Electrogastrography: Current Issues in Validation and Methodology

Stern, Robert M.; Koch, Kenneth L.; Stewart, William R.; Vasey, Michael W.

doi:10.1111/j.1469-8986.1987.tb01862.x

Cited by 59 publications

(33 citation statements)

References 22 publications

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“…EGG was performed according to a modification of methods previously described (Stern et al, 1987). After gentle skin abrasion to enhance electrical conduction, six Ag-AgCl electrodes (Accutac diaphoretic ECG electrodes; NDM, Dayton, OH) were affixed to the abdomen.…”

Section: Methodsmentioning

confidence: 99%

Ginger Reduces Hyperglycemia-Evoked Gastric Dysrhythmias in Healthy Humans: Possible Role of Endogenous Prostaglandins

Gonlachanvit

Chen

Hasler³

et al. 2003

J Pharmacol Exp Ther

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Acute hyperglycemia evokes gastric slow wave dysrhythmias via endogenous prostaglandin generation. Ginger exhibits slow wave antiarrhythmic effects in other models, but its actions on hyperglycemia-evoked gastric dysrhythmias are unexplored. We hypothesized that ginger prevents disruption of slow wave rhythm by acute hyperglycemia via inhibition of prostaglandin production but not its actions. Twenty-two healthy humans underwent fasting electrogastrography during hyperglycemic clamping to 250 to 290 mg/dl after double-blind placebo or ginger root (1 g). Responses were compared with the prostaglandin E 1 analog misoprostol (400 g). Dominant frequencies (DF) and the percentage of recording times in the bradygastric [0.5-2 cycles/min (cpm)], normal (2-4 cpm), and tachygastric (4 -9 cpm) frequency ranges were analyzed. After placebo, hyperglycemia reduced normal 2 to 4 cpm activity from 94.4 Ϯ 2.6 to 66.0 Ϯ 10.4%, increased the DF from 2.96 Ϯ 0.04 to 4.09 Ϯ 0.45 cpm, and increased tachygastria from 2.0 Ϯ 1.4 to 29.3 Ϯ 10.7% (P Ͻ 0.05). Hyperglycemia effects on normal activity (77.3 Ϯ 8.3%), DF (3.46 Ϯ 0.37 cpm), and tachygastria (15.6 Ϯ 8.6%) were significantly reduced by ginger (P Ͻ 0.05). Misoprostol evoked decreases in normal activity from 95.4 Ϯ 2.0 to 81.7 Ϯ 3.0% and increases in tachygastria from 3.1 Ϯ 1.6 to 11.2 Ϯ 2.4% (P Ͻ 0.05). However, ginger did not correct these abnormalities versus placebo (P ϭ N.S.). In conclusion, acute hyperglycemia evokes gastric slow wave dysrhythmias that are prevented by ginger root. Conversely, the compound has no effect on dysrhythmias elicited by a prostaglandin E 1 analog, indicating that ginger likely acts to blunt production of prostaglandins rather than inhibiting their action. These findings suggest novel mechanisms for the traditional Chinese herbal remedy ginger.

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Section: Methodsmentioning

confidence: 99%

Ginger Reduces Hyperglycemia-Evoked Gastric Dysrhythmias in Healthy Humans: Possible Role of Endogenous Prostaglandins

Gonlachanvit

Chen

Hasler³

et al. 2003

J Pharmacol Exp Ther

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“…Under normal conditions, mean signal amplitude and power increases in the postprandial period are compared with fasting. The normal frequency is 2-4 cpm for at least 75% of the postprandial period (19,96) or 2.4 -3.6 cpm (69,116). Dominant frequencies Ͻ2 and Ͼ4 cpm after a meal for Ͻ25% of the recording time probably indicates poor signal acquisition or signal noise rather than a true dysrhythmia.…”

Section: Testing Gastric Myoelectrical Activitymentioning

confidence: 99%

Methods for measurement of gastric motility

Szarka¹,

Camilleri²

2009

American Journal of Physiology-Gastrointestinal and Liver Physi

103

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Szarka LA, Camilleri M. Methods for measurement of gastric motility. Am J Physiol Gastrointest Liver Physiol 296: G461-G475, 2009. First published January 15, 2009 doi:10.1152/ajpgi.90467.2008There is an array of tests available to measure gastric motility. Some tests measure end points, such as gastric emptying, that result from several different functions, whereas other tests are more specific and test only a single parameter, such as contractility. This article reviews the tests most commonly available in practice and research to evaluate in vivo the gastric functions of emptying, accommodation, contractility, and myoelectrical activity. The rationale for testing, the relative strengths and weaknesses of each test, and technical details are summarized. We also briefly indicate the applications and validations of the tests for use in experimental animal studies. contractility; emptying; accommodation; gastroparesis; dyspepsia ASSESSMENT OF THE MOTOR FUNCTIONS (motility) of the stomach is important in studies of gastric physiology and pathophysiology. Although not generally applied in gastroenterological practice, there is increasing use of tests to evaluate gastric function, particularly less invasive tests in clinical settings.There is an array of tests available to measure gastric motility. Some tests measure end points, such as gastric emptying, that result from several different functions, whereas other tests are more specific and test only a single parameter, such as contractility. This article reviews the tests most commonly available in practice and research to evaluate in vivo the gastric functions of emptying, accommodation, contractility, and myoelectrical activity. The rationale for testing, the relative strengths and weaknesses of each test, and technical details are summarized. A brief discussion is also provided for methods that have been used in animals to study motor functions of the stomach in animals. Tests to Evaluate Gastric Emptying of SolidsGastric emptying is a composite end point reflecting a variety of functions including gastric accommodation, the pressure gradient between the proximal and distal stomach, and antropyloroduodenal contractility and coordination. The trituration of solids and emptying of solid and liquid food from the stomach are arguably the most important physiological functions of the stomach. Abnormal gastric emptying, either accelerated at 1 h or delayed at 4 h, is among the factors that contribute to reporting of dyspepsia or the development of postprandial symptoms after meal challenge (35). For all tests of gastric motility and emptying, there are standard precautions (1): 1) Drugs affecting gastric motility (e.g., anticholinergics, narcotics, and prokinetics) are stopped for 48 h prior to the test, and the study is performed in the morning after an overnight fast. 2) Diabetic subjects should have a glucose level Ͻ275 mg/dl. 3) At the time the meal is ingested, Type 1 diabetic patients should receive half of their normal insulin dose. Gastric Emptying Scintigrap...

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“…The gastric slow wave regulates the direction of propagation and the maximal frequency of phasic contractions in the distal stomach, thus abnormal slow wave patterns are postulated to underlie many gastric dysmotility syndromes (Stern et al, 1987b). Slow wave activity is measured using EGG, the findings of which show close correlations with recordings from serosal electrodes (Chen et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…EGG was performed according to a modification of previously described methods (Stern et al, 1987b). After gentle skin abrasion to enhance electrical conduction, six Ag-AgCl electrodes (Accutac diaphoretic electrocardiograph electrodes; New Dimensions in Medicine, Dayton, OH) were affixed to the abdomen.…”

Section: Methodsmentioning

confidence: 99%

Selective Reversal of Hyperglycemia-Evoked Gastric Myoelectric Dysrhythmias by Nitrergic Stimulation in Healthy Humans

Coleski

Gonlachanvit

Owyang³

et al. 2004

J Pharmacol Exp Ther

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Acute hyperglycemia disrupts gastric myoelectric rhythm in healthy humans. Defective nitrergic function is a factor in animal models of diabetic gastropathy. We tested participation of nitrergic pathways in hyperglycemia-evoked myoelectric dysrhythmias and compared their role in preventing dysrhythmic actions of experimental motion sickness. Twelve healthy volunteers underwent electrogastrography (EGG) with and without intravenous 20% dextrose to produce plasma glucoses of 250 mg/dl. EGG continued for 2 h after oral nitroglycerin (9 mg) or the cyclic GMP-specific phosphodiesterase inhibitor sildenafil (100 mg). In separate studies, 12 volunteers underwent circular vection (60°/s) without and 90 min after nitroglycerin (9 mg) or sildenafil (100 mg) with concurrent EGG. Hyperglycemia decreased recording time in normal rhythm, increased tachygastria more than 3-fold, and decreased power of the dominant frequency (P Ͻ 0.05). Nitroglycerin and sildenafil reversed effects of hyperglycemia, improving normal rhythm, decreasing tachygastria (both P Ͻ 0.05), and blunting power decreases. Neither agent affected EGG rhythm during euglycemia. Vection decreased time in normal rhythm and increased tachygastria (P Ͻ 0.05). However, nitroglycerin and sildenafil did not reverse dysrhythmic effects of vection (P ϭ N.S.). In conclusion, administration of a nitric oxide (NO) donor or an inhibitor of cyclic GMP-selective phosphodiesterase reverses the dysrhythmic effects of hyperglycemia on gastric myoelectric activity in healthy humans. These agents have no effect on dysrhythmias during motion sickness. These findings are consistent with selective impairment of nitrergic function in this model of diabetic gastropathy and suggest that NO donors and other agents that increase NO activity may be useful for treating diabetic dysrhythmias.

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Electrogastrography: Current Issues in Validation and Methodology

Cited by 59 publications

References 22 publications

Ginger Reduces Hyperglycemia-Evoked Gastric Dysrhythmias in Healthy Humans: Possible Role of Endogenous Prostaglandins

Ginger Reduces Hyperglycemia-Evoked Gastric Dysrhythmias in Healthy Humans: Possible Role of Endogenous Prostaglandins

Methods for measurement of gastric motility

Selective Reversal of Hyperglycemia-Evoked Gastric Myoelectric Dysrhythmias by Nitrergic Stimulation in Healthy Humans

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