Myoelectric Activity Of Small Intestine Research Articles

Neuropeptide S inhibits gastrointestinal motility and increases mucosal permeability through nitric oxide.

Neuropeptide S (NPS) receptor (NPSR1) polymorphisms are associated with enteral dysmotility and inflammatory bowel disease (IBD). This study investigated the role of NPS in conjunction with nitrergic mechanisms in the regulation of intestinal motility and mucosal permeability. In rats, small intestinal myoelectric activity and luminal pressure changes in small intestine and colon, along with duodenal permeability, were studied. In human intestine, NPS and NPSR1 were localized by immunostaining. Pre- and postprandial plasma NPS was measured by ELISA in healthy and active IBD humans. Effects and mechanisms of NPS were studied in human intestinal muscle strips. In rats, NPS 100-4,000 pmol·kg(-1)·min(-1) had effects on the small intestine and colon. Low doses of NPS increased myoelectric spiking (P < 0.05). Higher doses reduced spiking and prolonged the cycle length of the migrating myoelectric complex, reduced intraluminal pressures (P < 0.05-0.01), and increased permeability (P < 0.01) through NO-dependent mechanisms. In human intestine, NPS localized at myenteric nerve cell bodies and fibers. NPSR1 was confined to nerve cell bodies. Circulating NPS in humans was tenfold below the ∼0.3 nmol/l dissociation constant (Kd) of NPSR1, with no difference between healthy and IBD subjects. In human intestinal muscle strips precontracted by bethanechol, NPS 1-1,000 nmol/l induced NO-dependent muscle relaxation (P < 0.05) that was sensitive also to tetrodotoxin (P < 0.01). In conclusion, NPS inhibits motility and increases permeability in neurocrine fashion acting through NO in the myenteric plexus in rats and humans. Aberrant signaling and upregulation of NPSR1 could potentially exacerbate dysmotility and hyperpermeability by local mechanisms in gastrointestinal functional and inflammatory reactions.

Hyperglycemia-induced small intestinal dysrhythmias attributed to sympathovagal imbalance in normal and diabetic rats.

Hyperglycemia is known to induce dysrhythmias in the stomach; however, it is unknown whether they are also induced in the small intestine. Autonomic dysfunction is commonly noted in diabetes but the role it plays in hyperglycemia-induced dysrhythmias remains unknown. This study aimed to explore the effects of hyperglycemia on intestinal myoelectrical activity and the role of autonomic functions in hyperglycemia. Small intestinal myoelectrical activity (slow wave and spike activity) and autonomic functions (assessed by the spectral analysis of heart rate variability) were measured in Goto-Kakizaki diabetic rats and control rats treated with acute glucagon. Blood glucose was measured and its correlation with intestinal slow waves was determined. (1) The diabetic rats showed reduced regularity in intestinal slow waves in fasting and fed states (p < 0.001 for both), and increased sympathovagal balance (p < 0.05) in comparison with the control rats. The regularity in intestinal slow waves was negatively correlated with the HbA1c level in all rats (r = -0.663, p = 0.000). (2) Glucagon injection in the control rats induced transient hyperglycemia, intestinal slow wave dysrhythmias and impaired autonomic functions, similar to those observed in the diabetic rats. The increase in blood glucose was correlated with the decrease in the regularity of intestinal slow waves (r = -0.739, p = 0.015). Both spontaneous and glucagon-induced hyperglycemia results in slow wave dysrhythmias in the small intestine. Impairment in autonomic functions (increased sympathovagal balance) may play a role in hyperglycemia-induced dysrhythmias.

Dose-related effects of cerulein short infusions on proximal small bowel motility in sheep

The effect of cholecystokinin (CCK) upon the intestinal motility has not been entirely explored in ruminants. The aim of this study was to examine the precise effects of CCK amphibian analogue, cerulein, on small-intestinal myoelectric activity in rams in the course of chronic experiments. Five rams underwent implantation of bipolar platinum electrodes to the duodenal bulb, the distal duodenum and jejunum. During continuous myoelectrical and motor recordings, 0.15 M NaCl or the various doses of cerulein were administered intravenously. Short infusions of the smallest dose of cerulein exerted a slight and mostly insignificant effect on the duodenalbulb and the duodenal myoelectric activity index (MAI) values. In the duodenal bulb, the effects of cerulein on myoelectric activity were dose-dependent and closely related to the phase of the MMC. In the duodenum, the higher doses of the hormone evoked short stimulatory response followed by longer inhibitory biphasic effects on MAI. These effects were inversely related to the duration of hormone injection. Infusions of hormones at the higher doses caused a less pronounced biphasic effect. It is concluded that cerulein exerts an inhibitory effect upon the myoelectric activity of the duodenal bulb and a strong stimulatory and inhibitory (biphasic) effect on duodenal motility in sheep.

Dose-related effects of cholecystokinin octapeptide administered during various phases of the migrating motor complex on small-intestinal motility in sheep

Cholecystokinin (CCK) may affect intestinal motility, but in ruminants its precise effects have not been entirely explored. The aim of this study was to examine the effects of CCK-octapeptide (CCK-OP) on small-intestinal myoelectric activity in rams in the course of chronic experiments. Five rams underwent implantation of bipolar platinum electrodes to the duodenal bulb, distal duodenum, and jejunum as well as a strain gauge force transducer attached near the duodenal electrode. During continuous myoelectric recordings, 0.15 M NaCl or CCK-OP were injected slowly into the jugular vein. Injections of CCK-OP at doses of 20 (over 30 s), 200 (over 30 or 60 s) and 2000 (over 30, 60 or 120 s) ng/kg of body weight were each administered 5 or 30-40 min after the onset of the duodenal phase 1 or phase 2 of the migrating myoelectric complex (MMC), respectively. Most of these CCK doses were considered physiological. Injections of the smallest dose of CCK-OP exerted a slight and mostly insignificant inhibitory effect on the duodenal bulb and the duodenal myoelectric activity index (MAI) values. In the duodenal bulb, the effects of CCK-OP on myoelectric activity were dose dependent and closely related to the phase of the MMC. In the duodenum, the high dose of the hormone evoked short stimulatory and longer inhibitory biphasic effects on the MAI. These effects were inversely related to the duration of the hormone injection. It is concluded that CCK evokes a physiological stimulatory and inhibitory (biphasic) effect on the duodenal bulb and duodenal motility in sheep, with the inhibitory effect of the hormone being more pronounced in the duodenal bulb than in the duodenum. These effects were related to the CCK dose and the MMC phase. Therefore, CCK is an important regulator of upper small bowel motility in sheep.

Small-intestinal myoelectric activity in sheep: rebound excitation versus phase-3-like activity revealed by hexamethonium and atropine administration

Postinhibitory or rebound excitation (RE) is a known phenomenon in gastrointestinal motility, but its precise character and triggering mechanisms have not been defined so far. This study was thus devoted to analyzing its occurrence following hexamethonium (Hx) and atropine (At) administration during various phases of the migrating myoelectric or motor complex (MMC) in fasted, non-fasted, and fed sheep and to determine the nature of RE in comparison with phase 3 of the small-intestinal MMC. In the course of chronic experiments, various doses of Hx and At evoked RE alternating with phase-3-like activity (not the organized phase 3 of the MMC or its fragments) with periods and intensities related to the drug dose. In non-fasted sheep these changes were less pronounced and more delayed, while after feeding no excitatory response was observed. When the drug was given during phase 1 of the MMC, RE did not occur or was greatly reduced and delayed. Hx triggered RE mostly in the duodenum and At mostly in the jejunum. Rather, no RE was observed in the ileum. It is concluded that Hx and At inhibit small-intestinal motility and evoke RE and phase-3-like activity as a secondary stimulatory response in conscious sheep.

The Aging Gut Motility Decay: May Symbiotics Be Acting as "Implantable" Biologic Pace-Makers?

Motility recording of small and large intestine was performed in old Wistar rats divided into three groups: (a) standard diet, (b) standard diet plus a symbiotic preparation, and (c) standard diet plus a heat-inactivated symbiotic preparation. SCM-III. significantly increased the myoelectric activity of small intestine and colon (p < 0.01 versus [a] and [c]) paralleling "young" values of 4-month-old rats and increased the spike burst frequency in the proximal-distal colon (p < 0.05). SCM-III significantly increased the frequency and duration of spike bursts in the jejunum, transverse-distal colon, and defecation frequency, while decreasing the intervals of migrating motor complex in the colon (p < 0.01) to "young" values with an increased mRNA expression of VIP (p < 0.05). Gut flora manipulation aimed to modulate myoelectric activity can tentatively help reversing age-related motility decay.

Inhibitory Effects of Sildenafil on Small Intestinal Motility and Myoelectrical Activity in Dogs

Previous studies have shown that sildenafil inhibits the esophageal motility in both humans and animals. The aim of this study was to investigate the effects of sildenafil on intestinal myoelectrical activity and motility. The study was composed of 2 experiments and performed in 7 healthy female dogs with a duodenal cannula 20 cm beyond pylorus (19-26 kg). The first experiment was designed to study the effects of sildenafil on intestinal myoelectrical activity and it included 2 sessions each consisting of 30-minute baseline, 15-minute posttreatment (placebo or 100 mg sildenafil) and 90 minutes after a liquid meal. Intestinal myoelectrical activity was recorded during the entire experiment period. The second experiment was aimed to investigate the effect of sildenafil on intestinal motility and was performed immediately after a solid meal. Intestinal motility was measured by a manometric catheter inserted into the small intestine via the duodenum cannula for 30 minutes at baseline and 60 minutes after sildenafil. Sildenafil significantly reduced the amplitude but had no effect on the frequency and regularity of the intestinal myoelectrical activity. Sildenafil significantly inhibited postprandial intestinal contractions. Although the frequency of the contractions was not altered, the mean area under the curve was significantly reduced during the first 30 minutes (P < .03) and second 30 minutes after sildenafil (P < .03); the power of intestinal contractile activities was also significantly reduced during the first 30 minutes (P < .0004) and second 30 minutes after sildenafil (P < .0003) in comparison with baseline. In conclusion, sildenafil inhibits the amplitude of both intestinal contractile activity and intestinal slow waves.

The role of muscarinic and nicotinic receptors in the control of the ovine pyloric antral myoelectric response to nutrients during individual phases of the migrating myoelectric complex

The precise role of the muscarinic and especially of nicotinic receptors as well as the extent of the influence of individual phases of the migrating myoelectric complex (MMC) in the control of postprandial motility in sheep have been incompletely recognized. To gain further understanding of these, the antral and small-intestinal myoelectric activity was continuously recorded in six conscious sheep with implanted bipolar platinum electrodes. The amplitude of antral spike bursts observed during phase 1, 2a or 2b MMC in non-fasted animals gradually increased (77 ± 13, 87 ± 16 and 102 ± 9 μV, respectively), while in the fasted animals these values exhibited a similar tendency, although the values were lower (67 ± 12, 88 ± 14 and 91 ± 6 μV, respectively). Feeding performed during phase 2b MMC increased the antral spike burst amplitude in fasted and non-fasted animals, compared to the relevant pre-feeding value. When feed was administered during phase 1 or 2a of the MMC cycle, a significant response was recorded only in the non-fasted sheep. When feed was given following hexamethonium (2.0 mg/kg i.v.), atropine (0.1 mg/kg i.v.) or pirenzepine (0.5 mg/kg i.v.) administration, the response was still significant. Furthermore, the anticholinergic drugs often exerted more pronounced effect in non-fasted than in fasted animals. Thus, the muscarinic and nicotinic receptors contribute substantially, but not entirely to the control of the postprandial gastric motility in sheep and the roles of various MMC phases in this control can differ.

Cholinergic control of pacemaker initiating phase III of the migrating myoelectric complex in sheep

1. Small-intestinal myoelectric activity in sheep: rebound excitation versus phase-3-like activity revealed by hexamethonium and atropine administration K. W. Romański Comparative Clinical Pathology CrossRef

Small intestinal transections decrease the occurrence of tapeworm-induced myoelectric patterns in the rat.

Abstract Luminal infection by the noninvasive tapeworm, H. diminuta, alters rat small intestinal myoelectric activity. The significance of continuity between small intestinal enteric nervous system (ENS) and that of both the stomach/pylorus and colon/caecum regarding the induction of tapeworm-altered myoelectric patterns was evaluated. A total of 32 rats were implanted with four serosal electrodes placed at sites in the duodenum through the mid-jejunum. Sixteen of the 32 rats underwent intestinal transections and anastomoses at both the duodenum and ileum. After recording myoelectrical activity of both normal and transected intestines, eight rats from each group (normal and transected) were infected with H.diminuta. Phase III frequency, duration of the migrating myoelectric complex (MMC), slow wave frequency, percentage of slow waves associated with spike potentials and the occurrence of the the two tapeworm-initiated myoelectric patterns, repetitive bursts of action potentials (RBAP) and sustained spike potentials (SSP), were measured. In infected rats, the frequency of the RBAP and SSP electric patterns were significantly reduced by the double transection. Intestinal transection did not affect the other changes caused by infection, such as decreased MMC phase III frequency and percentage of slow waves associated with spike potentials. In conclusion, a small intestinal ENS in continuity with other segments of the GI tract is required to generate maximal numbers of tapeworm-induced SSP and RBAP myoelectric activity in the small intestine of the rat.

Influence of microbial species on small intestinal myoelectric activity and transit in germ-free rats.

The effect of an intestinal microflora consisting of selected microbial species on myoelectric activity of small intestine was studied using germ-free rat models, with recording before and after specific intestinal colonization, in the unanesthetized state. Intestinal transit, neuropeptides in blood (RIA), and neuromessengers in the intestinal wall were determined. Clostridium tabificum vp 04 promoted regular spike burst activity, shown by a reduction of the migrating myoelectric complex (MMC) period from 30.5 +/- 3.9 min in the germ-free state to 21.2 +/- 0.14 min (P < 0.01). Lactobacillus acidophilus A10 and Bifidobacterium bifidum B11 reduced the MMC period from 27.9 +/- 4.5 to 21.5 +/- 2.1 min (P < 0.02) and accelerated small intestinal transit (P < 0.05). Micrococcus luteus showed an inhibitory effect, with an MMC period of 35.9 +/- 9.3 min compared with 27.7 +/- 6.3 min in germ-free rats (P < 0.01). Inhibition was indicated also for Escherichia coli X7 gnotobiotic rats. No consistent changes in slow wave frequency were observed. The concentration of neuropeptide Y in blood decreased after introduction of conventional intestinal microflora, suggesting reduced inhibitory control. Intestinal bacteria promote or suppress the initiation and aboral migration of the MMC depending on the species involved. Bacteria with primitive fermenting metabolism (anaerobes) emerge as important promoters of regular spike burst activity in small intestine.

TNBS-induced inflammation impairs organized myoelectric activity in the rat small intestine

Background It has been known for several years that nematode-induced enteric inflammation impairs myoelectric and contractile activity, More recently, several studies showed that trinitrobenzene sulfonic acid (TNBS) induced inflammation alters in vitro muscle strip contractility. To our knowledge, the effect of TNBS-induced inflammation on small intestinal motility has not been studied in viva in the rat. Aim: To characterize the changes in small intestinal myoelectric activity caused by TNBS-induced inflammation. Methods: 4 bipolar electrodes were implanted at regular intervals on the antimesenterial side of the proximal jejunum of 13 male Wistar rats (250-350 g). During surgery, we administered intraluminally 30 mg TNBS in 0.25 ml ethanol 40% (n=5), 0.25 ml ethanol 40% (n=4) or 0.25 ml water (n=4). One week later, fasting myoelectric activity was recorded during at least 1 hour. The tracings were analyzed semiautomatically and several parameters concerning phase 3 (P3) and the migrating myoelectric complex (MMC) were examined. Results (mean 4SEM) were compared using ANOVA and Chi-square test. Results: Anaiysis of parameters at a single electrode site

Endotoxin induces biphasic alterations in small intestinal myoelectric activity in fasted newborn piglets.

Previous studies have shown that i.v. endotoxin infusion causes gastrointestinal dysfunction and intestinal injury in piglets. The aim of this study was to investigate the effects of endotoxin on intestinal myoelectric activity in newborn swine and to correlate this with gastrointestinal and hemodynamic events. Three pairs of electrodes were implanted in the jejunal wall of piglets, and after recovery, intestinal myoelectric activity was continuously recorded in the conscious, fasted condition. The intestinal myoelectric activity on the control day showed regular, repeating migrating myoelectric complex (MMC) cycles, each of which was composed of the classic phases I, II, and III. Mean cycle duration was 67.0 +/- 18.7 min (+/- SD), and phase III comprised 9.1 +/- 2.2% of each cycle. On the next day, infusion of 30 micrograms/kg endotoxin caused an initial, prolonged quiescent period and delayed the appearance of the first postendotoxin phase III complex. After the quiescent period, there was a period of irregular spiking activity followed by several shortened MMC cycles (47.9 +/- 22.7 min, p < 0.01 versus control) with a prolongation of the percentage of time spent in phase III (15.4 +/- 11.3%, p < 0.01). Endotoxin thus produced biphasic alterations in intestinal myoelectric activity characterized by an initial quiescence followed by increased gastrointestinal smooth muscle activity. Animals developed diarrhea, hypotension, and tachycardia about 1 h after endotoxin infusion in temporal association with increased spiking activity and MMC cycling. These studies are the first to show this biphasic response to endotoxin.

Small intestinal myoelectrical activity and bacterial flora after Roux-en-Y reconstruction

Small bowel myoelectrical activity and intestinal microflora were examined after partial gastrectomy and Roux-en-Y reconstruction in six dogs. Bacteriological analysis revealed a predominance of faecal bacteria. The basal electrical rhythm of the Roux limb was significantly decreased, while the frequency of phase III was increased (P < 0.05). In the bypassed duodenum, activity fronts occurred in only 25 per cent of experiments. Food intake led to an increase in the mean(s.e.m.) motility index in the Roux limb (from 46.1(9.4) to 75.0(21.5), P < 0.05), but not in the bypassed intestine (from 27.0(3.6) to 27.8(4.1), P not significant). Stimulation of the hypomotile bypassed intestine with cisapride induced an increase in the motility index from 27.0(3.6) to 111.2(16.5) (P < 0.001).

Small intestinal myoelectrical activity and bacterial flora after Roux-en-Y reconstruction

Small intestinal myoelectrical activity and bacterial flora after Roux-en-Y reconstruction

Luteinizing hormone and human chorionic gonadotropin fragment the migrating myoelectric complex in rat small intestine.

We hypothesized that sex hormones may affect motility disorders because these diseases occur more often in women than in men, and symptoms often occur or worsen after ovulation. Luteinizing hormone (LH) is predominantly secreted by the anterior pituitary midway through the menstrual cycle; it results in the development of the corpus luteum. LH levels also increase after bilateral gonadectomy. LH and human chorionic gonadotropin (hCG) bind to the same receptor, but rats lack hCG. To assess how LH and hCG influence myoelectric activity of the small intestine and to test the specificity of the LH receptor, we implanted electrodes on the jejunum of female rats. LH (0.1 or 0.5 NIH units) was administered intraperitoneally to intact and gonadectomized rats and 0.5 NIH units to rats that had been both hypophysectomized and gonadectomized; intact animals were treated with 100 units USP of hCG. Recordings were made with the rats in fasted and in fed states, and their intestinal motility was analysed. The most striking effects of LH, hypophysectomy, and hCG were the same: phase III of the migrating myoelectric complex was markedly fragmented and its duration lengthened (P < 0.0001). Gonadectomy alone and gonadectomy with hypophysectomy also increased fragmentation and phase III duration (P < 0.01 or better). LH receptors respond similarly to LH and hCG, and both hormones alter myoelectric activity of the rat small intestine in comparable ways.

Myoelectric activity and absorptive capacity of rat small intestinal isografts

The effect of transplantation on small intestinal absorption, digestive capacity, myoelectric activity, and morphology was assessed in inbred Lewis rats. Electrodes were sutured to the duodenum and isografted jejunoileum or to the native jejunoileum in controls. The frequency of migrating myoelectric complexes (MMCs) in the duodenum was 3.3 +/- 0.3/hr in controls and 1.8 +/- 0.4/hr in transplants (P < 0.05). MMC frequency in the jejunoileum was 5.1 +/- 1.3/hr in controls and 3.2 +/- 0.9/hr in transplants (P > 0.05). MMCs appeared to migrate from the duodenum to the jejunoileum 80 +/- 3% of the time in controls and 59 +/- 7% of the time in transplant rats (P < 0.05). Absorption in the transplanted jejunoileum demonstrated a 35-40% decrease in glucose and electrolytes absorption. Villus height and number of nuclei per villus was reduced. Intestinal length (dry) was 103 +/- 6 cm for controls and 51 +/- 3 cm for transplant rats (P < 0.05). Brush border sucrase activity was unchanged. We conclude that small intestinal isografts display similar myoelectric activity as controls, but the decreased absorptive capacity and villus height may require longer segments of intestine to be transplanted in order to support normal nutrition.

Intestinal microflora stimulates myoelectric activity of rat small intestine by promoting cyclic initiation and aboral propagation of migrating myoelectric complex.

Microbial modulation of myoelectric activity in small intestine was studied. Germ-free male Sprague-Dawley rats were equipped with bipolar electrodes from the duodenojejunal junction to the midpoint of small intestine. Prior to and one week after introduction of conventional intestinal microflora, 32 +/- 5% and 61 +/- 5% (mean +/- SE), respectively, of activity fronts of the migrating myoelectric complex reached the midpoint (P < 0.05), and the interval between activity fronts in proximal jejunum was reduced from 31.2 +/- 2.0 min to 17.5 +/- 0.8 min, respectively (P < 0.01). The pattern of propagation was more regular after conventionalization. Slow-wave frequency in proximal jejunum was 38.5 +/- 1.2/min in germ-free rats and 43.0 +/- 0.8/min in conventional rats (P < 0.01), but introduction of microflora failed to increase the frequency in germ-free rats. The frequency of spike potentials succeeding jejunal infusion of 5 ml of 12.5% glucose remained unchanged after conventionalization. Statistical analyses showed that the interval between activity fronts varied mainly within rats, whereas the propagation velocity showed statistically significant variability between rats (P < 0.01), regardless of intestinal microflora. Luminal control by the resident microflora is important for physiological cycling and aboral propagation of the migrating myoelectric complex, but seems to be of no major consequence for postprandial myoelectric response.

Ketorolac prevents postoperative small intestinal ileus in rats

The effect of ketorolac, a parenterally administered, nonsteroidal anti-inflammatory drug, was examined in a rat model of postoperative ileus. Small intestinal transit was measured by calculating the geometric center (GC) of distribution of 51CrO4. Laparotomy significantly delayed transit (GC: 2.2 +/- 0.2 after laparotomy versus 5.6 +/- 0.5 for unoperated controls, p < 0.01). The administration of ketorolac (1 mg/kg) improved the GC to 5.2 +/- 0.2 (p < 0.01), indicating normal intestinal transit after surgery in ketorolac-treated animals. Small intestinal myoelectric activity was recorded in rats with implanted electrodes. Animals treated with saline 2 hours postoperatively did not show return of the migrating myoelectric complex (MMC) in 183 +/- 25 minutes. In contrast, rats receiving ketorolac postoperatively had return of MMC activity in 59 +/- 18 minutes (p < 0.01). Preoperative ketorolac treatment reduced the duration of MMC inhibition after surgery from 197 +/- 55 minutes to 13 +/- 5 minutes (p < 0.05) when compared with saline. In summary, ketorolac hastens the return of MMC activity when given postoperatively. When ketorolac is administered preoperatively, it completely prevents the delay in intestinal transit and the inhibition of myoelectric activity seen in postoperative ileus. We concluded that ketorolac may be of benefit in the prevention and treatment of postoperative ileus.

Effect of substance P on small intestinal and caecal myoelectrical activity in the conscious piglet

Effect of substance P on small intestinal and caecal myoelectrical activity in the conscious piglet