography alone in five others during two hours of fasting and for two hours after one 2,100-kJ meal. One patient with an ileostomy was also studied by the same method to record the migrating myoelectric complex from the terminal ileum during fasting. RESULTS: Three kinds of spike bursts were observed in the pelvic colon: rhythmic short spike bursts, migrating long spike bursts, and nonmigrating long spike bursts. The meal significantly increased the number of migrating and nonmigrating long spike bursts (from 25 to 38.7 percent of the recording time; P <0.01). These bursts of potentials showed a peak 15 minutes after the meal, which may be caused by the gastrocolic reflex. Migrating long spike bursts started anywhere along the rectosigmoid and migrated from there aborad 82 percent of the time and orad or in both directions in 10 or 7 percent of the time, respectively. They originated pressure waves 99 percent of the time. Short spike bursts were more frequent before the meal (15.1 percent before and 9.6 percent after the meal), but the difference was not significant; they neither propagated nor initiated pressure waves detected by the miniballoon. CONCLUSIONS: Migrating long spike bursts were the only potentials that migrated, sometimes for short distances. Short spike bursts are a different phenomenon from the small-bowel migrating myoelectric complex because they do not migrate; they can occur during the postprandial period and never originated intraluminal pressure waves.Supported by a grant from the Instituto Nacional de Investigação Científica, Proc. DBI-22086.Presented at the meeting of the Portuguese Congress of Gastrenterology, Vila Moura, Portugal, June 2 to 5, 1993.     

Caloric content of a meal affects duration but not contractile pattern of duodenal motility in man

The variability of the fasted duodenal contractile pattern and the patterns of contraction during the fed phase was examined in normal volunteers. Prolonged recordings from the duodenum and proximal jejunum were achieved using a series of transducers mounted on a 2.3-mm catheter. A total of 58 interMMC intervals and the response to 18 meals was examined. There was marked inter- and intrasubject variability in the fasted state, even within one study. The phase II pattern was examined in detail and propagated single peaks, propagated clusters, and repeated propagated clusters are described. Single peaks could be propagated as rapidly as 16 cm/sec. Single peaks were propagated more rapidly than propagated multiple peaks. During phase III, duodenal contractions occurred at 11.3 +/- 0.09/min and jejunal contractions at 10.73 +/- 0.15/min. The rate of progression of the onset of phase III was 0.145 +/- 0.015 cm/sec. The effect of the caloric content of the meal was examined by determining the effect of 150-kcal, 300-kcal, and 600-kcal meals on the fed pattern. Increasing caloric content increased the duration of the fed pattern but had no effect on the total or normalized motility index or on the change in motility index over time during the fed pattern. The types of contractions seen during the fed pattern are described. Propagated clusters over at least 16 cm are common during the fed phase in normals, with 10% of all contractions seen during the fed phase being propagated over 28 cm. No difference in the patterns of contractions or their propagation was seen with the different caloric contents of the meals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of migrating motor complex on esophageal motility

In most fasting mammals motility of the foregut and small intestine undergoes regular cycles of activity. The phenomenon has been called the interdigestive migrating myoelectric complex or the migrating motor complex. As shown in published literature, feeding interrupts the cycle and changes the interdigestive fasted pattern into a pattern of irregular spiking activity, which has been called the fed pattern. The mapping of the migrating motor complex throughout the upper gut demonstrated major regional variations. The incidence of migrating motor complex at multiple sites from distal esophagus to cecum approximated a normal distribution. In the course of esophageal manometric studies the influence of migrating motor complex on lower esophageal sphincter was observed. This observation raised the question whether future pharmacomanometric studies should be performed with volunteers in the fasting state as done until now. According to published literature, lower esophageal sphincter pressure is significantly higher during migrating motor complex phase III than phase I; differences are approximately twofold. Fifty percent of migrating motor complexes involve the esophagus. The migrating motor complex in some individuals interferes significantly with esophageal pharmacomanometry provided the volunteers are fasted. On the other hand postprandial lower esophageal sphincter pressure was rather constant at a level comparable with that measured in migrating motor complex phase I. The consequences of this phenomenon for the study design in pharmacomanometry are discussed.     

Role of pylorus in the control of the canine migrating motor complex

The cyclic myoelectric activity of the gastroduodenal area and the antral mucosal ionic permeability, measured by the transmural potential difference, were simultaneously evaluated in the dog. These parameters were recorded before and after section of the omental attachments to the pyloric area, section of the terminal antrum, and excision of a 2-cm segment at the pylorus. None of the surgical procedures modified the duration of the postprandial disruption of the migrating motor complexes, whereas the potential difference was increased. In fasted dogs resection of the omentum increased the migrating motor complex intervals and the duration of the phase of regular spiking activity; however, the regular spiking activities still occurred in a sequential manner. Transection of the terminal antrum was associated with a decrease in duration of the regular spiking activity phases that started simultaneously on the antrum and duodenum, without changes in the migrating motor complex intervals, and prevented the occurrence of the increase in potential difference associated with feeding. After pylorectomy, the migrating motor complex intervals were reduced by 46% on both antrum and duodenum. Our observation that only pylorectomy was able to consistently increase the frequency of migrating motor complexes suggests a pyloric inhibition of the normal pacing of the cyclic motor events at both antral and duodenal levels.     

Evaluation of colonic myoelectrical activity in health and functional disorders.

Electrical activity of the colon was investigated in six healthy volunteers and 22 patients presenting functional colonic disorders associated with pain, constipation, or diarrhoea. Myoelectrical activity during 10 hours, including two daily meals, was recorded from eight groups of nickel-chrome electrodes using a 1.5 m length probe introduced by the rectal route. Electromyograms of volunteers consisted of slow waves at two distinct rhythms, approximately 3 and 10 cycles per minute, during 16 to 28% of the recording time respectively for each site. Action potentials were also recorded as 11 to 80 short spike bursts (SSB) per hour lasting 1.5 to 3.5 s at any site and 20-26 long spike bursts (LSB) per hour, lasting 17 to 21 s, occurring in series of four to eight propagated bursts. Additional high-velocity propagated bursts were recorded during the three hour postprandial period. Three typical changes in spike activity patterns were detected: an increase by 170-420% of the number of SSB associated to a high spiking activity was recorded in 13 patients (group I), the absence of SSB, a low spiking activity level and only 3 to 8 LSB per hour (group II), in six patients; and the postprandial response was absent (group III) in three other investigated patients. Evidence for three groups of motor disturbances and their possible relation to clinical manifestations of functional disorders is presented.     

Effects of cisapride on postcibal jejunal motor activity

In the jejunum of fasting humans, cisapride induces a phase 2-like, highly propagative motor pattern. This study investigated cisapride's effects on the fed pattern of the jejunum. Starting 5 min after a phase 3 of the migrating motor complex, 18 healthy men received 5 or 10 mg cisapride or placebo orally in random double-blind fashion and ingested meals containing 1000 and 4200 kJ, respectively. Jejunal pressures were recorded pneumohydraulically with five catheter orifices 10–30 cm aborad the ligament of Treitz. After the 4200-kJ meal, total number and number of propagated contractions as well as area under the curve increased significantly more than after 1000 kJ. Following the 1000-kJ but not the 4200-kJ meal, 10 mg cisapride increased total number of contractions, number of propagated contractions, mean amplitude, and area under curve significantly more than placebo. Fed-pattern duration increased with the meal's caloric content but was not influenced systematically by cisapride. In conclusion, cisapride stimulates jejunal motor activity and induces a propagative pattern after a 1000-kJ but not after a 4200-kJ meal, suggesting that it can produce no further stimulation when motor activity is near maximally enhanced already.     

Disruption of canine jejunal interdigestive myoelectrical activity by artificial ileocolonic sphincter

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)     

Twenty four hour manometric recording of colonic motor activity in healthy man.

The motor activity of the transverse, descending, and sigmoid colon was recorded for 24 hours in 14 healthy volunteers with a colonoscope positioned catheter. During the study the patients ate two 1000 kcal mixed meals and one continental breakfast. Colonic motor activity was low before meals and minimal during sleep; the motility index increased significantly after meals and at morning awakening. Most of the motor activity was represented by low amplitude contractions present singly or in bursts, which showed no recognisable pattern. All but two subjects also showed isolated high amplitude (up to 200 mmHg) contractions that propagated peristaltically over long distances at approximately 1 cm/sec. Most of these contractions occurred after morning awakening, and some in the late postprandial period, with a mean of 4.4/subject/24 h. The peristaltic contractions were often felt as an urge to defecate or preceded defecation, and could represent the manometric equivalent of the mass movements.     

Colonic motor response to a meal in acute colitis

The symptoms of urgency, diarrhea, and abdominal discomfort are exaggerated after a meal in inflammatory disorders of the colon, such as ulcerative colitis. The possible motor correlates of these symptoms were investigated in a model of acute colitis in six dogs. Each dog was instrumented with seven strain gauge transducers, two on the proximal, three on the middle, and two on the distal colon. After an overnight fast, 4-hour fasted recordings were made from the normal colon and after the colon had been cleansed on the previous day with Colyte (Reed & Carnrick, Piscataway, NJ). A 1300-kcal meal was then fed, and the recordings were continued for another 8 hours. Acute colitis was then induced by the perfusion of 10 mL of 75% acetic acid and confirmed with colonoscopy and biopsy. The fasted and postprandial recordings were repeated during the next 5 days. In the control state, ingestion of the meal increased the total duration per hour of contractile activity in the early (0-2 hours) and late (2-8 hours) postprandial periods in the distal colon. In the proximal and the middle colon, a significant increase in motor activity occurred only during the late postprandial period. Similar effects were observed in the cleansed colon. By contrast, there was no significant increase in motor activity after a meal during colitis in any of the postprandial periods in the cleansed or the uncleansed colon. During colitis, there was a significant increase in the incidence of giant migrating contractions in the fasted state. The ingestion of a meal further increased the frequency of giant migrating contractions in the uncleansed colon from 0.4 +/- 0.1 to 1.3 +/- 0.5 per hour in the late postprandial period. There was no significant increase during the early postprandial period. The increase in the late postprandial frequency of giant migrating contractions was associated with an increase in defecation frequency. It is concluded that the motor response of the colon to a meal is absent in acute colitis. The entry of new ingesta into the colon during the late postprandial period stimulates enteric mechanisms to initiate an excessive number of giant migrating contractions. These giant migrating contractions may be related to increased postprandial abdominal discomfort and increased frequency of defecation.     

Effect of somatostatin on gallbladder volume and small intestinal motor activity in humans

The effects of different doses of somatostatin (36, 180, 360 pmol/kg/h) on the motor patterns of the duodenum and on gallbladder volume in the postprandial period were evaluated. Gallbladder volume and small intestinal motor activity were monitored simultaneously in 9 normal subjects. Gallbladder volume was measured every 5 min throughout the study by real-time ultrasonography while intestinal motility was recorded manometrically by means of a low-compliance pneumohydraulic system. On day 1, the response of the gallbladder to a 972-kcal test meal was evaluated ultrasonographically to assure a normal response. On day 2, at least 2 consecutive phase III complexes of the interdigestive motor cycle were recorded. Gallbladder volume varied cyclically during the interdigestive motor cycle, with the minimum value late in phase II and the maximum early in phase I (p less than 0.01); the test meal was then administered. Following the induction of a typical pattern of postprandial motility, somatostatin infusion was started and continued for 150 min. Somatostatin, at the 180- and 360-pmol/kg/h doses, interrupted the fed pattern and induced consecutive bursts of propagated clustered activity. The characteristics of these somatostatin-induced motor patterns were similar to the spontaneous phase III of the interdigestive motor cycle. An initial reduction in gallbladder volume cycle. An initial reduction in gallbladder volume followed the ingestion of the meal; during somatostatin infusion, gallbladder volume increased to values greater than fasting values and varied cyclically with minimum values before the second episode of propagated clustered activity. These results show that somatostatin interrupts the fed pattern and elicits consecutive clusters of propagated motor activity in the duodenum that are coordinated with cyclic fluctuations in gallbladder volume.     

Influence of coronavirus (transmissible gastroenteritis) infection on jejunal myoelectrical activity of the neonatal pig

Four silver-silver chloride electrodes were surgically implanted at 5-cm intervals on the jejunal serosa of 7 neonatal pigs. Daily recordings, 7 h in duration, were made from each piglet beginning 3 days after surgery. Characteristic migrating motility complexes and short, distinct (2.5-5.0 s), rapidly aboral migrating bursts of intense spike activity ("migrating action potential complexes") were seen in all preinfection recordings. Piglets were inoculated with a 1-ml oral dose of a 0.1% gut suspension from coronavirus (transmissible gastroenteritis) infected pigs. This resulted in inappetence, vomiting, and diarrhea, most marked on the second day postinfection, but which had abated by the third day. When compared to recordings from both fed and fasted noninfected (control) animals, infection significantly altered jejunal myoelectrical activity by (a) shortening the duration of the migrating motility complex on day 1 postinfection and prolonging it on day 2, (b) increasing the number of abnormal activity fronts, and (c) decreasing the number of migrating action potential complexes. Slow wave frequency and the duration of phase 3 of the migrating motility complex were unaffected. When compared to fed control animals, infected piglets also showed a slight shortening of phase 1 of the migrating motility complex on day 1 postinfection and a prolongation on days 2 and 3, as well as a shortening of phase 2 on the second and third days postinfection. Changes in myoelectrical activity were not solely due to decreases in food intake, as abnormalities persisted when food intake returned to normal on postinfection day 3, and disruption of the activity front and migrating motility complex duration were purely transmissible-gastroenteritis-virus-induced phenomena. These findings suggest that infection with transmissible gastroenteritis virus disrupts organized propulsive activity in the jejunum of the neonatal pig.     

Motility of rabbit proximal colon

To better define the physiologic relevance of the cholinergic muscarinic input to the rabbit colon and the role of different muscarinic receptor subtypes, we studied the effects of atropine, telenzepine (M₁ antagonist) and DF594 (M₃ antagonist) on colonic motility in eight conscious rabbits fitted with bipolar electrodes and strain gauges along the proximal colon. In some experiments, the chronotropic and mydriatic effect of the pharmacological agents were also assessed. Two main patterns of spike activity were identified: short spike bursts (SSBs), which were usually stationary, and long spike bursts (LSBs), which were usually propagated. Both myoelectrical patterns were dose-dependently inhibited by atropine (0.06–4 mol/kg). Atropine, at the doses of 2–4 mol/kg, abolished both myoelectrical and mechanical activity. Telenzepine (0.008–0.125 mol/kg) dose-dependently inhibited migrating LSBs without significant effect on SSBs. Higher doses (0.25–0.5 mol/kg) inhibited both LSBs and SSBs. DF594 (0.06–2 mol/kg) dose-dependently inhibited both migrating LSBs and SSBs. The three antimuscarinic agents, at doses that inhibited colonic spike activity by approximately 80% (equiactive doses), behaved as follows on heart rate and pupil diameter: atropine induced tachycardia and mydriasis, telenzepine had no effect, and DF594 induced slight mydriasis with no effect on heart rate. We conclude that spontaneous motility in the rabbit proximal colon depends on a muscarinic excitatory input. M₃ receptors are involved in the control of both LSBs and SSBs, while M₁ receptors play an important role in the regulation of LSBs. The development of selective antimuscarinic drugs, acting on a given motility pattern and with minimal side effects, may offer new perspectives in the treatment of functional bowel motor disorders.This work was supported in part by a grant from the Ministero dell'Università e della Ricerca Scientifica e Tecnologica.A preliminary report of this paper was presented at the Fifth European Symposium on Gastrointestinal Motility held in Augsburg, Germany, June 13–16, 1990, and appears in abstract form inJ Gastrointest Motil 2:156, 1990.     

Effects of central and peripheral administration of dopamine on pattern of intestinal motility in dogs

The central vs peripheral effects of dopamine on the motility pattern of the small intestine were investigated by electromyography in four conscious dogs, chronically fitted with transparietal duodenal and jejunal electrodes. In the fasted dog intracerebroventricular administration of dopamine (10g/kg) increased the duration of the interval between two consecutive migrating myoelectric complexes (MMC) while the intravenous administration at a 10-fold higher dose induced in 37.5% of trials a phase of regular spiking activity propagated over the duodenum and the jejunum. When dopamine was centrally administered 1 hr before a daily meal, the duration of the postprandial disruption of the MMC pattern was significantly (P<0.01) reduced from 9.4±1.8 to 3.2±1.3 hr at the level of the duodenum. Peripheral administration of dopamine did not modify the duration of the postprandial disruption. All of the central and peripheral effects persisted after vagotomy. It is concluded that in the dog dopamine acts centrally to modify the food-induced disruption of the MMC pattern and the frequency of the interdigestive myoelectric complexes.This study was supported by INRA (Animal Pathology Department).