PMC:4110358 / 11526-19300
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4110358","sourcedb":"PMC","sourceid":"4110358","source_url":"http://www.ncbi.nlm.nih.gov/pmc/4110358","text":"Changes in the EGG record due to medication for reasons other than gastrological\nProgress in the prevention and treatment of chronic diseases, has resulted in the life expectancy in Poland to increase each year. Therefore, an increasing proportion of people use prolonged pharmacotherapy, often with combinations of different drugs. The consequences are relatively common undesirable side effects of chronic drug use, and decreased quality of life. The most common side effects are gastrointestinal tract disorders, including those of the stomach. Drugs that have proven to affect the gastric myoelectrical activity include the following:\n\nAntidepressants\nOne of the best-known and most often used antidepressants is fluoxetine. Wu et al. [16] reported in EGG traces that patients with functional dyspepsia and depression had significantly lower relative time proportion of normogastria, both in fasting and postprandial periods. At the same time, the relative time proportion of tachygastria increased in this group of patients. Treatment with fluoxetine with a dose of 20 mg daily for 1 month caused a decrease in DFIC, but there was no significant drop in the relative time-share of tachygastria in electrogastrograms [16]. Doxepin, in a single oral dose of 25 mg, significantly reduced the meal-evoked ries of the dominant power of gastric slow waves in healthy volunteers [17].\n\nDrugs acting on the autonomic system\nNon-selective cholinergic agonist substances, such as edrophonium, have strong stimulating gastric motility properties. The influence of this drug on the EGG record mainly relates to increasing the amplitude of the dominant slow wave rhythm without changes in dominant frequency [18]. Anti-cholinergic drugs, such as scopolamine, have the opposite effect, as they reduce the amplitude of gastric slow waves in an electrogastrogram, but at the same time an increase in the frequency of dominant waves is observed [19].\nA case report indicates that cevimeline, a selective muscarinic M3 receptor agonist, applied for the symptomatic treatment of dryness of conjunctiva of eyes and mucosa of the mouth in Sjögren's syndrome, may increase the dominant frequency of gastric slow waves, especially during the interdigestive period [20].\n\n(Neuro)hormones and hormonal drugs\nMotilin administered by intravenous infusion, despite the stimulating motility effect on the gastric antrum, did not elicit perceptible changes in the EGG record of GMA in healthy volunteers [21]. Intravenous infusion of cholecystokinin octapeptide (CCK-8) resulted in a decrease dominant power of gastric slow waves in the postprandial period, without changing their dominant frequency [22].\nGlucagon, like scopolamine, decreased the amplitude of gastric slow waves in an electrogastrogram while increasing their dominant frequency [19].\nCalcitonin – a drug that strongly delays stomach evacuation [23] – administered intranasally, reduced the relative time share of bradygastria, but did not significantly affect the contribution of normogastria in postprandial electrogastrogram [24].\nIn pharmacological doses, vasopressin is an exemplary drug causing bradygastria [25].\n\nCardiac medications\nNitrates have significant effects on GMA. Although the dominant frequency of gastric slow waves was not altered after 1 week of treatment with isosorbide dinitrate, a significant reduction was observed in meal-evoked signal amplitude increase on electrogastrogram [26].\n\nDrugs used in anaesthesia\nThe main indication for the use of naloxone is to reverse the effects of opioids, for example in narcotic agent intoxication or awaking from sedation after anaesthesia. Naloxone is also a drug that is sometimes used in situations very different from its main indications. It was found, for example, that it can be effective in cases of aggravating itchiness in liver disorders with cholestasis. Naloxone has the ability to accelerate intestinal transit time with partial normalisation of the electrogastrographic record, as demonstrated in the case of gastrointestinal pseudo-obstruction [27]. A study done with healthy volunteers did not show any significant effect of naloxone on GMA, or on the rate of gastric emptying [28].\nAnother drug often used in anaesthesia with documented significant effect on the myoelectric activity of the stomach is fentanyl, a painkiller drug belonging to the family of opioid analgesics. Approximately half of the patients undergoing anaesthesia with fentanyl showed a significant decrease in both the dominant frequency and dominant power in the electrogastrographic record [29].\n\nStimulants\nAlcohol, cigarettes (containing nicotine), and coffee (due to the caffeine content) are the most common stimulants used in European countries. Each of these substances has a documented strong effect on the human body, including actions potentially disrupting the GMA.\nEthyl alcohol is a substance with a proven effect on motility of the upper gastrointestinal tract. Most of the work evaluating the effect of alcohol on myoelectrical activity and gastric emptying suggest that consumption of ethanol delays gastric emptying [30]. Pfaffenbach et al. [31] showed that, in comparison to healthy subjects, GMA in alcoholics was characterised by a relatively lower time-share of bradygastria. On the other hand, in conditions of acute exposure, Levanon et al. [32] observed a significant decrease in dominant power of gastric slow waves after consumption of white wine with 12.5% volume ethanol content. However, Turkish researchers found that orange juice with 40% volume ethanol content did not significantly modify any of the evaluated electrogastrographic parameters [33]. In a recent study, Kasicka-Jonderko et al. [30] showed that the influence of alcoholic beverages on GMA depends on ethanol concentration. Whisky and an aqueous solution of ethanol with the same concentration of 43.5%volume significantly impaired the dominant power of the gastric slow waves in the electrogastrographic GMA record. However, neither red wine (13.7% vol.) nor beer (4.7% vol.) nor aqueous ethanol solutions of the corresponding concentrations exerted a noticeable effect on the GMA [30].\nNicotine administered in a controlled manner via transdermal patches resulted in a significant impairment of GMA. In the study on non-smoking volunteers, administration of 14 mg of nicotine caused an increase in the relative time-share of tachygastria, from an average of 2% to as much as 16%, and an increase in DFIC. Electrogastrographic disturbances were accompanied by severe nausea [34]. Transdermal application of nicotine in the same dose of 14 mg did not cause any problems on GMA in heavy smokers [34]. Under conditions of acute exposure, smoking of 2 cigarettes of nominal nicotine content of 1 mg/piece did not cause definite changes in GMA during the postprandial period in heavy smokers [35].\nAnimal studies have shown that the main effect of caffeine is an increase in contractile activity of the colon, and not the stomach [36]. In a pilot study with healthy volunteers, there was no significant effect on the GMA of 4 mg/kg of caffeine administered in grapefruit juice [37].\n\nOther substances\nComparable to the properties of some drugs, certain substances present in food, or in the form of so-called dietary supplements, also have an effect on the GMA record. An example is ginger, a rhizome with a specific odour and a characteristic pungent taste. In folk medicine, it is a known herbal medication with antiemetic, antiseptic and stimulating properties. Research has shown that ginger administered prophylactically significantly reduces the severity of both subjective symptoms, and objective changes in the electrogastrographic record associated with motion sickness 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