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Motor cycles with phase III in antrum are associated with high motilin levels and prolonged gallbladder emptying.

We examined the relationship of interdigestive gallbladder emptying with the different phases of the migrating motor complex (MMC) and with plasma levels of cholecystokinin (CCK) and motilin. In 10 volunteers 20 cycles of the MMC were recorded. In 11 cycles phase III occurred in antrum and duodenum (group 1). In nine cycles phase III was observed only in duodenum (group 2). In group 1 gallbladder emptying started at 30% of total cycle length and continued until the end of the cycle. Maximal gallbladder emptying was 33.3 +/- 3.3% (SE). In group 2 gallbladder emptying also started at 30% of total cycle length but ended at 60%. Maximal gallbladder emptying in this group was 24.3 +/- 3.1% (P < 0.05). Motilin levels were higher in group 1 than in group 2 during phase IIB (240.1 +/- 28.5 and 142.1 +/- 30.9 pg/ml, respectively, P < 0.05) and during phase III (210.8 +/- 24.3 and 93.5 +/- 12.5 pg/ml, respectively, P < 0.05). We conclude that: 1) phase III activities starting in the antrum are preceded by greater and prolonged gallbladder emptying, higher motilin levels, and higher intraduodenal bile acid concentrations than phase III activities starting in the duodenum and 2) no relationship between interdigestive gallbladder motility and CCK levels could be demonstrated.

Adult↗

The nocturnal jejunal migrating motor complex: defining normal ranges by study of 51 healthy adult volunteers and meta-analysis.

Interdigestive human small bowel motility is characterized by the migrating motor complex (MMC). The aims of this study were to: (i) establish the normal range of variables of the nocturnal jejunal MMC and (ii) incorporate these data in a subsequent meta-analysis. Eighty-one recordings were performed by prolonged (24 h) ambulatory manometry in 51 subjects in two centres. Quantitative analysis was undertaken of 419 Phase III and 332 Phase II episodes. Adjusted mean values of seven variables were calculated using a mixed-effects model. Meta-analysis of pooled published data to generate a reliable 95% reference range was also performed. Adjusted mean values and confidence intervals are presented for all seven variables. Intrasubject variances were large in comparison with intersubject. Meta-analysis of 19 studies (356 pooled patients) meeting inclusion criteria produced wide reference ranges. At least five such ranges are useful for the detection of abnormality in the individual. This is the largest study of normal volunteers presented to date, with ranges for many variables produced using appropriate statistical methodology. A model for definition of abnormality has been proposed. We recommend that these data may be used by investigators in this field as a complement to other existing indicators of small bowel dysmotility.

Adolescent↗

Intraduodenal neuropeptide levels, but not plasma levels, vary in a cyclic fashion with the migrating motor complex.

The neurohormonal control of the migrating motor complex (MMC) is not fully understood. The hypothesis of the present study was that neuropeptide levels might vary with the different phases of the MMC and that a similar variation might be found in the secretions of the gastrointestinal tract. Thus, plasma and intraduodenal concentrations of vasoactive intestinal peptide (VIP), somatostatin (SOM), substance P (SP) and neurokinin A (NKA) were determined by radioimmunoassay every 10 min during two complete MMC cycles in eight male subjects. For comparison, plasma motilin (MOT) concentrations were measured. Plasma concentrations of MOT (mean peak value +/- SEM; 39 +/- 6 pmol L-1), but none of the neuropeptides studied, showed a cyclic variation in plasma with the different phases of the MMC. Peak intraduodenal concentrations of VIP (79 +/- 23 pmol L-1), SOM (2437 +/- 432 pmol L-1) and SP (718 +/- 326 pmol L-1) occurred at or at the time point before the onset of phase III of the MMC. No such correlation was observed for NKA. These results demonstrate that intraduodenal but not plasma concentrations of the neuropeptides VIP, SOM and SP show an association with phase III of the MMC. The biological relevance of this finding is yet unclear, but the results raise the possibility that gut neuropeptides may regulate fasting motility through a luminal release.

Adult↗

Adrenergic blockage does not restore the canine gastric migrating motor complex during vagal blockade.

Bilateral cervical cooling blockade of the vagi abolishes the gastric migrating motility complex (MMC), except for the pylorus. The present study investigated if this finding is caused by adrenergic inhibition of the stomach via sympathetic nerves entering the vagi below the level of the blockade. Stomach and upper small bowel motor activity was monitored in five chronic dogs whose vagosympathetic nerve trunks were previously isolated in bilateral, cervical skin loops to permit blockade by cooling. Adrenergic blockade was performed by an initial bolus injection of phentolamine (0.3 mg/kg) and propranolol (0.3 mg/kg) followed by a continuous intravenous infusion of the combined drugs at a rate of 1.5 mg.kg-1.h-1 for phentolamine and 0.3 mg.kg-1.h-1 for propranolol. Bilateral cervical vagal blockade abolished the gastric MMC, with persistence of phase III of the MMC in the upper small bowel. During combined vagal and adrenergic blockade, gastric contractions were absent in 4 of the 22 duodenal complexes observed. In the other duodenal complexes, intermittent gastric contractions were associated with all phases of the intestinal MMC, including phase I. At times, this contractile activity was accentuated during phase III but never reached the intensity of activity or showed the typical coordination features of the gastric MMC seen with the vagi intact. Therefore, unopposed adrenergic inhibition of the stomach does not explain the absence of the gastric MMC during vagal cooling blockade. Under normal circumstances, the vagus nerve is the most important pathway for central control of the appearance of the gastric MMC.

Analysis of Variance↗

Pain associated with phase III of the duodenal migrating motor complex in patients with postcholecystectomy biliary dyskinesia.

BACKGROUND: Correlation between various gastrointestinal events and particular aspects of the migrating motor complex has been reported. This study correlates postcholecystectomy pain to variations in biliary pressure associated with the duodenal motor cycle. METHODS: In 18 patients with postcholecystectomy pain and 10 control subjects, biliary and duodenal pressures were recorded simultaneously with microtransducers. After recording a spontaneous cycle, morphine was administered to induce a premature phase III and spasm of the sphincter of Oddi, and then cerulein was administered to stop the spasm. RESULTS: Transient but significant elevations of biliary pressure occurred at duodenal phase III in both groups, but a greater percentage of the patients developed pain during phase III (89% vs. 20%, p<0.01). Morphine produced premature phase III and biliary pressure elevation, which were accompanied by pain more frequently in the patients than in the control subjects (78% vs. 30%, p<0.05). Biliary pressure dropped after the cerulein injection, relieving the pain in 13 of 14 patients and in 2 of 3 control subjects who had morphine-induced pain. The phase III-related pain was relieved by endoscopic sphincterotomy in 14 of 15 patients. CONCLUSIONS: The cyclic elevation of biliary pressure in coordination with phase III of the duodenal motor cycle may contribute to the development of pain in patients with postcholecystectomy biliary dyskinesia.

Adult↗

Adrenergic modulation of small bowel haemodynamics in interdigestive motility state of man.

OBJECTIVE: We previously reported a new application of semi-invasive laser-Doppler flowmetry (LDF) to record small intestinal haemodynamics in man under basal motor conditions, i.e. during phase I of the migrating motor complex (MMC). In the present study, we evaluated the complete MMC cycle and its haemodynamics in humans; specifically, adrenergic influence on blood flow in all three MMC phases was studied. DESIGN: Twenty-one fasting healthy male volunteers (21-44 years) were studied during two complete MMC cycles: the first as control period, the second as experimental period with different adrenergic drugs or saline. METHODS: Recording of LDF of intestinal blood flow was performed by attaching two single-fibre microprobes to a small intestinal manometry tube, which simultaneously monitored luminal pressure changes. RESULTS: Clonidine and oxymetazoline, two alpha2-adrenoceptor agonists, significantly decreased blood flow during all phases of the MMC cycle. In contrast, the non-selective beta-adrenoceptor agonist isoprenaline induced phase II-like activity with a significant increase in blood flow. Propranolol, a beta-adrenoceptor antagonist, did not alter motility but decreased blood flow throughout the MMC cycle. CONCLUSIONS: Both alpha- and beta-adrenergic mechanisms modifying small bowel haemodynamics are in operation throughout phases I, II and III of MMC. Our findings support the use of the semi-invasive LDF technique to measure drug-induced haemodynamic changes in the fasting gut.

Adrenergic alpha-Agonists↗

Predicting the clinical response to cisapride in children with chronic intestinal pseudo-obstruction.

We assessed upper gastrointestinal anatomy and function with contrast radiology and antroduodenal manometry in 51 children with chronic intestinal pseudo-obstruction (CIP) prior to entering these patients into an open-label outpatient trial of cisapride. The diagnosis of CIP was based on characteristic symptoms requiring special nutritional support (parenteral in 30, tube feeding in 12) or interfering with daily activities (documented by diary in nine). At a time the subjects were not acutely ill, antroduodenal pressures were recorded for > 4 h fasting and > 1 h after a complex liquid meal. Results were categorized by the most prominent manometric abnormality as myopathy (n = 6), absent migrating motor complex (MMC) (n = 27), failure to induce fed pattern (n = 7), MMC plus discrete abnormalities (n = 7), and postprandial duodenal hypomotility (n = 4). Patients in the first two categories did not have effective MMCs, but those in the last three categories did. Compared to children without MMCs, those with MMCs rarely required parenteral nutrition (p < 0.001). All children were treated with oral cisapride 0.2 mg/kg/dose t.i.d., and evaluated every 2 months for up to 1 yr. Of 49 evaluable subjects, the final global assessment was unchanged in 25, fair (improved symptom score) in 17, or excellent (change from TPN to tube feeding or tube feeding to oral feeding) in seven. Children with MMCs (13 of 18) responded more often to cisapride than those without MMCs (11 of 31), p < 0.02. All four subjects with postprandial duodenal hypomotility had excellent responses. Children with normal diameter bowel responded more often than those with dilated bowel, p < 0.004. To summarize, in children with CIP, absence of the MMC was associated with need for greater intensity of nutritional support and decreased response rate to cisapride. The response to cisapride was highly variable within the study group, but often could be predicted by the presence or absence of bowel dilation and MMCs.

Child, Preschool↗

Cholinergic and nitrergic regulation of in vivo giant migrating contractions in rat colon.

The aim of this study was to characterize in vivo rat colonic motor activity in normal and inflamed states and determine its neural regulation. Circular muscle contractions were recorded by surgically implanted strain-gauge transducers. The rat colon exhibited predominantly giant migrating contractions (GMCs) whose frequency decreased distally. Only a small percentage of these GMCs propagated in the distal direction; the rest occurred randomly. Phasic contractions were present, but their amplitude was very small compared with that of GMCs. Inflammation induced by oral administration of dextran sodium sulfate suppressed the frequency of GMCs in the proximal and middle but not in the distal colon. Frequency of GMCs was suppressed by intraperitoneally administered atropine and 4-diphenylacetoxy-N-methyl-piperidine methiodide and was enhanced by N(w)-nitro-L-arginine methyl ester. Serotonin, tachykinin, and calcitonin gene-related peptide receptor or receptor subtype antagonists as well as guanethidine and suramin had no significant effect on the frequency of GMCs. Verapamil transiently suppressed the GMCs. In conclusion, unlike the canine and human colons, the rat colon exhibits frequent GMCs and their frequency is suppressed in inflammation. In vivo GMCs are stimulated by neural release of acetylcholine that acts on M3 receptors. Constitutive release of nitric oxide may partially suppress their frequency.

Animals↗

Variability of migrating motor complex in humans.

Fasting gastrointestinal motility in the human is characterized by the regular cycling activity of the migrating motor complex (MMC). Our purpose was to define the variability of the MMC within and between a group of six healthy subjects studied for 6-9 hr over six separate days with a perfused catheter system. A total of 88 phase III events was observed during 255 hr of recording in this group. The mean MMC cycling time varied significantly between subjects (range 113-230 min, P less than 0.001), and variation within subjects also was wide (SD range 58-70 min). Seventy-one percent of phase III events commenced in the gastric antrum, 18% in the proximal duodenum, 10% in the distal duodenum, and 1% in the proximal jejunum. For each subject, the velocity of propagation of phase III decreased significantly (P less than 0.001), and phase III duration increased significantly (P less than 0.001), with increasing distance from the os. In the antrum, phase I was predominant, and significant (P less than 0.006) variation between subjects was noted for percentage of MMC cycle occupied by phase I (overall mean +/- SD 55 +/- 23%). Phase II was predominant in both duodenum and jejunum (mean range 70-80%), and no significant variation was noted between subjects for percentage of MMC occupied by phase II. We conclude that human MMC activity varies widely between individuals and within the same individual when studied on separate days.

Adult↗

Relation between gastroduodenal interdigestive migrating motor complex and postoperative gastrointestinal symptoms before and after cisapride therapy following distal gastrectomy for early gastric cancer.

A total of 30 patients (18 men, 12 women; 43-79 years, mean 58.9 years) 1.0 to 1.5 years (mean 1.25 years) after distal gastrectomy for early gastric cancer (Billorth I, D2 lymph node dissection, curability A) were divided into two groups based on the occurrence of interdigestive migrating motor complex (IMMC) phase III (pIII) from the duodenum and their postoperative gastrointestinal symptoms. They were compared before and after cisapride therapy (at an oral dose of 7.5 mg/day for 3 months). Results were as follows. Before cisapride therapy: (1) Patients in the IMMC-pIII-positive group (n = 20) had more appetite and ate more food with less decrease in body weight than those in the IMMC-pIII-negative group (n = 10); (2) patients in the IMMC-pIII-positive group clearly had fewer symptoms, such as early dumping (systemic) symptoms, symptoms of reflux esophagitis (e.g., heartburn, feeling of regurgitation, difficult swallowing), nausea, abdominal pain, diarrhea, abdominal distension, and borborygmus, than the IMMC-pIII-negative group. After cisapride therapy: eight patients (80%) in the IMMC-pIII-negative group became IMMC-pIII-positive, and their appetite and food consumption were obviously improved; body weight increased in six patients (60%), with alleviation of other abdominal symptoms and disappearance of the early dumping syndrome. These results showed a more satisfactory condition in regard to gastrointestinal symptoms in the IMMC-pIII-positive group than in the IMMC-pIII-negative group. It is concluded that cisapride therapy results in the occurrence of IMMC-pIII and subsequently alleviates various abdominal symptoms, contributing to the improved postoperative gastrointestinal condition of patients after gastrectomy.

Adult↗

Abnormalities of gastrointestinal motility in children with nonulcer dyspepsia and in children with gastroesophageal reflux disease.

In 11 children (mean age 44.2 months) with symptoms suggesting upper intestinal dysfunction (nonulcer dyspepsia), in nine children (mean age 27.3 months) with gastroesophageal reflux (GER) disease, and in seven controls (mean age 20.4 months) we investigated fasting [for 3 hr or until two migrating motor complexes (MMC) were observed] and fed (90 min) antroduodenal motility by means of perfused catheter system; furthermore, we measured both gastric emptying of a radiolabeled milk formula and fasting duodenogastric reflux during manometry by assessing bile salt concentration in gastric aspirates. No structural abnormalities of gastrointestinal tract and organic disorders were detected in the patients. In a high proportion of both groups of patients we found manometric abnormalities of interdigestive and fed motor patterns that were not seen in the controls: absence of antral phase III of MMC; significant decrease of antral and/or duodenal motor activity during fasting and/or fed periods; abnormal propagation or configuration of MMC phase III that was significantly shorter than in controls; bursts of sustained fasting and/or fed phasic duodenal activity, frequently uncoordinated with adjacent gut segments. When compared to controls, the mean intragastric concentration of bile salts during all MMC phases and the mean 1-hr percent gastric activity of the radiolabeled milk were significantly higher in the two groups of patients. We conclude that in a high proportion of children with nonulcer dyspepsia and of children with GER disease, gastrointestinal manometry may reveal significant irregularities of antral and duodenal motility, which are associated with increased duodenogastric reflux and delayed gastric emptying.

Bile Acids and Salts↗

Interdigestive small bowel motility and duodenal bacterial overgrowth in experimental acute pancreatitis.

The objective of this study is to investigate the effects of an acute necrotizing pancreatitis (ANP), without biliary obstruction, on the migrating motor complex (MMC), small bowel bacterial overgrowth (SBBO), bacterial translocation (BT) and infection of the pancreas simultaneously. Rats were divided into four groups: mild pancreatitis, control, ANP and sham operated control. Jejunal myoelectrodes were used to measure MMCs. Blood, peritoneal fluid, bile, and abdominal organs were harvested for microbial culturing 72 h after induction of pancreatitis. The splenic portion of the pancreas was taken for histology. During ANP the MMC cycle length was significantly increased from 14.1 +/- 0.2 to 22.4 +/- 1.9 min (P < 0.05). The duodenum of ANP rats was in contrast with the other groups characterized by Enterobacteriacae (> 3 log 10 CFU g-1 in seven of 12 rats, P < 0.05). A positive correlation (r = 0.78, P < 0.01) existed between duodenal Gram-negative and anaerobic flora and the MMC cycle. Correlation between MMC cycle length and BT to the pancreas was positive as well (r = 0.70, P < 0.01). A positive correlation (r = 0.85, P < 0.01) was found between the severity of pancreatitis and duodenal bacterial overgrowth. During ANP without biliary obstruction, the jejunal MMC is disturbed and consequently SBBO occurs. The correlation between the severity of pancreatitis, the disturbance of the MMC and SBBO suggests an important pathophysiological role of the proximal small bowel in the infection of pancreatic necrosis.

Animals↗

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.

Animals↗

Electrical events underlying organized myogenic contractions of the guinea pig stomach.

The stomach generates a characteristic pattern of coordinated activity whereby rings of contraction regularly start in the corpus and migrate slowly down the stomach to the duodenum. This behaviour persists after isolating the stomach and after blocking nervous activity; hence the response is myogenic, resulting from organized contractions of smooth muscle cells lying in the stomach wall. Each ring of contraction is triggered by a long lasting wave of depolarization, termed a slow wave. Slow waves are now known to be generated by sets of interstitial cells of Cajal (ICC), which intermingle with gastric smooth muscle cells. This article describes some studies which identify the roles played by ICC in the on-going generation of coordinated gastric movements. Intramuscular ICC in the corpus generate slow waves and these provide the dominant pacemaker frequency in the stomach. Corporal slow waves, in turn, activate a network of myenteric ICC, which starts in the antrum and slowly conducts waves of depolarization down the stomach. As these waves pass over bundles of circularly orientated muscle cells, they activate a set of intramuscular ICC which lie in the circular muscle layer: these generate slow waves that rapidly spread radially, so triggering each ring of contraction.

Action Potentials↗

The effect of e-, i-, and n-nitric oxide synthase inhibition on colonic motility in normal and muscular dystrophy (mdx) mice.

To explore the origin of diarrhea or constipation in human Duchenne muscular dystrophy (DMD), the effect of the inhibition of e- , i-, and n-nitric oxide synthase (NOS) on the motility of proximal and distal segments of colon of muscular dystrophy (mdx) and control mice was studied. The frequency of migrating motor complexes (MMC) was higher in the proximal than in the distal segments in mdx colon (0.56 vs. 0.25 cpm) and in the control colon (0.7 vs. 0.25 cpm), and there was no difference when mdx was compared to control segments. High concentrations of NOS inhibitors, including 1,3-PBIT dihydrobromide (1,3-PBIT) and spermine, inhibited MMC. The dose of spermine required to inhibit MMC was lower for the proximal mdx colon than for the distal mdx or control colon. In the presence of tetrodotoxin, spermine (1 mM) and 1,3-PBIT (5 mM) reduced the magnitude of local, rhythmic contractions (LC) paced by the interstitial cells of Cajal (ICC), but 1,3-PBIT (50 microM) increased their magnitude. There was no difference in the effect of spermine and 1,3-PBIT on the LC between mdx and control colon. The results suggest an inhibition of MMC by high concentrations of e-, i-, and n-NOS inhibitors, modulation of ICC activity by e-NOS, and greater susceptibility of MMC to n-NOS inhibition in the mdx proximal than in the control colon, which is very likely because of a deficit in n-NOS in the mdx smooth muscle affecting the MMC pacemaker. A deficit in the effect of mdx smooth muscle n-NOS on an MMC pacemaker may be the origin of diarrhea or constipation in human DMD.

Animals↗

Disruption of intestinal motility by a calcium channel-stimulating autoantibody in type 1 diabetes.

BACKGROUND & AIMS: Autonomic neuropathy, including gastrointestinal dysfunction, is a common complication of type 1 diabetes; however, its cause is uncertain. This study aimed to test whether functional autoantibodies cause the gastrointestinal dysfunction. METHODS: We used isolated mouse colon undergoing colonic migrating motor complex (MMC) activity to test for autoantibodies that disrupt colonic motility. Purified immunoglobulin G (IgG) from patients with type 1 diabetes or from controls was tested either in vitro or after passive transfer. Pharmacological studies of the interaction between the IgG and L-type calcium channel activator (Bay K8644) and inhibitors (nicardipine and verapamil) were performed. The effect of IgG on nerve-evoked contraction of the vas deferens longitudinal smooth muscle was also assessed. RESULTS: MMC activity was disrupted by IgG (0.2 mg/mL) from 8 of 16 patients with type 1 diabetes but not by control IgG. Passive transfer of diabetic IgG to mice also disrupted MMCs, showing access to the antigen in vivo. The acute effect of the autoantibody was mimicked by the dihydropyridine agonist, Bay K8644 (2-10 nmol/L), and both Bay K8644 and the autoantibody competitively inhibited the effect on MMC contraction of the dihydropyridine antagonist, nicardipine. Diabetic IgG, but not control IgG, altered the nerve-evoked contractile activity of vas deferens smooth muscle effects mimicked by Bay K8644. CONCLUSIONS: A novel functional autoantibody that activates smooth muscle L-type calcium channels at the dihydropyridine binding site is produced specifically by patients with type 1 diabetes and may mediate gastrointestinal and autonomic dysfunction in these patients.

Adult↗

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

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

Animals↗

The effects of ischemia and reperfusion on intestinal motility.

The interdigestive migrating motor complex (MMC) has been demonstrated to be a reliable indicator of intestinal motility and function. The effects of low perfusion on the MMC have never been studied. Fourteen newborn Yorkshire piglets (5 to 18 days old, weighing 2.9 +/- 0.4 kg) underwent celiotomy under general anesthesia with placement of four jejunal electrodes (50 cm apart) as well as a superior mesenteric artery (SMA) Doppler flow probe and a pericardial catheter. Group 1 (n = 5) had operation alone. Group 2 (n = 9) had nonocclusive mesenteric ischemia induced by reversible cardiac tamponade for 5 hours between postoperative days 6 to 12. All subjects had MMC phase III electrical activity, cycling time, and propagation velocity recorded daily. In group 2 MMCs were recorded prior to and during ischemia, and during reperfusion. Group 2 animals had 75% +/- 4% decrease in SMA flow during the tamponade period. During the ischemic period, the MMC cycling time (CT) increased from 67 +/- 10 (mean +/- SEM) to 98 +/- 12 minutes (P < .05) and MMC propagation velocity (PV) decreased to 4.2 +/- 2.2 from a baseline value of 10.5 +/- 1.5 cm/min (P < .05). During reperfusion CT and PV values were not significantly different from baseline. The validity of this model is confirmed by the comparable baseline recordings in groups 1 and 2, and by the return of MMC to baseline values within 4 to 7 hours of reperfusion, as seen in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗