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PubMed1996

Frequency of gastric pacesetter potential depends on volume and site of distension.

Little is known about the response of the frequency of gastric pacesetter potential (PP) to luminal distension. When volume distension occurs as a result of a meal, gastric emptying may play an important role, since the site of distension shifts as the meal is displaced from the stomach to the small bowel. In this study, using does equipped with duodenal fistulas and serosal electrodes on the antrum, we compared the frequency of gastric PP during the course of gastric emptying while isolating the volume distension to either the stomach or the small bowel. We found that 1) the frequency of gastric PP decreased linearly with greater initial meal volume when volume distension was isolated to either the stomach -P<0.05, analysis of variance (ANOVA)- or small bowel (P<0.01, ANOVA), and 2) the frequency of gastric PP decreased linearly with increased volume remaining in the stomach or increased volume entering the small intestine. We conclude that the frequency of gastric PP depends on the volume and site of distension.

Analysis of Variance↗
PubMed1997

Inflammation modulates in vitro colonic myoelectric and contractile activity and interstitial cells of Cajal.

Inflammation suppresses phasic contractile activity in vivo. We investigated whether inflammation also suppresses in vitro phasic contractile activity and, if so, whether this could in part be due to the alteration of specific slow wave characteristics and morphology of the interstitial cells of Cajal (ICC). Circular muscle strips were obtained from normal and inflamed distal canine colon. Inflammation was induced by mucosal exposure to ethanol and acetic acid. The amplitudes of spontaneous, methacholine-induced, substance P-induced, and electrical field stimulation-induced contractions were smaller in inflamed muscle strips than in normal muscle strips. Inflammation reduced the resting membrane potential and the amplitude and duration of slow waves in circular muscle cells. Inflammation did not affect the amplitude of inhibitory junction potentials but did decrease their duration. Ultrastructural studies showed expansion of the extracellular space between circular muscle cells, reduction in the density of ICC and associated neural structures, damage to ICC processes, vacuolization of their cytoplasm, and blebbings of the plasma membrane. We conclude that inflammation-induced alterations of slow wave characteristics contribute to the suppression of phasic contractions. These alterations may, in part, be due to the damage to ICC. Inflammation impairs both the myogenic and neural regulation of phasic contractions.

Acetic Acid↗
PubMed1998

Effects of pacing parameters on entrainment of gastric slow waves in patients with gastroparesis.

The aim of this study was to investigate the effect of pacing parameters on the entrainment of gastric slow waves in patients with gastroparesis. Four pairs of cardiac pacing wires were placed on the serosal surface of the stomach in 13 patients with gastroparesis. After a baseline recording for 30 min, gastric pacing was performed in a number of sessions with different effective parameters, each lasting for 30 min. The following parameters were found to be effective for the entrainment of the gastric slow wave: a pacing frequency 10% higher than the intrinsic gastric slow wave frequency (IGF), 300 ms pulse width, and 4 mA pacing amplitude. A reduction of pacing amplitude from 4 to 2 mA and 1 mA reduced the percentage of entrainment of the gastric slow wave to 79 +/- 10% and 50 +/- 11%, respectively. Pacing with a pulse width of 30 or 3 ms was not able to entrain the gastric slow wave in any of the patients. An ectopic pacemaker of tachygastria found in three patients was reversed with gastric pacing. It was concluded that gastric pacing at a frequency up to 10% higher than the IGF and with an amplitude of 4 mA and a pulse width of 300 ms is able to completely entrain the gastric slow wave and normalize gastric dysrhythmias in patients with gastroparesis.

Adult↗
PubMed1998

Effects of meal volume and composition on gastric myoelectrical activity.

The absence of a standard meal in electrogastrography may limit its clinical significance. Different meals may fail to produce the expected postprandial motility pattern. The aim of this study was to investigate the effect of meal volume and composition on postprandial myoelectrical activity. Fourteen healthy subjects were given four meals that differed from a "reference meal" in one single parameter (volume, calorie, or fiber content). Gastric myoelectrical activity was measured using surface electrogastrography. Spectral and statistical analyses were performed to investigate the effect of food properties on electrogastrogram (EGG) parameters. It was found that the reference meal produced a postprandial increase in the dominant frequency (P < 0.007), dominant power (P < 0.04), and percentage of normal 2-4 cycle/min gastric slow waves (P > 0.05). Similar changes were observed with the low-volume and high-fiber meals but not with the reduced-calorie meal. Fasting EGG parameters in all four sessions showed no significant difference. It was concluded that low-calorie meals do not result in expected postprandial physiological responses and thus are not appropriate for EGG tests. A volume reduction of down to one-half the volume of a regular meal does not affect postprandial changes of the EGG; thus a condensed test meal may be recommended for symptomatic patients.

Adult↗
PubMed1998

Rat gastroduodenal motility in vivo: involvement of NO and ATP in spontaneous motor activity.

Our studies of fasted anesthetized rats have shown that all spontaneous relaxations of the antrum are nitric oxide (NO) dependent. Duodenal motility is patterned into propagating "grouped" motor activity interposed with "intergroup" periods of nonpropagating motor activity; in the duodenum, only intergroup relaxations are NO dependent. We examined the involvement of NO and ATP in spontaneous motor activities of the gastroduodenum in vivo: contractions and relaxations were recorded and analyzed simultaneously from the antrum (S1) and proximal duodenum (D1) of anesthetized Sprague-Dawley rats (n = 10/group), using extraluminal foil strain gauges. Treatment with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg iv) attenuated (P < 0.05) antral and intergroup relaxations, whereas grouped relaxations were enhanced (P < 0.05). These effects were reversed with L-arginine (300 mg/kg iv). L-NAME also increased (P < 0.05) the amplitude of duodenal contractions. ATP (8 mg. kg-1. min-1 iv) stimulated relaxations at S1 and D1 that were blocked by the P2-purinoceptor antagonist suramin (60 mg/kg iv). This treatment did not affect spontaneous antral relaxations; however, duodenal grouped relaxations were attenuated. Desensitization to the P2x-purinoceptor agonist alpha,beta-methylene ATP (300 micrograms/kg iv) gave results similar to suramin. In contrast, the P2y-purinoceptor agonist 2-methylthio-ATP (2-MeS-ATP; 360 micrograms/kg iv) evoked duodenal relaxations that were attenuated by L-NAME, and desensitization to 2-MeS-ATP attenuated intergroup relaxations. Spontaneous relaxations of the rat antrum and duodenal intergroup relaxations are NO dependent. Both gut regions relax in response to systemically administered ATP; this response is sensitive to suramin. Grouped duodenal relaxations display functional sensitivity to suramin and P2x- purinoceptor desensitization, indicative of the involvement of ATP and P2x purinoceptors. P2y purinoceptors must also be present; however, these occur on elements releasing NO. Although NO does not mediate grouped relaxations or duodenal contractions, the sensitivity of these responses to L-NAME indicates that the pathway(s) controlling these responses is modulated by NO.

Adenosine Triphosphate↗
PubMed1998

Rat gastroduodenal motility in vivo: interaction of GABA and VIP in control of spontaneous relaxations.

Spontaneous relaxations occurring within motor activity in the rat gastroduodenum in vivo can be distinguished by their dependence on either nitric oxide (NO) or ATP. We examined the interaction of gamma-aminobutyric acid (GABA) and vasoactive intestinal peptide (VIP) within pathways controlling this activity in the antrum (S) and duodenum (D) of anesthetized Sprague-Dawley rats, using miniaturized extraluminal foil strain gauges oriented perpendicular to (S1, D1) or in the axis of (S2) the circular smooth muscle. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg iv) attenuated (P < 0.05) antral relaxations and, in the duodenum, nonpropagating "intergroup" relaxations. The GABAA receptor antagonist bicuculline (350 micrograms/kg sc) had similar effects. The GABAA agonist 3-amino-1-propanesulfonic acid stimulated L-NAME-sensitive relaxations at S1 and D1. Propagating "grouped" responses were unchanged. VIP (6 micrograms/kg iv) always induced a relaxation of the duodenum, which was attenuated by bicuculline and L-NAME. VIP caused simultaneous responses at S1 and S2; however, the antrum displayed either contraction or relaxation in response to VIP. All antral relaxations in response to VIP were attenuated (P < 0. 05) by L-NAME; however, only VIP-induced relaxations at S1 were sensitive to bicuculline. VIP-induced contractions were also unaffected. GABAA receptors mediate the pathway(s) controlling NO-related spontaneous relaxations of the antrum and duodenal circular muscle. All VIP-induced relaxations are mediated by NO. Spontaneous relaxations of the rat gastroduodenum include responses that involve a GABAAergic NO-related pathway, which is targeted by VIP. In addition, VIP can target NO relaxations of the antrum via other pathways.

Animals↗
PubMed1998

Short-chain fatty acids modify colonic motility through nerves and polypeptide YY release in the rat.

Short-chain fatty acids (SCFAs) are recognized as the major anions of the large intestinal content in humans, but their effect on colonic motility is controversial. This study explores the colonic motor effect of SCFAs and their mechanisms in the rat. Colonic motility (electromyography) and transit time (plastic markers) were measured in conscious rats while SCFAs were infused into the colon, either alone or after administration of neural antagonists or immunoneutralization of circulating polypeptide YY (PYY). SCFA-induced PYY release was measured by RIA and then simulated by infusing exogenous PYY. Intracolonic infusion of 0.4 mmol/h SCFAs had no effect, whereas 2 mmol/h SCFAs reduced colonic motility (36 +/- 3 vs. 57 +/- 4 spike bursts/h with saline, P < 0.05) by decreasing the ratio of nonpropulsive to propulsive activity. This resulted in an increased transit rate (P < 0.01). Neither alpha-adrenoceptor blockade nor nitric oxide synthase inhibition prevented SCFA-induced motility reduction. Intraluminal procaine infusion suppressed the SCFA effect, indicating that a local neural mechanism was involved. SCFA colonic infusion stimulated PYY release in blood. Immunoneutralization of circulating PYY abolished the effect of SCFAs on colonic motility, whereas exogenous PYY infusion partly reproduced this effect. SCFAs modify colonic motor patterns in the rat and increase transit rate; local nerve fibers and PYY are involved in this effect.

Animals↗
PubMed1999

Normalization of atropine-induced postprandial dysrhythmias with gastric pacing.

Gastric pacing has received increasing attention recently. However, few studies have systematically assessed the effect of pacing on gastric dysrhythmias. The aims of this study were to investigate the effect of gastric pacing on gastric dysrhythmia and to explore whether the effect of gastric pacing was mediated via cholinergic nerves. Eight hound dogs implanted with three pairs of serosal electrodes were studied. Three study sessions were performed on each dog. The experiment was conducted sequentially as follows: a 30-min myoelectrical recording immediately after a meal, intravenous injection of atropine or saline, and three sequential 20-min myoelectrical recordings with or without gastric pacing during the second 20-min recording. The percentage of regular slow waves (3.5-7. 0 cycles/min) was calculated using spectral analysis. The percentage of the regular slow waves was progressively reduced from 96.7 +/- 1. 7% at baseline to 29.6 +/- 9.0 (P < 0.001), 23.1 +/- 7.1 (P < 0.001), and 27.3 +/- 4.3% (P < 0.001), respectively, during the first, second, and third 20 min after atropine injection. Normalization of the gastric slow wave was achieved with gastric pacing 2.3 +/- 1.0 min after the initiation of pacing. The percentage of regular slow waves was significantly increased both during pacing (93.6 +/- 2.4 vs. 23.1 +/- 7.1%, P < 0.002) and after pacing (70.9 +/- 6.8 vs. 27. 3 +/- 4.3%, P < 0.003) in comparison with the session without pacing. We conclude that 1) atropine induces gastric myoelectric dysrhythmia in the fed state, 2) gastric pacing is able to normalize gastric postprandial dysrhythmia induced by atropine, and 3) the effect of gastric pacing is not mediated by vagal cholinergic mechanism.

Animals↗
PubMed2001

Gastroparesis: prevalence, clinical significance and treatment.

The application of novel techniques to quantify gastric motor function and gastric emptying has yielded important insights into the prevalence, pathogenesis and clinical sequelae of gastroparesis. Both acute and chronic gastroparesis occur frequently; gastric emptying of solids is delayed in 30% to 50% of patients with diabetes mellitus, functional dyspepsia and gastroesophageal reflux disease. While many patients with gastroparesis experience upper gastrointestinal symptoms that adversely affect quality of life, the concept that symptoms are inevitably the direct outcome of delay in gastric emptying is now recognized to be overly simplistic. In contrast, the potential impact of gastroparesis on oral drug absorption and blood glucose control in patients with diabetes mellitus has probably been underestimated. While the use of prokinetic drugs (cisapride, domperidone, metoclopramide and erythromycin) forms the mainstay of therapy in symptomatic patients with gastroparesis, a number of novel pharmacological therapies are being evaluated, and preliminary studies using gastric pacing show promise.

Gastric Emptying↗
PubMed2002

Cutaneous electrical stimulation of acupuncture points may enhance gastric myoelectrical regularity.

BACKGROUND/AIM: Cutaneous electrical stimulation has been reported to be as effective as electroacupuncture. The aim of this study was to test whether cutaneous electrical stimulation had the same effect as electroacupuncture to enhance the regularity of myoelectrical activity. METHODS: Fifteen healthy male volunteers were enrolled for this study. Electrogastrography (EGG) was performed for 30 min at the baseline, 30 min during electroacupuncture or cutaneous electrical stimulation, and for an additional 30 min thereafter. RESULTS: During 3 Hz of electroacupuncture on the Zusanli point, there was a significant increase in the percentage of normal frequency. The percentage of normal frequency in the post-acupuncture period was also increased, but it was not statistically significant when compared to the baseline. There was a significant decrease in the tachygastric and bradygastric rhythm during electroacupuncture on the Zusanli points. There were similar changes of EGG parameters with cutaneous electrical stimulation on the Zusanli points. The percentage of normal frequency during cutaneous electrical stimulation increased significantly. However, the percentage of normal frequency in the post-cutaneous electrical stimulation period was similar to the baseline. There was a significant decrease in the percentage of tachygastric rhythm during cutaneous electrical stimulation on the Zusanli points. However, there was no significant change in the percentage of bradygastric rhythm during and after the cutaneous electrical stimulation periods. CONCLUSIONS: The effect of cutaneous electrical stimulation on the percentage of normal frequency and tachygastria is similar to electroacupuncture. Nonetheless, the changes of the percentage in bradygastria are not significant.

Acupuncture Points↗
PubMedDate not supplied

Electromotor activity of the cecum and ascending colon: the concept of 'individual pacemakers'.

BACKGROUND/AIMS: The cecum is described as differing anatomically from the ascending colon (AC); yet their similarity or difference in terms of motile activity has not been studied sufficiently. The cecum is separated from the AC by the cecocolonic junction (CCJ) which contains a cecocolonic sphincter. We assumed that the motile activity of the AC is different from that of the cecum and hypothesized that both the AC and the cecum might have different pacemakers which initiate the motile activity. This hypothesis was investigated in the current study. METHODS: The study was performed in 10 subjects (mean age 41.6 +/- 12.8 SD years; 7 women) during the repair of huge abdominal incisional hernias. The electric activity was recorded from 2 monopolar electrodes applied each to the cecum, CCJ and AC. The CCJ was then anesthetized by xylocaine and the electric waves of the cecum, CCJ and AC were registered after 10 and 90 min. The test was repeated using normal saline instead of xylocaine. RESULTS: Electric waves were recorded from the cecum, CCJ and AC in the form of monophasic pacesetter (PPs) and action potentials (APs). The PPs occurred regularly and the APs randomly. The frequency, amplitude and conduction velocity of the waves recorded from the CCJ and AC had higher readings than those from the cecum (p < 0.05). The CCJ and AC showed similar frequency and conduction velocity (p > 0.05). Ten minutes after CCJ anesthetization, electric waves were recorded from the cecum but not from the CCJ or AC; however, electric activity returned after 90 min. Saline injection did not affect the electric activity of the cecum, CCJ and AC. CONCLUSION: The electric wave parameters of the cecum differed from those of the CCJ and AC, suggesting that the motile activity of the CCJ and AC is not a continuation of the motile activity of the cecum and that it might be evoked by 2 different pacemakers. The similarity in frequency and conduction velocity of electric waves of the CCJ and AC, however, most likely denotes that the AC waves are a continuation of those of the CCJ, and that both are evoked by the same pacemaker probably located in the CCJ. The higher amplitude of cecal waves might be due to the thicker cecal musculature compared to that of the AC.

Adult↗
PubMed2005

Utility of electrogastrography in differentiating Parkinson's disease with or without gastrointestinal symptoms: a prospective controlled study.

BACKGROUND/AIMS: Parkinson's disease (PD) may be associated with various gastrointestinal symptoms. This study was designed to assess the gastric myoelectrical functioning in patients with PD and in healthy controls by using electrogastrography (EGG) with the water load test and to determine the clinical utility of EGG in differentiating PD patients with or without upper gastrointestinal symptoms. METHODS: Twenty patients (13 men, mean age 63 years) with PD and 11 healthy controls (5 men, mean age 55 years) were studied. The PD patients were stratified into two subgroups: 9 were assessed as PD without upper gastrointestinal symptoms (group A) and 11 as PD with upper gastrointestinal symptoms (group B). The gastric myoelectrical activity was assessed using cutaneous electrodes to record EGG before and after the subjects ingested water until full. RESULTS: The PD patients drank significantly less water until full as compared with the controls (303 +/- 45 vs. 627 +/- 67 ml, p < 0.05). At baseline, the PD patients had a significantly higher 1.0- to 2.5-cpm activity as compared with the controls (44 +/- 3 vs. 33 +/- 3%, p < 0.05). These differences persisted after ingestion of the water load. The PD patients had a significantly lower 2.5- to 3.75-cpm activity late after ingestion of the water load as compared with the controls (33 +/- 4 vs. 49 +/- 5%, p < 0.05). No statistically significant differences were found in any EGG variables or the water load between the two groups of PD patients. CONCLUSIONS: This study has shown that the gastric myoelectrical activity is impaired in both groups of PD patients. EGG appears to have a limited, if any, clinical utility in the differentiation of PD patients with or without upper gastrointestinal symptoms.

Administration, Oral↗
PubMed2005

Pathophysiological roles of ectopic tachygastria induced with antral electrical stimulation.

AIM: To investigate the pathophysiological roles of tachygastria using antral electrical stimulation (AES). METHODS: The study was performed on 13 healthy female hound-type dogs chronically implanted with three pairs of serosal electrodes and a gastric cannula (n = 7). In the first experiment (n = 7), the antral motility was measured for three 30-min periods right after a solid meal. AES was performed during the second 30-min period at a tachygastric frequency. In the second experiment (n = 6), gastric slow waves and animal behavior were monitored in the fasting state at baseline and with various parameters of AES. RESULTS: (1) AES at tachygastric frequencies (7-14 cpm) significantly reduced the percentage of normal 4- to 6-cpm slow waves and induced tachygastria; (2) AES significantly and substantially inhibited the antral motility in the fed state; (3) AES in the fasting state energy dependently induced symptoms, and the symptom score was linearly correlated with the stimulation frequency, and (4) there was a significant negative correlation between percentage of tachygastria and index of antral motility. CONCLUSIONS: AES induces tachygastria and inhibits the antral motility. Tachygastria is correlated with antral motility.

Animals↗
PubMed2006

Gastric electrical stimulation in gastroparesis: where do we stand?

Gastroparesis is a chronic disabling condition of impaired gastric motility that results in decreased quality of life. Currently available medical therapy consists of prokinetic and/or antiemetic therapy, dietary modifications, and nutritional supplementation. For patients with medication-resistant gastroparesis a non-pharmacological therapy, gastric electric stimulation, has evolved over the last decade. Based on the frequency of the electrical stimulus, gastric electric stimulation can be classified into low- and high-frequency gastric electric stimulation. The first method aims to normalize gastric dysrhythmia and entrain gastric slow waves and accelerates gastric emptying, whereas high-frequency gastric electric stimulation is unable to restore normal gastric emptying, but nevertheless stunningly reduces symptoms, such as nausea and vomiting, re-establishes quality of life, nutritional state in all patients, and metabolic control in patients with diabetic gastroparesis. Gastric electric stimulation presents a new possibility in the treatment of gastroparesis.

Electric Stimulation Therapy↗
PubMed1990

Relationship between fluctuations of pH and pressure in the human stomach and duodenum.

The normal patterns of pressure activity in the antrum, pylorus and duodenum and associated pH changes were monitored in 9 healthy volunteers under fasted conditions and after ingestion of 300 ml of chocolate milk. The manometric assembly incorporated three side holes in the antrum, four side holes in the duodenum, a sleeve sensor positioned across the pylorus, and pH electrodes situated in the terminal antrum and proximal duodenum. The most common motor pattern recorded under fasting conditions consisted of regular co-ordinated contractions, most of which involved the antrum and duodenum, showed evidence of propagation and was associated with transient decreases in duodenal pH and transient increases in antral pH. Ingestion of milk changes the motor pattern to one that was composed of pressure waves which were confined to the pylorus with few or no pressure waves in the terminal antrum or proximal duodenum. Isolated pyloric pressure waves were gradually replaced by propagated antropyloroduodenal contractions which were associated with transient decreases in duodenal pH. Isolated pyloric pressure waves were not associated with episodes of duodenal acidification under fed conditions.

Adult↗
PubMedDate not supplied

Intestinal motor function in irritable bowel syndrome.

Irritable bowel syndrome is widely considered to be associated with disordered gastro-intestinal motility. The evidence for a motor disorder in the colon and small intestine of patients with irritable bowel syndrome is reviewed. Results of myoelectric, motility and transit studies in both the colon and small intestine are inconsistent. Difficulties in interpreting colonic motility have led investigators to address the small intestine as a possible site of dysmotility. An increase in the number of clustered contractions in the proximal small intestine has been reported by some, but not all investigators. Methodological differences as well as patient selection, symptom severity and fluctuation may all contribute to discrepancies between the results of different studies. Motility disturbances may be present which are currently unrecognised due to an inadequate understanding of the propagation of colonic contractions, and of small intestinal contractions during phase II and postprandially. Whether the reported motor disturbances arise locally in the gut or originate from higher centres in the central nervous system has not been established.

Colon↗
PubMedDate not supplied

Clinical significance of gastric myoelectrical dysrhythmias.

Normal rhythmic myoelectrical activity of the human stomach is 3 cpm, regulating gastric contractile activity. Dysrhythmia in gastric myoelectrical activity is found to be associated with functional disorders of the stomach. Gastric dysrhythmias are classified into tachygastria (frequency higher than normal), bradygastria (frequency lower than normal) and arrhythmia (no rhythmic activity). Clinical significance of gastric dysrhythmias is discussed in this paper, outlined as follows: (a) What is normal gastric myoelectrical activity and what is dysrhythmia? (b) How to detect gastric dysrhythmias? (c) Gastric dysrhythmias in clinical settings. (d) What may cause gastric dysrhythmias? (e) How to normalize gastric dysrhythmias?

Electrodiagnosis↗