Inhibitory reflexive effect of rectal distension on postprandial gastric myoelectrical activity

The aim of the study was to determine the effects of low-volume rectal distension on gastric myoelectrical activity. The study was performed in 14 healthy volunteers in 2 randomized sessions. In the control session, a small balloon was inserted into the rectum 10 cm beyond the anal verge and inflated with 20 ml of air. Gastric myoelectrical activity was recorded for 30 minutes in the fasting state and 30 minutes after a meal; and then the balloon was deflated and removed, and another 30-min recording was followed. The study session was the same except that after the 30-min baseline recording the balloon was inflated to reach a volume with which the subject felt an urgency for defecation. Spectral analyses were performed to compute the dominant frequency, power, and regularity (2–4 cycles/minutes, cpm) of the gastric slow waves and the percentage of gastric dysrhythmia. Results: 1). In comparison with our previously published data, the placement of the rectal balloon with a volume of 20 ml air did not affect the regularity of the slow waves (84.2 ± 3.6% in fasting, 85.3 ± 4.3% in fed); In comparison with the control session, the rectal distension inducing an urgency for defecation (average volume of air: 72.5 ml) significantly reduced the regularity of gastric slow waves in the fed state (72.0 ± 5.7%, P < 0.03 vs baseline; P < 0.02, vs control session) but not in the fasting state (80.1 ± 4.5%, P = 0.1). This postprandial change was attributed to a significant increase in bradygastria (3.1 ± 1.0% vs 7.9 ± 2.6%, P < 0.04) and a marginal increase in tachygastria (7.4 ± 2.5% vs 15.8 ± 4.3%, P = 0.06). The normal postprandial increases in the dominant frequency and power of the gastric slow wave were abolished in both sessions. conclusions, rectal distension evoking an urgency for defecation impairs postprandial gastric slow waves with an increase in the percentage of both bradygastria and tachygastria.     

Inhibitory effect of white wine on gastric myoelectrical activity and the role of vagal tone

Although extensively investigated throughout the gastrointestinal tract, the influence of alcohol on gastric motility is still unclear. Our aim was to investigate the effect of wine on gastric myoelectrical activity and vagal activity. Ten healthy subjects were studied in two sessions with the electrogastrogram (EGG) for 30 min at baseline, 30 min after ingesting the test liquid [white wine (12.5% alcohol) or matched juice], and 60 min after a standard test meal. Spectral analysis was performed to compute EGG parameters and their postprandial changes. The vagal activity was assessed based on spectral analysis of the heart rate variability (HRV) signal derived from the ECG recording. White wine preload significantly diminished the postprandial increase in EGG dominant power compared to juice preload (1.16 ± 1.57 vs 5.48 ± 1.01 dB, P < 0.001). A significant decrease in vagal activity was observed after wine (23.40 ± 4.30 vs 17.43 ± 3.40%, P < 0.005), which remained unchanged after the test meal (23.40 ± 4.30 vs 16.77 ± 4.40%, P < 0.05). This decrease was not noted in the juice session. A correlation was established between changes after wine consumption in EGG dominant power and in the percentage of the vagal activity (r = 0.89, P < 0.05). In conclusion, white wine preload inhibits the postprandial EGG dominant power, suggesting a possible inhibition of postprandial gastric contractions. This effect may be associated with diminished vagal activity.     

Postprandial Response of Jejunal Slow Waves and Mediation via Cholinergic Mechanism

The postprandial characteristics of jejunalmyoelectrical activity and its mediation via cholinergicnerves were investigated in this study. Four pairs ofbipolar electrodes were implanted on the serosa of the proximal jejunum of nine female hounddogs (14-22 kg). In the control session, the recordingof jejunal myoelectrical activity was made for 30 min inthe fasting state and for 90 min after a solid meal (0.45 kg, 838 kcal). The study sessionfollowed the same protocol except that a bolus of 0.25mg/kg atropine was injected intravenously 30 min afterthe meal. Computerized spectral analysis was performed to calculate the frequency, power, andpercentage of 17-22 cycles/min (cpm) slow waves. Aspecial artificial neural network program was applied tocompute the spike bursts superimposed on slow waves. All data were expressed as mean ± SE. Thepostprandial frequency of the jejunal slow waves wassignificantly increased from 18.42 ± 0.28 cpm inthe fasting state to 18.95 ± 0.22, 19.28 ±0.23, and 19.28 ± 0.22 cpm during the first, second, andthird 30-min periods after the meal (all P < 0.03 incomparison with the fasting state). The percentage ofthe slow waves superimposed with spike bursts was increased from 19.33 ± 3.90% at fastingstate to 35.16 ± 2.76%, 32.87 ± 4.06%, and34.88 ± 3.51% during the first, second, and third30-min periods after the meal (all P < 0.03 incomparison with fasting state). Atropine abolished thepostprandial increases in the frequency of slow wavesand the number of spike bursts. No significantpostprandial changes in the power and the percentage of17-22 cpm slow waves were observed. In conclusion,the postprandial response of the jejunal slow wavesafter a solid meal presents as an increase of thefrequency of slow waves and the number of the spikebursts which can be abolished by atropine, and thepostprandial response of the jejunal slow waves is aneural reflex dominantly mediated via vagal cholinergicnerves.     

Electrogastrographic characteristics in patients of stomach cancer

Using a homemade electrogastrography (EGG) system, we studied the characteristics of myoelectrical rhythm in gastric cancer (GC) patients. Based on a short-term Fourier transform, recorded slow waves could be automatically analyzed to obtain the following parameters: dominant frequency/power, percent of normal rhythm (2.4–3.7 cpm), power ratio, etc. Fifty histologically confirmed GC patients (34 men, 16 women) were enrolled before surgical intervention to measure their fasting and postprandial EGG parameters for 30 min. The cancerous parameters of GC patients were then obtained postoperatively. In addition, 46 healthy subjects were enrolled for comparison. When compared to controls, GC patients had the following characteristics: absence of postprandial increase in dominant frequency (GC: 3.04 ± 0.47 vs 3.07 ± 0.44 cpm, NS; controls: 3.02 ± 0.31 vs 3.21 ± 0.25 cpm, P < 0.001), marked power response after meal (P < 0.05), and obvious power ratio (4.58 ± 7.38 vs 2.27 ± 2.05, P < 0.05). Multivariate analysis indicated that advanced GC was the factor responsible for the obvious dominant power enhancement after meal (P < 0.05). Other demographic, clinical, and cancerous factors did not influence EGG parameters. We conclude that apparent arrhythmia is not encountered in GC patients, although they mainly exhibit obvious postprandial power response. Advanced GC is likely responsible for this power enhancement on EGG recording.     

Impairment of Gastric and Jejunal Myoelectrical Activity During Rectal Distension in Dogs

It is known that distension of the rectum induces gastric hypomotility and delays gastric emptying. Its effect on gastrointestinal myoelectrical activity has not been well studied, however. The aim of this study was to investigate the effects of rectal distension on gastrointestinal myoelectrical activity in dogs. Six hound dogs implanted with electrodes on the serosa of the stomach and proximal jejunum were studied. The protocol consisted of a 30-min baseline recording and another 30-min recording during rectal distension. Gastric myoelectrical activity was severely impaired by rectal distension. The dominant power was significantly decreased from –2.79 ± 0.52 dB at baseline to –4.84 ± 1.26 dB during distension (P < 0.05). The percentage of normal 4–6 cycles per minute gastric slow waves was reduced from 95.08 ± 1.11% to 83.63 ± 4.00% (P < 0.02), and the percentage of tachygastria was increased during distension (0.33 ± 0.19% vs 6.03 ± 1.27%, P < 0.02). The instability coefficient of the dominant frequency was significantly increased (0.134 ± 0.012 vs 0.326 ± 0.074, P < 0.05). The percentage of slow wave coupling was reduced from 93.99 ± 0.76% to 73.43 ± 2.07% (P < 0.00003). In the small bowel, only the instability coefficient of dominant frequency showed a significant increase during distension. Other parameters were not affected by rectal distension. We conclude that rectal distension severely impairs gastric myoelectrical activity. The induced gastric dysrhythmia and reduced slow wave amplitude and coupling may be the underlying pathophysiology of gastric hypomotility and delayed gastric emptying observed during rectal distension.     

Impaired Postprandial Gastric Myoelectrical Activity in Chinese Patients with Nonulcer Dyspepsia

Using a homemade electrogastrography (EGG) system, we studied the characteristics of the myoelectrical rhythm in Chinese patients with nonulcer dyspepsia (NUD). Based on short-term Fourier transformation, recorded slow waves could be automatically analyzed to obtain the following parameters: dominant frequency/power, percent of normal frequency (2–4 cpm), power ratio, etc. EGG parameters, Helicobacter pylori status, histological examination of gastric mucosa, and dyspeptic symptoms were recorded in 27 NUD patients. Compared to 32 healthy controls, the Chinese NUD patients had abnormal postprandial EGG parameters including a lower percentage of regular 2–4 cpm slow waves (70.10 ± 2.97% vs 79.08 ± 2.95%, P < 0.05), a lower level of increment of dominant power (0.62, ± 0.91 vs 3.76 ± 0.58 dB, P < 0.05), lower power ratio (1.42 ± 0.28 vs 2.79 ± 0.39, P < 0.05) and a higher instability coefficient (0.36 ± 0.03 vs 0.26 ± 0.03, P < 0.05). However, Helicobacter pylori infection and its associated gastritis did not influence any EGG parameters in NUD patients. Six main dyspeptic symptoms and total symptom score had no correlation with any EGG parameters. In conclusion, Chinese NUD patients may have abnormal postprandial stomach myoelectrical activity, but these EGG abnormalities are not a direct result of Helicobacter pylori infection and its related gastritis and do not contribution to the dyspeptic symptoms.     

Cutaneous gastric electrical stimulation alters gastric motility in dogs: New option for gastric electrical stimulation?

Background and Aim:  We investigated the effects of cutaneous gastric electrical stimulation (CGES) on gastric myoelectrical activity, postprandial antral contractions and gastric tone in dogs.
Methods:  CGES was carried out via abdominal surface electrodes over the stomach. After an overnight fast, gastric slow waves were recorded from the serosal electrodes in six dogs at a frequency of 4.4 cycles/min (c.p.m.) or 10 c.p.m. Nine dogs were used for the measurement of postprandial antral contractions. Gastric tone at baseline and during CGES was measured in six of the dogs.
Results:  We found that: (i) CGES at 4.4 c.p.m. decreased slow wave frequency (5.1 vs 4.6 c.p.m., P  < 0.05) and increased slow wave power (−6.2 vs 2.7 c.p.m., P  < 0.05); CGES at 10 c.p.m. increased slow wave frequency (5.1 vs 9.2 dB, P  < 0.05) and decreased normal slow waves (85.4% vs 60.0%, P  < 0.05); (ii) CGES at 10 c.p.m. significantly suppressed postprandial antral contractions ( P  < 0.01); (iii) CGES had no effects on gastric tone.
Conclusions:  CGES is capable of altering gastric slow waves and inhibiting gastric motility. It may have therapeutic potential for treating eating disorders, such as obesity. However, clinical studies are needed to explore the potential of CGES.     

Inhibitory effects of cholecystokinin on postprandial gastric myoelectrical activity

While a number of studies have investigated the effects of cholecystokinin (CCK) on gastrointestinal motility, little is known on the effects of CCK on gastric myoelectrical activity, which regulates gastric motility. The aim of this study was to investigate the effects of intravenous infusion of CCK-8 on gastric myoelectrical activity in normal humans. Gastric myoelectrical activity was measured in 10 healthy subjects with a noninvasive electrogastrographic technique by placing abdominal electrodes on the epigastric area. Two study sessions were performed in each subject on two separate days with double-blinded infusion of either saline or CCK (24 pmol/kg/hr). The procedure for each session was as follows: (A) 30-min baseline fasting electrogastrogram (EGG); (B) start infusion, another 30-min EGG; (C) give meal, 60-min EGG; and (D) stop infusion, another 60-min EGG. The dominant frequency and peak power (amplitude) of the EGG, and the percentage of normal 2–4 cycles/min slow waves during each recording session were computed and compared between placebo and CCK. It was found that normal 3 cpm slow waves were recorded in all EGGs. Infusion of CCK had no effect on the frequency of the gastric slow wave and did not induce gastric dysrhythmias. It was also found that intravenous infusion of CCK significantly decreased the EGG peak power (amplitude) during the first hour after the meal (the infusion was given during this period) in comparison with placebo (P<0.05). This inhibitory effect on EGG peak power was sustained but not significant during the second postprandial hour (the infusion was not given during this period). It was concluded that intravenous infusion of CCK at a physiological concentration significantly decreased the postprandial EGG amplitude in normal humans, suggesting an inhibitory effect on postprandial gastric motility, but did not change the frequency and regularity of the gastric slow wave.     

Intestinointestinal Inhibitory Reflexes

The motor response induced by intraluminal distension of the small intestine has been well investigated. However, little is known of the myoelectrical response to intraluminal distension. The aim of this study was to investigate the effects of oral- and anal-side distension on jejunal slow waves in dogs. The study was performed in 10 healthy female hound dogs implanted with three pairs of electrodes on the jejunum and an intestinal fistula. The first study session was designed to investigate the effects of anal-side distension on jejunal myoelectrical activity in fasting state. The protocol consisted of a 30-min baseline recording, a 30-min recording during anal-side balloon distension located 5 cm distal to the most distal pair of electrodes, and another 30-min recording after distension. The second session was designed to investigate the effect of oral-side distension with the balloon 5 cm proximal to the most proximal pair of electrodes. Jejunal slow waves were severely impaired by both anal- and oral-side distension. The dominant power was significantly reduced from –2.96 ± 0.90 dB at baseline to –6.00 ± 0.64 dB during anal-side distension (P < 0.0005) and from –3.90 ± 0.85 dB at baseline to –7.17 ± 0.90 dB during oral-side distension (P < 0.001). The percentage of normal 17 to 22-cpm slow waves was significantly decreased from 97.39 ± 0.88% to 83.48 ± 3.12% during anal-side distension (P < 0.0005) and from 92.49 ± 2.42% to 68.80 ± 7.24% during oral-side distension (P < 0.002). The percentage of slow wave coupling was decreased from 95.08 ± 2.27% to 52.48 ± 7.73% during anal-side distension (P < 0.0005) and from 84.82 ± 6.75% to 49.21 ± 8.91% during oral-side distension (P < 0.001). The instability coefficient of the dominant frequency was significantly increased during anal-side distension. In conclusion, intraluminal distension of the jejunum severely impairs jejunal slow waves. The slow waves on both sides of distension become less coupled, less regular, and are of lower amplitude.     

Effects of Octreotide and Erythromycin on Gastric Myoelectrical and Motor Activities in Patients with Gastroparesis

Simultaneous recordings of gastric manometry andmyoelectrical activity were made in 10 patients withgastroparesis. Intravenous erythromycin (100 mg) wasadministered in the fasting state for a period of 30 min. Subcutaneous injection of octreotide(100 g) was administered before one of the fouridentical test meals. It was found that octreotidesignificantly decreased the antral motility index(30-min fasting: 4.51 ± 1.04 vs 1.75 ±0.97, P < 0.02; 60-min fed: 5.16 ± 1.44 vs 3.4± 1.41, P < 0.05) and the dominant power ofthe EGG (fasting power: 35.19 ± 1.54 vs 30.84± 1.57 dB, P < 0.004; postprandial powerincrease: 5.52 ± 1.06 vs 0.27 ± 0.87, P< 0.001). Erythromycin significantly increased theantral motility index (3.16 ± 0.96 vs 9.5± 0.61, P < 0.001) and the dominant power ofthe EGG (28.86 ± 1.57 dB vs 33.55 ± 1.59dB, P < 0.005) in the fasting state. An improvement in theregularity of the gastric slow wave was also noted witherythromycin. It was concluded that: (1) the inhibitoryeffect of octreotide on postprandial gastric motility and myoelectrical activity suggests thatcaution should be exercised when octreotide is used inpatients with gastroparesis; and (2) the stimulatoryeffect of erythromycin on gastric myoelectrical activity may enhance gastric motility and gastricemptying in patients with gastroparesis.     

Enhanced postprandial gastric myoelectrical activity after moderate-intensity exercise

OBJECTIVE: The aim of this study was to investigate the change of postprandial gastric myoelectrical activity and its relation with vagal activity after exercise. METHODS: Nine subjects were studied in two sessions. In the control session, gastric myoelectrical activity was recorded using electrogastrography (EGG) for 30 min in the fasting state and 60 min after a test meal. In the exercise session, after the baseline recording of both the EGG and electrocardiogram (ECG), the subject was put on a cycle ergometer for exercise until reaching 50% of the maximum age-predicted heart rate for 10 min. The test meal was then given and the recording was resumed for 60 more minutes. Spectral analyses were performed on both the EGG and the heart rate variability derived from the ECG. RESULTS: The postprandial increment of the dominant power (p<0.05) and the percentage of the 2-4 cpm slow waves (p = 0.01) were significantly higher with exercise. The standard deviation of the postprandial dominant frequency was significantly decreased (more stable slow waves) with exercise (p<0.04). While cardiac vagal activity was significantly decreased after the meal, exercise did not significantly affect the postprandial change. CONCLUSIONS: Gastric slow waves become more regular, more stable, and of higher amplitude after exercise, and this enhancement is probably not mediated via the vagal pathway.     

Impaired Gastric Myoelectrical Activity in Patients with Chronic Renal Failure

Dysmotility and delayed emptying of the stomachhave been reported in patients with chronic renalfailure (CRF). The aim of this study was to investigatewhether gastric myoelectrical activity was impaired in patients with CRF using electrogastrography.The electrogastrogram (EGG) was recorded in 24symptomatic patients with CRF (15 with diabetes) and 12normal subjects. Two 30-min EGG recordings before and after a test meal were analyzed using spectralanalysis methods. It was found that patients with CRFshowed a significantly lower percentage of normal 2-4cpm slow waves in both fasting and fed states in comparison with healthy controls (in fastingstate: 88.9 ± 2.5% vs 67.4 ± 6.6%/63.27.0%, P < 0.01; in fed state: 89.6 ± 1.8% vs64.6 ± 6.2%/62.0 ± 8.3%, P < 0.01;controls vs diabetic patients/nondiabetic patients). Both patient groups showed a significantlyhigher prevalence of the abnormal EGG, which was definedas the percentage of 2-4 cpm slow waves lower than 70%(fasting state: 8% vs 60%/56%, P < 0.01/0.05; fed state: 0% vs 53%/56%, P < 0.005/0.002;controls vs diabetic patients/nondiabetic patients). Nosignificant difference was observed in the regularity ofthe gastric slow waves between the two patient groups. The healthy controls showed a significantincrease in the dominant power and frequency of the EGGafter the test meal. However, this increase was absentin the two patient groups. It was concluded that patients with chronic renal failure haveabnormal gastric myoelectrical activity, includingimpaired regularity of the gastric slow wave and afailed increase in the power of the EGG at 3 cpm.Electrogastrography is an attractive noninvasive method for thestudy of gastric motility in patients with severechronic renal failure.     

Gastric Myoelectrical Activity in Patients with Parkinson's Disease (Evidence of a Primary Gastric Abnormality)

Parkinson's disease patients may experiencevarious gastrointestinal symptoms; however, the exactpathophysiology of these symptoms is not fullyunderstood. Therefore, the aim of this study was toinvestigate the pattern of gastric myoelectrical activityin patients with Parkinson's disease. Eleven patientswith Parkinson's disease and 10 healthy subjectsparticipated in the study. Patients were stratified as receiving dopaminergic therapy (N= 5) and off therapy (N = 6). Gastricmyoelectrical activity was measured by means of surfaceelectrogastrography (EGG) for 30 min before and for 90 min after a standardized meal. The dominantfrequency, postprandial EGG power change, and thepercentage of normal 2-4 cycles/min (cpm) slow-waveactivity in the three groups were calculated andcompared. The mean postprandial EGG power increase in theuntreated patients was smaller than in the treatedpatients (–3.11 ± 1.01 and 1.17 ±1.96 dB; P = 0.072). Moreover, both of these values weresignificantly decreased when compared to the control group(untreated vs control: d–3.11 ± 1.01 vs8.01 ± 1.86 dB; P = 0.04 and treated vs control:1.17 ± 1.96 vs 8.01 ± 1.86 dB; P = 0.02).The percentage of normal 2-4 cpm slow waves in untreated patients wasnot different from the treated patients (82.6 ±6.6% vs 75.8 ± 13.6%, P = NS) or from the controlgroup (88.2 ± 5.4%, P = NS). The dominantfrequency after the meal was similar to that in thefasting state both in the untreated (3.3 ± 0.1 vs3.2 ± 0.2 cpm; P = NS) and treated patients (3.2± 0.1 vs 3.1 ± 0.1 cpm, P = NS), whereasthe dominant frequency significantly increasedpostprandially in the control group (2.88 ± 0.12vs 3.05 ± 0.16; P < 0.05). Abnormalities ingastric myoelectrical activity in untreated Parkinson'sdisease patients reflect direct involvement of thegastrointestinal tract by the primary disease process.EGG can be regarded as a useful diagnostic tool inevaluating gastrointestinal involvement inneurodegenerative diseases.     

Abnormal gastric myoelectrical activity and delayed gastric emptying in patients with symptoms suggestive of gastroparesis

Gastric myoelectrical activity modulates gastric motor activity. Abnormalities in gastric myoelectrical activity may be associated with gastric motility disorders. The aim of this study was to investigate the correlation of gastric myoelectrical activity with gastric emptying in symptomatic patients with and without gastroparesis. Ninety-seven patients with symptoms suggestive of gastroparesis participated in the study. Gastric myoelectrical activity was recorded using surface electrogastrography. The electrogastrogram (EGG) was recorded for 30 min in the fasting state and for 120 min after a solid test meal. Gastric emptying of the solid meal was simultaneously monitored for 120 min. Patients with delayed gastric emptying showed a significantly lower percentage of normal gastric slow waves (P<0.03) and a significantly reduced increase of the dominant power in the postprandial EGG (P<0.02). Postprandial EGG parameters were found to be able to predict delayed emptying of the stomach. Postprandial gastric dysrhythmia predicts delayed gastric emptying with an accuracy of 78%, while the abnormality in postprandial EGG power predicts delayed gastric emptying with an accuracy of 75%. All patients with abnormalities in both the rhythmicity and the power had delayed gastric emptying. Patients with delayed gastric emptying have a lower percentage of normal gastric slow waves in the EGG and a lower postprandial increase in the dominant power. Abnormalities in the postprandial EGG seem to be able to predict delayed emptying of the stomach. However, a normal EGG does not seem to guarantee normal emptying of the stomach.     

Effects of muscarinic receptor stimulation and nitric oxide synthase inhibition on gastric tone and gastric myoelectrical activity in canines

Aims:  This study was designed to assess whether the muscarinic receptor stimulation and nitric oxide synthase inhibition were equally effective on gastric fundic tone or gastric myoelectrical activity (GMA) in canines, and the correlation between gastric fundic tone and GMA.
Methods:  Gastric fundic tone and GMA were recorded on seven dogs implanted with serosal electrodes and a gastric cannula.
Results:  Bethanechol and L-nitro-N-arginine (L-NNA) significantly increased gastric fundic tone; gastric volume was decreased with bethanechol or L-NNA ( P  < 0.05). Increased spike activities were observed after both bethanechol and L-NNA. The percentage of slow waves superimposed with spikes was increased with bethanechol ( P  < 0.001) and L-NNA ( P  < 0.05). There was a significant reduction in dominant frequency (DF) ( P  < 0.05), dominant power (DP) ( P  < 0.05) and percentage of normal slow waves (%N) ( P  < 0.05) with bethanechol, while no significant change was observed with L-NNA. The variation of gastric tone was not correlated with parameters of GMA.
Conclusions:  Muscarinic receptor stimulation and nitric oxide synthase inhibition have similar effects on gastric tone and gastric spike activities, but different effects on gastric slow waves. Gastric fundic tone does not correlate with gastric slow waves.     

Effect of Peritoneal Dialysis on Gastric Myoelectrical Activity in Patients with Chronic Renal Failure

Impaired gastric myoelectrical activity has been reported in patients with chronic renal failure (CRF). The effect of peritoneal dialysis on this function has not previously been described. The aim here was to investigate the effect of peritoneal dialysis on gastric myoelectrical activity. Gastric myoelectrical activity was recorded by electrogastrography (EGG) in 23 patients with CRF (18 with dyspepsia) during peritoneal dialysis and with the peritoneal cavity empty of dialysis fluid (14 patients), and in 20 healthy controls. Two 30-min EGG recordings before and after a solid test meal were analyzed using spectral analysis methods. No significant difference in the percentage of normal 2- to 4-cpm slow waves was found in patients on peritoneal dialysis compared to those with the peritoneal cavity empty of dialysis fluid or to controls (in fasting state 83 ± 3%, 80 ± 5% and 89 ± 4%, in fed state 91 ± 3%, 86 ± 4% and 83 ± 4%, respectively). It was found that the power ratio (change in power of normal slow waves in fed state) was significantly higher in the 14 patients on peritoneal dialysis compared to the same patients with the peritoneal cavity empty of dialysis fluid (27.2 ± 10.7 vs 8.6 ± 4.8, P < 0.05). There was no significant difference in the power ratio between patients with the peritoneal cavity empty of dialysis fluid and controls (8.6 ± 4.8 vs 7.5 ± 2.2). The subgroup of patients with no dyspepsia had a significantly higher power ratio compared to those with dyspepsia both on dialysis and with the peritoneal cavity empty of dialysis fluid (39.4 ± 13.7 vs 12.4 ± 5.2 and 29.2 ± 21.5 vs 2.8 ± 0.4 respectively, P < 0.05). In conclusion, there was no significant difference in gastric myoelectrical activity between patients with the peritoneal cavity empty of dialysis fluid and controls. Dialysis fluid in the peritoneal cavity seems to enforce the gastric myoelectrical signal.     

Impaired Postprandial Gastric Slow Waves in Patients with Functional Dyspepsia

The aim of this study was to investigate gastricmyoelectrical activity in patients with functionaldyspepsia. Thirteen healthy subjects and 14 patientswith functional dyspepsia participated in the study. The electrogastrogram (EGG) recording was madein each subject for 30 min in the fasting state and 120min after a standard test meal of 475 calories. Spectralanalysis methods were applied to derive quantitative EGG parameters. There was no difference in theEGG between the patients and controls in the fastingstate. However, abnormalities in the postprandial EGGwere found in the patients. The percentage of 2-4 cpmwaves was significantly lower (74.4 ± 4.0% vs85.7 ± 1.6%, P < 0.03) and the postprandialincrease in EGG dominant power was significantly less(–0.52 ± 0.92 dB vs 2.24 ± 0.88 dB,P < 0.03) in patients than in controls. It was alsofound that the percentage of postprandial 2-4 cpm wavescould be used to differentiate the patients withfunctional dyspepsia from the healthy controls with a specificity of 100% and a sensitivity of 43%. It was concluded that a subset of patients withfunctional dyspepsia have impaired gastric myoelectricalactivity in the fed state.     

Impaired gastric myoelectricity in patients with chronic pancreatitis： Role of maldigestion

AIM: To investigate whether gastric myoelectrical activity was impaired in patients with chronic pancreatitis (CP) and to explore the role of pancreatic enzyme in regulating gastric myoelectrical activity. METHODS: Twenty CP patients and 20 controls participated in the study. Gastric myoelectrical activity was recorded by a homemade electrogastrography (EGG) device. Two experiments were carried out. In experiment one, EGG was recorded in both controls and CP patients. While in experiment two, either pancreatic enzymes or placebo was given together with test meals. Spectral analysis was used to generate various EGG parameters. RESULTS: The control subjects, but not the CP patients, showed typically increased postprandial dominant frequency. The postprandial dominant power (DP) increment (2.24±1.13 vs 5.35±0.96 dB, P= 0.04) and the percentage of normal 2-4 cpm slow waves (63.0±3.8% vs 77.4±3.1%, P<0.05) were lower in CP patients when compared with the control. In the 20 CP patients, the DP increment (4.76±1.02 vs 2.53±1.20 dB, P<0.05) and the postprandial percentage of normal 2-4 cpm (74.4±2.8% vs 64.8±5.7%, P<0.05) were significantly higher with pancreatic enzyme replacement than the placebo. CONCLUSION: CP patients have an abnormal postprandial stomach myoelectricity showing poor response in dominant frequency/power and regularity, whereas these abnormalities are corrected after pancreatic enzyme replacement. Maldigestion is likely to be the factor leading to abnormal postprandial gastric myoelectricity of CP patients.     

Impaired Gastric Myoelectrical Activity in Patients with Parkinson's Disease and Effect of Levodopa Treatment

The aim of this study was to evaluate gastric myoelectrical activity in patients with Parkinson's disease during and after levodopa treatment. Thirteen Parkinson's patients and 13 age-matched Parkinson's-free controls were enrolled. Electrogastrography was used to record gastric myoelectrical activity in all subjects for 30 min before and 30 min after a standard meal. In the group with Parkinson's disease, gastric myoelectrical activity was recorded during both the "on" (with levodopa treatment) and the "wearing-off" (without levodopa for at least 12 hr) periods. Results were as follows. (1) The patients without treatment showed a significantly lower percentage of regular slow waves and a significantly higher instability coefficient of the dominant frequency; (2) the patients showed an absence of the normal postprandial increase in gastric slow wave frequency which was seen in the controls: and (3) treatment with levodopa resulted in an improvement in the fed state, including a marginal increase in the percentage of regular slow waves (P = 0.1), a significant decrease in the instability coefficient, and an enhanced postprandial power increase. In conclusion, patients with Parkinson's disease have reduced slow wave rhythmicity and an impaired postprandial response in gastric myoelectrical activity. These abnormalities may be partially corrected with levodopa treatment in the fed state.     

Gastric Myoelectrical Activity in Healthy Children and Children with Functional Dyspepsia

The aim of this study was to investigateabnormalities in pediatric patients with functionaldyspepsia. Fifteen symptomatic pediatric patientsdiagnosed with functional dyspepsia and 17 aged-matchedhealthy controls were studied. Gastric myoelectricalactivity was recorded using surface electrogastrographyfor 1 hr in the fasting state and 1 hr after a testmeal. It was found that, in comparison with thecontrols, the children with functional dyspepsia had alower percentage of 2- to 4-cpm slow waves in bothfasting state (66.0 ± 4.7% vs 79.7 ± 3.1%,P < 0.07) and fed state (72.4 ± 5.4% vs 85.0± 2.9%, P < 0.04), and a significantly higherinstability of the dominant frequency in both fastingstate (0.50 ± 0.05 vs 0.31 ± 0.04, P <0.01) and fed state (0.39 ± 0.05 vs 0.25 ±0.03, P < 0.05). It was also found the postprandial increase inEGG dominant power in the patients was inverselycorrelated with the total symptom score (r = 0.63, P =0.03). It was concluded that abnormal gastricmyoelectrical activity may play a role in the pathogenesis ofpediatric functional dyspepsia.