Intestinal Myoelectric Activity Research Articles

Role of Peptide YY in Intestinal and Gallbladder Motility in Dogs

The purpose of this study was to characterize the action of exogenous PYY, an ileocolonic peptide released by fatty meal, and that released by Heal perfusion with oleate on intestinal and gallbladder motility patterns and the posssible role of the adrenergic pathway in this action. Dogs were equipped with chronic duodenal electrodes for recording myoelectric activity and with a cannula in the gallbladder fundus for measuring the gallbladders intraluminal pressure and volume and calculating its motility index (MI) and emptying rate. After intravenous infusion of PYY, there was a dose-dependent prolongation of the migrating motor complex (MMC) interval and almost complete abolition of the contractions and emptying of gallbladder during the duodenal activity front. After meat feeding or during intravenous infusion of cerulein, 50 pmol/(kg · h), the MMC was interrupted and replaced by irregular spike activity, accompanied by a marked increase in the gallbladder MI and about 80% to 90% reduction of its volume. PYY, 200 pmol/(kg · h), reduced significantly the meal- or cerulein-induced duodenal spike activity but failed to affect the MI and volume of the gallbladder. Similar changes in fasted and fed patterns of motility were observed after Heal oleate (16 mM/h), producing plasma PYY levels in a range similar to that observed after infusion of exogenous PYY. The inhibitory effects of PYY or Heal fat on intestinal myoelectric activity were reversed in part by α-adrenergic blockade (phentolamine). We conclude that exogenous PYY or endogenous hormone released by Heal oleate inhibits the interdigestive and postprandial motility pattern of the small bowel but does not affect gallbladder motility, and that the inhibition of intestinal motility involves, at least in part, the adrenergic pathway.

Use of multichannel electrointestinography for noninvasive assessment of myoelectrical activity in the cecum and large colon of horses

To evaluate whether changes in myoelectrical activity in the cecum and large colon of horses can be detected via multichannel electrointestinography (EIG). 6 healthy mature horses. Each horse underwent 3 EIG procedures. Intestinal myoelectrical activity (cecum and large colon) was recorded during a 20-minute period following i.v. administration of physiologic saline (0.9% NaCl) solution (20 mL; baseline), erythromycin lactobionate (0.5 mg/kg), or detomidine (0.015 mg/kg); intestinal contractions were concurrently viewed via B-mode ultrasonography. By use of computer software, 8-channel EIG recordings were analyzed and the mean of the dominant frequency (a measure of the rhythmicity of gastric electrical activity) expressed in cycles per minute (cpm) was obtained. Total power (muV(2)) was calculated, and treatment effect was expressed as the power ratio (ie, treatment-associated power divided by the baseline power). The dominant frequency cpm values were not stable, and no significant differences between treatments were detected. Compared with the effects of saline solution treatment, detomidine significantly reduced the mean cecal and colonic power ratios. Erythromycin significantly reduced the cecal power ratio and increased the colonic power ratio, although the increase was significant in only 1 channel. Ultrasonographic findings and total power (predominantly from the long-distance electrode pairs) were significantly correlated. In horses, EIG was useful for assessment of changes in myoelectrical activity in the cecum and large colon. Multiple electrodes should be used to cover a larger area of the intestine, and agreement between multiple channels is needed to make the analysis meaningful.

The uncut Roux-en-Y with jejunal pouch: a new reconstruction technique for total gastrectomy

Roux Stasis Syndrome is a well-known complication after Roux-en-Y reconstruction. It has been hypothesized that reconstruction with an uncut Roux limb and jejunal pouch after total gastrectomy would preserve unidirectional intestinal myoelectrical activity, improve postoperative weight gain and nutritional parameters, and diminish Roux Stasis Syndrome in canines. A total gastrectomy was performed, and 2 methods were used for reconstruction: Roux-en-Y esophagojejunostomy (RY) was performed on 5 canines (control), and the uncut Roux-en-Y with a jejunal pouch (URYJP) was performed on 5 other canines (experimental). The canines were monitored for 10 weeks postoperatively. Serial weight and nutritional parameters were measured. Emptying profiles and motility studies were performed in the fasting and postprandial states. Ten weeks after operation, the URYJP group had significantly improved nutritional parameters, including weight, total protein, albumin, hemoglobin, serum total iron binding capacity, and serum IgA, IgG, and IgM. The emptying times for both groups were similar, with an increase of disordered propagation of the jejunal pacesetter potential in the RY group. The aboral propagation occurred more frequently in the URYJP group during fasting and after feeding (98% +/- 1% vs 39% +/- 16%; P = .02, and 99% +/- 1% vs 43% +/- 18%; P = .03). The sites of luminal occlusions were intact in the URYJP group at 10 weeks. The combination of jejunal pouch and uncut Roux limb improved overall nutritional parameters when compared with the traditional Roux-en-Y, while preserving aboral propagation of jejunal pacesetter potentials.

The Chinese herbal preparation Qing Yi Tang (QYT) improves intestinal myoelectrical activity and Increases intestinal transit during acute pancreatitis in Rodents

The aim was to investigate alterations of intestinal motility in models of acute pancreatitis and to investigate the effects of the Chinese herbal preparation Qing Yi Tang (QYT) on these alterations. Upper gastrointestinal transit was evaluated in mice following induction of mild acute pancreatitis (MAP) using caerulein. Myoelectrical activity was recorded in rats after induction of severe acute pancreatitis (SAP) using sodium deoxycholate (SDOC). The contractility of jejunum segments was evaluated in the presence of SDOC, lipopolysaccharide (LPS) and trypsin. QYT accelerated the transit in MAP mice in a concentration dependent manner. Slow wave activity of smooth muscle in rat stomach and jejunum remained unchanged following SAP, but the spiking activity was significantly decreased, with bursts of 7.2 +/- 2.6/10 min compared with 47.9 +/- 13.2/10 min without SAP (p < 0.01). QYT reversed this decrease. Additionally, the amplitudes of slow waves and spikes were enhanced by QYT in SAP rats. The tension and amplitude of spontaneous contractile activity was reduced by SDOC and LPS and increased by trypsin. Gastrointestinal (GI) transit is altered by SAP but not by MAP. The Chinese herbal preparation QYT improves disturbed motility in AP by stimulating myoelectrical activity and accelerating GI transit.

Little or no ability of obestatin to interact with ghrelin or modify motility in the rat gastrointestinal tract.

Obestatin, encoded by the ghrelin gene may inhibit gastrointestinal (GI) motility. This activity was re-investigated. Rat GI motility was studied in vitro (jejunum contractility and cholinergically-mediated contractions of forestomach evoked by electrical field stimulation; EFS) and in vivo (gastric emptying and intestinal myoelectrical activity). Ghrelin receptor function was studied using a GTPgammaS assay and transfected cells. Contractions of the jejunum or forestomach were unaffected by obestatin 100 nM or 0.01-1000 nM, respectively (P>0.05 each; n=4-18). Obestatin (0.1-1 nM) reduced the ability of ghrelin 1 microM to facilitate EFS-evoked contractions of the stomach (increases were 42.7+/-7.8% and 21.2+/-5.0 % in the absence and presence of obestatin 1 nM; P<0.05; n=12); higher concentrations (10-1000 nM) tended to reduce the response to ghrelin but changes were not statistically significant. Similar concentrations of obestatin did not significantly reduce a facilitation of contractions caused by the 5-HT(4) receptor agonist prucalopride, although an inhibitory trend occurred at the higher concentrations (increases were 69.3+/-14.0% and 42.6+/-8.7% in the absence and presence of 1000 nM obestatin; n=10). Obestatin (up to 10 microM) did not modulate recombinant ghrelin receptor function. Ghrelin increased gastric emptying and reduced MMC cycle time; obestatin (1000 and 30,000 pmol kg(-1) min(-1)) had no effects. Obestatin (2500 pmol kg(-1) min(-1), starting 10 min before ghrelin) did not prevent the ability of ghrelin (500 pmol kg(-1) min(-1)) to shorten MMC cycle time. Obestatin has little ability to modulate rat GI motility.

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.

Absorptive and motor function of orthotopically vascularized segmental ileal autografts.

In 24 dogs a 100 cm length of terminal ileum was autografted as an orthotopically vascularized Thiry-Vella segment. In six dogs absorption, motility and histology were studied in detail and in two intestinal myo-electrical activity was recorded. At a second operation 5 weeks after autotransplantation the Thiry-Vella segment was returned to its normal anatomical position in the intestinal stream and 2 months later all the non-transplanted intestine was resected. Eighteen grafts were technically successful. Intestinal myo-electrical activity was normal by the second day after transplantation while intestinal transit and contractile activity recovered within 10 days. Mucosal morphology and intestinal absorption had largely recovered by 10 days after grafting but absorption of oleic acid was impaired for 4 weeks. Ten dogs with severe short, bowel syndrome but intact ileocaecal valve were maintained in good health for more than 7 months by a 100 cm ileal autograft.

Noninvasive Measurement and Analysis of Intestinal Myoelectrical Activity Using Surface Electrodes

Intestinal myoelectrical activity (IMA), which determines bowel mechanical activity, is the result of two components: a low-frequency component [slow wave (SW)] that is always present, and a high-frequency component [spike bursts (SB)] which is associated with bowel contractions. Despite of the diagnostic significance of internal recordings of IMA, clinical application of this technique is limited due to its invasiveness. Thus, surface recording of IMA which is also called electroenterogram (EEnG) could be a solution for noninvasive monitoring of intestinal motility. The aim of our work was to identify slow wave and spike burst activity on surface EEnG in order to quantify bowel motor activity. For this purpose, we conducted simultaneous recordings of IMA in bowel serosa and on abdominal surface of five Beagle dogs in fast state. Surface EEnG was studied in spectral domain and frequency bands for slow wave and spike burst energy were determined. Maximum signal-to-interference ratio (7.5 dB +/- 36%) on SB frequency band was obtained when reducing upper frequency limit of signal analysis. Energy of external EEnG in reduced SB frequency band (2-7.9 Hz) presented a high correlation (0.71 +/- 7%) with internal intensity of contractions. Our results suggest that energy of SB can be quantified on external EEnG which could provide a noninvasive method for monitoring intestinal mechanical activity.

Effects of vasopressin and long pulse–low frequency gastric electrical stimulation on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs

The aim of this study was to investigate the effect of vasopressin and long pulse-low frequency gastric electrical stimulation (GES) on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs. The study was performed in eight healthy female dogs implanted with four pairs of gastric serosal electrodes and two pairs of small bowel serosal electrodes, and a duodenal fistula for the assessment of gastric emptying. Each dog was studied in three sessions on three separate days in a randomized order with recordings of gastric and small bowel slow waves. Each study session consisted of 30-min baseline, 30-min stimulation and 30-min recovery period. In sessions 1 and 2, infusion of either saline or vasopressin (0.75 U kg(-1) in 30 mL saline instilled in 30 min) was given during the second 30-min period. The protocol of session 3 was the same as session 2 except long pulse-low frequency GES was performed during the second 30-min period. It was found that: (i) Vasopressin significantly delayed gastric emptying 30 and 45 min after meal and GES did not improve the vasopressin induced delayed gastric emptying; (ii) Vasopressin induced gastric dysrhythmias and GES significantly improved vasopressin induced gastric dysrhythmia; (iii) Vasopressin also induced intestinal slow wave abnormalities but GES had no effect on vasopressin induced small bowel dysrhythmia; (iv) Vasopressin induced symptoms and behaviours suggestive of nausea that were not improved by GES. We conclude that: (i) Vasopressin delays gastric emptying and induces gastric and small bowel dysrhythmias and symptoms in the fed state, and (ii) long pulse-low frequency GES normalizes vasopressin induced gastric dysrhythmia with no improvement in gastric emptying or symptoms.

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.

Effect of the acupoints ST-36 (Zusanli) and SP-6 (Sanyinjiao) on intestinal myoelectric activity of Wistar rats.

Despite its ancient use as a therapeutic tool to treat several ailments, acupuncture still faces the challenge of scrutiny by Western science both in terms of its efficacy and in terms of the characterization of its effects and mechanisms of actions underlying these effects. We investigated under well-controlled and carefully characterized conditions the influence of electrical stimulation of acupuncture points ST-36 (Zusanli) and SP-6 (Sanyinjiao) on the myoelectric activity of the small intestine of 38 adult male Wistar rats. Electrical recordings obtained by means of four electrodes chronically implanted in the small intestine were used to assess the effects of acupuncture (electroacupuncture stimulation set at 2 Hz, intermittent stimulation, 1 V, for 30 min). Immobilization of the animals was associated with a consistent decrease (-8 +/- 7%) in the myoelectric activity of the small intestine as measured by means of the root mean square. Conversely, acupuncture was able to significantly increase (overshoot) this activity compared to baseline (+44 +/- 7%). In contrast, immobilized animals subjected to sham acupuncture had only modest (nonsignificant) increases in myoelectric activity (+9 +/- 6%). Using carefully controlled conditions we confirmed previous noncontrolled studies on the ability of acupuncture to alter intestinal motility. The characterization of the topographic and temporal profiles of the effects observed here represents a basis for future dissection of the physiological and pharmacological systems underlying these effects.

Small doses of melatonin increase intestinal motility in rats.

Since melatonin receptors are present in the intestines, the possibility that this hormone may affect intestinal motility has been studied in the rat. Sprague-Dawley male rats were given a carmine cochineal powder meal and were injected intraperitoneally with 1, 10, 100, or 1000 microg/kg melatonin. Sixty minutes after treatment, intestinal transit was found to be faster in animals treated with small doses of melatonin (1 or 10 microg/kg) than in saline-injected controls. This effect, however, appear to be clearly reversed with 100 or 1000 microg/kg melatonin. In fact, these doses of the hormone reduced intestinal transit in rats. The nonselective melatonin receptor antagonist, luzindole (administered intraperitoneally in a dose of 0.25 mg/kg, 15 min prior to melatonin injection) totally prevented the accelerating effect of melatonin (10 microg/kg) on intestinal transit. Luzindole per se failed to affect gut motility. Injection of the reversible acetylcholinesterase inhibitor and cholinergic agent, neostigmine, accelerated intestinal transit but failed to influence melatonin effect on this parameter. In contrast, intraperitoneal injection of the muscarinic receptor antagonist atropine delayed intestinal transit per se but did not reduce the stimulating effect of melatonin on this parameter. Intestinal myoelectrical recording revealed that intestinal myoelectrical activity was increased by intraperitoneal injection of melatonin (10 microg/kg). Administration of luzindole totally prevented melatonin-induced increase of intestinal myoelectrical activity. These results indicate that melatonin may affect intestinal motility in rats when administered in small doses. This effect might be mediated by melatonin receptors in the intestines, although the involvement of central receptors for the hormone is also possible.

Interdigestive and postprandial intestinal myoelectric activity during ischemia/reperfusion

Interdigestive and postprandial intestinal myoelectric activity during ischemia/reperfusion

Interdigestive and postprandial intestinal myoelectric activity during ischemia/reperfusion

Interdigestive and postprandial intestinal myoelectric activity during ischemia/reperfusion

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.

The effect of change of the diet and feeding regimen at weaning on duodenal myoelectrical activity in piglets

AbstractThis study investigated the effect of the change of diet and feeding regimen at weaning on myoelectrical activity of the intestine of piglets. For this purpose the electromyographic recordings of duodenal myoelectrical activity were carried out in relation to the different weaning status of piglets. Six piglets, in two experimental trials were surgically modified with two serosal, bipolar electrodes on the duodenum. The myoelectrical activity was recorded in the same piglets before weaning when they were sucking their sow and after weaning when the diet was changed to solid dry food (standard commercial concentrate for weaned pigs). In sucking piglets the intestinal myoelectrical activity pattern exhibited triple-phased migrating myoelectric complex (MMC), undisturbed by sow nursing. After weaning, feeding with solid food induced a long-term post-prandial pattern with higher frequency of electrical response activity (ERA) when compared with phase II of the MMC. The duration of the MMC cycles increased with time over the experiment by proportionately 0•11 and 0•14 in the periods before and after weaning. However, weaning significantly shortened MMC cycle duration by proportionately 0•21. The duration of phase II was significantly prolonged with time over the experiment by 0•07 to 0•10 and it was not affected by weaning. Phase III of MMC were of constant duration over the whole experimental period.In summary, changes in the diet and feeding regimen have an influence on the characteristics of intestinal myoelectrical activity in piglets around weaning.

Distension-induced myoelectrical dysrhythmia and effect of intestinal pacing in dogs.

The aims of this study were to investigate the effect of duodenal distension on intestinal myoelectrical activity and to investigate whether intestinal pacing was able to reverse the effects of distension. Six female hound dogs with four pairs of electrodes on the proximal jejunum were involved in this study. The protocol consisted of 30 min of recording of jejunal myoelectrical activity as baseline and 90 min of recording during distension. Intestinal pacing was performed during the second 30 min of distension. Duodenal distension severely impaired intestinal myoelectrical activity. The percentage of normal slow waves was reduced from 90.8+/-8.4% at baseline to 73.8+/-10.2%, 57.2+/-11.4%, and 53.7+/-16.0% during the first, second and third 30 min of distension (P<0.05, ANOVA). The dominant power was similarly decreased and the minute-by-minute variation of dominant frequency was significantly increased after distension. Intestinal pacing reversed distension-induced dysrhythmia. The percentage of normal slow waves during the 30 min of distension with pacing was significantly higher than the corresponding 30 min of distension without pacing (88.5+/-6.6% vs. 57.2+/-11.4%, P<0.03). It was concluded that intestinal pacing can normalize distension-induced dysrhythmia and has a potential as a future therapeutic modality for intestinal motor disorders.

Entrainment of segmental small intestinal slow waves with electrical stimulation in dogs.

The aim of this study was to derive effective pacing parameters for the entrainment of segmental intestinal myoelectrical activity. The study was performed in 12 dogs. Four pairs of electrodes were implanted on the serosa of the jejunum. Electrical stimulation of the small intestine was performed via the most proximal pair. For the slow waves within a distance of 5 cm, a complete entrainment was achieved with a pacing frequency of 1.1 times the intrinsic frequency (IF), a pulse width of 140 msec, and an amplitude of 4 mA. The time required for the entrainment was 25.6 +/- 2.7 sec. The maximum driven frequency was 1.38 +/- 0.03 IF. The percentage of the entrainment at this frequency was 44.0 +/- 3.9%. The data indicate that pacing is able to completely entrain segmental intestinal myoelectrical activity, suggesting that normalization of intestinal myoelectrical dysrhythmia is feasible with pacing.

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

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

Myenteric neuronal antibodies in scleroderma: Passive transfer evokes alterations in intestinal myoelectric activity in a rat model

Although the mechanism for neuropathic gastrointestinal motility disturbances in scleroderma is unknown, we have previously described anti-myenteric antibodies in some patients with scleroderma. The aim of this study was to screen patients with scleroderma who had gastrointestinal symptoms for the presence of anti-myenteric neuronal antibodies and then purify the immunoglobulin G (IgG) fraction from serum samples for passive immunization into a rat model and observe for intestinal motility effects. Patients with scleroderma were screened, a serum sample from a patient with high titer anti-myenteric neuronal antibodies was obtained, and IgG was purified. Using a rat model with chronic indwelling intestinal electrodes to measure intestinal myoelectric activity, we passively transferred the IgG from either control subjects or this patient with scleroderma. We immunosuppressed the rats and intraperitoneally injected IgG from control subjects and this patient with scleroderma daily for 7 days. Recordings of myoelectric activity in control injected rats revealed no difference from baseline, but a prolongation in the activity front duration and interval and a disruption were seen after scleroderma IgG injections. IgG from a patient with scleroderma with antimyenteric neuronal antibodies, when passively immunized into a rat model, evokes intestinal myoelectric activity alterations. We hypothesize that these antibodies could account for the gastrointestinal neuropathic motility disturbances seen in scleroderma.