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Continuous administration of haloperidol, sulpiride, or cis-flupenthixol, but not of domperidone or apomorphine, to Wistar rats for up to 3 weeks caused an increase in spontaneous purposeless chewing movements. Treatment with physostigmine and pilocarpine, but not neostigmine, for up to 3 weeks increased chewing, whilst scopolamine decreased chewing. Metergoline and cyproheptadine, but not quipazine, increased chewing after only 1 and 7 days but not thereafter. Chewing was not altered following treatment with compounds acting on GABA or noradrenaline systems or by a range of non-neuroleptic agents inducing dystonia in man. The enhancement of chewing induced by neuroleptic and cholinomimetic drugs was reduced by acute treatment with scopolamine, and reverted to control levels following drug withdrawal. Neuroleptic-induced purposeless chewing in Wistar rats appears to be primarily influenced by cerebral dopamine and acetylcholine function and may resemble acute dystonia, rather than tardive dyskinesia.
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Solid dispersions were prepared by spray-drying with a polymer. The characterization of prepared solid dispersions was analyzed by scanning electron microscope, Fourier transform infrared spectroscopy, x-ray diffraction and differential scanning calorimeter. In vitro dissolution behavior was carried out in gastric juice (pH 1.2) and these results were compared with pure domperidone (active pharmaceutical ingredient). The dissolution rate was improved due to the influence of polymers. Stability assays were conducted by the same pre-experiment. Storage conditions of the solid dispersions were as follows: 25°C relative humidity 25% and 65°C relative humidity 80%.
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The relation between radiation-induced vomiting and gastric emptying is unclear and the treatment of this condition is not established. We explored, therefore, (a) the effect of cobalt 60 irradiation on gastric emptying of solids and liquids and (b) the possibility of preventing radiation-induced vomiting with the dopamine antagonist, domperidone. Twenty dogs were studied on two separate days, blindly and in random order, after i.v. injection of either a placebo or 0.06 mg/kg domperidone. On a third day, they received 8 Gy (800 rads) whole body irradiation with cobalt 60 gamma-rays after either placebo (n = 10) or domperidone (n = 10). Before each study, each dog was fed chicken liver tagged in vivo with 99mTc-sulfur colloid (solid marker), and water containing 111In-diethylenetriamine pentaacetic acid (liquid marker). Dogs were placed in a Pavlov stand for the subsequent 3 h and radionuclide imaging was performed at 10-min intervals. Irradiation produced vomiting in 9 of 10 dogs given placebo but only in 1 of 10 dogs pretreated with domperidone (p less than 0.01). Gastric emptying of liquids and solids was significantly suppressed by irradiation (p less than 0.01) after both placebo and domperidone. These results demonstrate that radiation-induced vomiting is accompanied by suppression of gastric emptying. Furthermore, domperidone prevents vomiting produced by ionizing radiation but does not alter the accompanying delay of gastric emptying.
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Abstracts were reviewed by two review authors, and relevant RCTs on study participants (birth to 16 years) with GOR receiving a pharmacological treatment were selected. Subgroup analysis was considered for children up to 12 months of age, and for children 12 months to 16 years of age, and for those with neurological impairment.
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The relationship of gastric emptying of liquid to the extent of fundal gastritis and gastrointestinal symptoms was investigated in a total of 37 subjects comprising healthy controls with no gastrointestinal symptoms and patients with constant gastrointestinal symptoms for at least 1 year. Gastric emptying was measured by the acetaminophen absorption method, and the extent of fundal gastritis was determined by the endoscopic Congo-red test developed at this hospital. Gastric emptying was significantly slower in patients with gastrointestinal symptoms than in healthy subjects. It was also significantly slower in patients with than in those without severe fundal gastritis. Gastrointestinal symptoms were significantly more frequent in patients with delayed gastric emptying. The acute effect of oral administration of domperidone on gastric emptying was examined. A single dose of domperidone (20 mg) significantly increased the rate of gastric emptying.
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Forty-two patients (51%) had microadenomas (less than 10 mm), 37 (46%) had macroadenomas and in three no tumour was found at operation. Preoperatively, normal responses of both TSH (incremental rise less than 2.0 mU/l) and PRL (greater than 100% rise) to domperidone were observed in two patients only: both had an abnormal vascular supply to the pituitary rather than an adenoma. Serum PRL was normalized in the early post-operative period (less than 72 h; 'early cure') in 65 patients (79%). The highest early cure rate (96%, n = 26) was in patients with adenomas of 5-9 mm, lower rates being achieved for lesions of 10-19 mm (80%, n = 30), less than 5 mm (63%, n = 19) or greater than or equal to 20 mm (57%, n = 7). The early cure rate was strongly correlated with preoperative PRL, ranging from 100% in patients with PRL less than 1000 mU/l (n = 13) to zero in those with PRL greater than 10,000 mU/l. Dopamine agonist therapy of between 5 weeks and 4 years duration prior to surgery was associated with a significantly reduced early cure rate (60 vs 94%, P less than 0.02) in macroadenoma but not microadenoma patients. Recurrent hyperprolactinaemia during mean follow-up of 51.7 months occurred in eight patients (12%), in five cases within 2 months of surgery and in the others at 26, 48 and 50 months. Recurrence could not be predicted from any preoperative parameter, but a serum PRL greater than 150 mU/l 1-3 days following microadenomectomy was associated with early recurrence and probably indicates failed surgery. An abnormal response of TSH to domperidone was documented 2 months post-operatively in 11/60 patients with normal basal PRL, and preceded all three late recurrences. Of four patients with abnormal responses of both PRL and TSH at this time, two have relapsed to date.
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The zona incerta (ZI) is a site of dopamine nerve terminals and part of the incertohypothalamic tract (I-H). Previous findings indicate that dopamine in the ZI has a stimulatory control on the release of luteinizing hormone (LH) and occurrence of ovulation. The effect of acute administration into anaesthetised rats of selective D1 and D2 dopamine agonists and antagonists injected into the ZI on plasma luteinizing hormone (LH) and on the occurrence of ovulation has now been investigated. It was found that bilateral injections on the day of pro-oestrus of a selective D1 antagonist, Sch 23390, inhibited ovulation at 10 micrograms/side/rat. Unilateral injections of a selective D1 agonist, SKF 38393, at 10 micrograms/rat stimulated a significant rise in plasma LH concentration in ovariectomised oestrogen-primed rats, and this was partially reversed by systemic pre-treatment with Sch 23390. The selective D2 agonist, LY 171555, and D2 antagonists, sulpiride and domperidone, had no effect on plasma LH levels or ovulation. This indicates that D1 receptors (but not D2 receptors) in the ZI are involved in the control of gonadotrophin release and may have a physiological function in reproductive processes.
Prokinetic drugs enhance the motility of the luminal organs of the gastrointestinal tract. Few drugs developed in this decade are likely to have a greater impact on the treatment of disorders of the gastrointestinal tract. Bethanechol and metaclopramide have proven the potential utility of this class of drugs, whereas newer agents promise to have both a greater margin of safety and tolerability and a broader scope of utility. The efficacy of these agents is reviewed for the treatment of impaired motility from gastroesophageal reflux to severe chronic constipation.
The prevalence of OH was 51.6%, almost equally divided into probably symptomatic and probably asymptomatic cases. Another 20.6% had possibly symptomatic OH. Importantly, only two patients with symptomatic OH had an OH diagnosis noted in their medical records. Five received domperidone, one received fludrocortison and none received midodrine.
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The response to domperidone (a dopamine blocking agent) of serum prolactin (PRL) levels was compared in 3 patients with amenorrhea-galactorrhea without evidence of a pituitary tumor, 23 patients with prolactinomas (10 cases with histologic confirmation), 7 patients with histologically verified large nonfunctioning pituitary adenomas with normal or moderately elevated basal PRL levels, and 6 patients with histologically verified craniopharyngiomas (3 with normal basal PRL levels and 3 with elevated PRL levels). The response was compared with that of 10 patients with postpartum hyperprolactinemia and 14 normal women. Ten milligrams of intravenous domperidone induced a rapid rise in PRL that was maximal at 30 to 45 minutes in normal, postpartum, and amenorrhea-galactorrhea patients who had no sign of tumor. In contrast, domperidone failed to induce significant changes in PRL in cases of prolactinoma, nonfunctioning pituitary adenomas, and craniopharyngioma with or without elevated basal PRL levels. The results suggest that dopaminergic control on PRL secretion was impaired in all tumor cases. The mechanisms of this abnormal dopaminergic control, however, may be different. Whereas dopamine control in cases of prolactinoma is altered at the level of pituitary dopamine receptors, alternative explanations must be found for those tumors with normal basal PRL levels and lack of response to domperidone.
Of the 85 FD patients, 2 females without nocturnal symptoms, who responded to placebo run-in treatment, were excluded from the study, 30 (36.1%) exhibited nocturnal dyspeptic symptoms with increased duodenogastric bile reflux time (intragastric bilirubin absorbance > 0.14) and mean gastric pH (confirming the existence of bile reflux) (P = 0.021, 0.023) at night were included in the study. Of these 30 patients, 21 (70%) had overt nocturnal duodenogastric bile reflux, which was significantly higher than that of those without nocturnal symptoms (P = 0.026). The 30 patients were allocated to domperidone group or placebo group (n = 15). The nocturnal duodenogastric bile reflux and gastric pH were significantly decreased after domperidone treatment (P = 0.015, 0.021). The severity score of nocturnal dyspeptic symptoms was also significantly decreased after domperidone treatment (P = 0.010, 0.015, 0.026), which was positively correlated with the reduced nocturnal bile reflux or gastric pH (r = 0.736, 0.784, 0.753 or r = 0.679, 0.715, 0.697, P = 0.039, 0.036, 0.037 or P = 0.043, 0.039, 0.040).
Prolactin (PRL) release induced by TRH was examined on each day of the estrous cycle in female rats in which pituitary dopamine (DA) receptors were blocked pharmacologically. The objective was to determine if an interaction exists between hypothalamic inhibitory and releasing hormones with regard to prolactin (PRL) secretion. Domperidone (0.01 mg/rat i.v.) followed 5 minutes later by the administration of the DA agonist 2-Br-alpha-ergocryptine maleate (CB-154, 0.5 mg/rat i.v.) were used to produce a transient (less than 1 hr) dopamine blockade. One hour later, thyrotropin-releasing hormone (TRH, 1.0 microgram/rat i.v.) was given to stimulate PRL release. On the morning of proestrus, TRH released a significantly greater quantity of PRL into the plasma after DA antagonism compared to control animals which did not receive the dopamine antagonist. Dopamine antagonism also enhanced the effectiveness of TRH on the mornings of estrus and metestrus. The response on estrus was significantly greater than the response on proestrus. However by the morning of diestrus, TRH-"releasable" PRL was greatly diminished. Our results suggest that DA antagonism is able to shift differing quantities of PRL into a TRH "releasable" pool on several days of the estrous cycle and that the control of this mechanism is acute.
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The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha-adrenergic, beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.
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A retrospective audit of domperidone dispensing among women with singleton pregnancies who delivered at the WCH between January 2000 and July 2010 was undertaken. Women dispensed domperidone were identified using WCH pharmacy dispensing records. Maternal and infant clinical data were obtained from the WCH Perinatal Statistics Collection. An audit of paper-based medical records was undertaken for a random sample of 261 mother-child pairs to collect prescribing and additional clinical data.
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We investigated the contractile mechanisms of action of three putative gastroprokinetic agents (cisapride, metoclopramide, and domperidone) on the linear phase of gastroduodenal emptying of solid meals in six healthy conscious dogs. The spatial and temporal parameters of gastric, pyloric, and duodenal contractions during the entire period of gastroduodenal emptying, during the 60-min period of drug infusion (ti), and during the postdrug infusion period (tpi) were analyzed by a computer method. Cisapride accelerated the total gastroduodenal emptying time (tfull), metoclopramide had no significant effect, and domperidone delayed the tfull. None of the drugs had a significant effect on gastroduodenal emptying during ti. Both cisapride and metoclopramide enhanced the rate of gastroduodenal emptying during tpi. Cisapride enhanced pyloric and duodenal motor activity but had no significant effect on antropyloroduodenal coordination during tfull and ti. During tpi, cisapride significantly enhanced both the pyloric and duodenal motor activity and antropyloroduodenal coordination. Metoclopramide exhibited only a few significant effects on the frequency, amplitude, duration, and area under contractions in the antrum, pylorus, and duodenum, but it enhanced antropyloroduodenal coordination during tfull and tpi. Domperidone decreased the frequency of corporeal, pyloric, and duodenal contractions and deteriorated antropyloroduodenal coordination by decreasing the frequency of contractions propagating from the antrum or the pylorus to the duodenum. Cisapride and metoclopramide, but not domperidone, increased the mean distance of propagation of duodenal contractions during tfull, ti, and tpi. We conclude that cisapride is more effective in accelerating gastroduodenal emptying because it stimulates the largest number of parameters of gastropyloroduodenal contractions that enhance gastric emptying. Most enhancement of gastric emptying rate with both cisapride and metoclopramide occurs during tpi.
Our laboratory has reported earlier that in leukocytes, phospholipase D2 (PLD2) is under control of Janus kinase 3 (JAK3), which mediates chemotaxis. Investigating JAK3 in cancer cells led to an important discovery as exponentially growing MDA-MB-231 human breast cancer cells, which are highly proliferative and metastatic, did not substantially use JAK3 to activate PLD2. However, in 2-h or 16-h starved cell cultures, JAK3 switches to a PLD2-enhancing role, consistent with the needs of those cells to enter a "survival state" that relies on an increase in PLD2 activity to withstand serum deprivation. Using a small-molecule tyrosine kinase inhibitor, the flavonoid 4',5,7-trihydroxyflavone (apigenin), as well as RNA silencing, we found that the invasive phenotype of MDA-MB-231 cells is mediated by PLD2 under direct regulation of both JAK3 and the tyrosine kinase, epidermal growth factor receptor (EGFR). Furthermore, serum-deprived cells in culture show an upregulated EGFR/JAK3/PLD2-PA system and are especially sensitive to a combination of JAK3 and PLD2 enzymatic activity inhibitors (30nM apigenin and 300nM 5-fluoro-2-indolyl des-chlorohalopemide (FIPI), respectively). Thus, a multi-layered activation of cell invasion by two kinases (EGFR and JAK3) and a phospholipase (PLD2) provides regulatory flexibility and maximizes the aggressively invasive power of MDA-MB-231 breast cancer cells. This is especially important in the absence of growth factors in serum, coincidental with migration of these cells to new locations.
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The relative potency of prokinetics in patients with gastroparesis has not been systematically studied. This study, therefore, aimed to assess the available data and to compare the effects of different prokinetics on symptoms and gastric emptying rates in patients with gastroparesis.
The effects of apomorphine on survival time of mice during lethal anoxic hypoxia were studied. Apomorphine induced hypothermia and an increase in survival time. Both these effects were mediated by cerebral dopamine receptors, however with different affinity for the neuroleptics haloperidol and sulpiride. These data suggest that apomorphine's antihypoxic effect is not only mediated by the classical effect of hypothermia but also by slowing of oxydative metabolism.
Dopamine agents (saline in control groups) were coadministered with indomethacin by either single or repeated application. The ulcerogenic effect (erosions and/or ulcers) of repeated given indomethacin on gastric mucosa differed clearly from that on intestinal mucosa. The effect on intestinal mucosa was markedly greater than after a single dose. The effects of dopamine agents appeared to be more consistent. Domperidone and haloperidol, given as single or repeated doses, strongly aggravated both the gastric and intestinal lesions. Bromocriptine and amantadine had a protective effect. The adverse effects of both dopamine antagonists (increased after repeated administration) were strongly inhibited by the simultaneous administration of either bromocriptine or amantadine. The involvement of the dopamine system (central or peripheral) in the mechanisms that maintain gastric (probably related to cytoprotection also) and intestinal mucosa integrity is therefore suggested.
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Atrial natriuretic peptide (ANP) can regulate aqueous humor production in the eye and has recently been suggested to play some functional roles in the retina. It has also been reported that ANP increases tyrosine hydroxylase (TH) mRNA levels and intracellular dopamine levels in PC12 cells. The effect of ANP on TH levels and the role of ANP in retinal excitotoxicity remain unknown. In this study, we investigated the effects of ANP on TH expression and dopamine levels in rat retina after intravitreal injection of NMDA. Immunohistochemistry localized natriuretic peptide receptor-A (NPRA) in the ganglion cell layer (GCL), the inner nuclear layer (INL) and the outer nuclear layer (ONL) in the rat retina. Quantitative real-time PCR and Western blot analysis showed a dramatic reduction in retinal TH levels 5 days after NMDA injection, while ANP, at a concentration of 10(-4) M, ameliorated this reduction in TH mRNA and TH protein levels. High-performance liquid chromatography (HPLC) analysis showed that NMDA reduced dopamine levels in the retina, and that ANP attenuated this reduction. Moreover, morphological analysis showed that ANP ameliorated NMDA-induced neurotoxicity through NPRA. The ameliorative effect of ANP was inhibited by a dopamine D(1) receptor antagonist. These results suggest that ANP may have a neuroprotective effect through possible involvement of dopamine induction.
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Forty-eight patients treated with domperidone participated in the study. DNA was successfully obtained from each patient. Age was associated with effectiveness of domperidone (p=0.0088). Genetic polymorphism in KCNH2 was associated with effectiveness of domperidone (p=0.041). The efficacious dose was associated with polymorphism in ABCB1 gene (p=0.0277). The side-effects of domperidone were significantly associated with the SNPs in the promoter region of ADRA1D gene.
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Domperidone is a commonly prescribed antiemetic drug but its side effects are rarely seen. Extrapyramidal side effects are a very rare complication of the drug occurring in 1/10,000 population. They usually occur in infants and very young children due to a poorly developed blood-brain barrier. We report a case of acute dystonia in a 13-year-old boy induced by domperidone. The boy was treated for viral fever and was started on domperidone 30 mg/day, sustained release form (0.7 mg/kg/day), for persistent vomiting along with other supportive treatment. On the fourth day of treatment, although the fever and vomiting subsided, the child developed oromandibular dystonia despite giving the drug in the recommended dose. Fortunately, drug-induced dystonias are a reversible condition and the child improved in 7-8 days after discontinuation of the drug. There was no recurrence at 1 month follow-up. Usually, dystonic reactions do not threaten life but are troublesome and life altering, so judicious use of the drug is advised.
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Cyclic AMP was measured in both striatal slices and in the incubation medium after exposure to dopamine and dopamine antagonist. Dopamine increased cyclic AMP in both tissue and medium. The effect of dopamine was enhanced by sulpiride and domperidone, and to a lesser extent by haloperidol, but alpha-fluphenthixol had only an inhibitory effect. The enhancement by sulpiride was stereoselective and totally suppressed by the D1 antagonist SCH 23390. Cyclic AMP in the medium provided the more sensitive measure of drug effect and increased linearly for up to 20 min., whereas the nucleotide in tissue remained stable or declined after 10 min. It is concluded that: the increase in dopamine-stimulated cyclic AMP efflux caused by D2 antagonists reflects increased intracellular cyclic AMP accumulation rather than an effect on the efflux mechanism; dopamine enhances cyclic AMP accumulation via a D1 receptor, and simultaneously inhibits it through a D2 receptor; and changes in D1 receptor-stimulated cyclic AMP formation in striatum may not be related to the clinical actions of neuroleptics. It remains possible that D2 receptor-mediated inhibition of cyclic AMP accumulation stimulated by a different agonist system may underlie some of the therapeutic actions of dopamine agonists and antagonists.
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Apomorphine (3.5 and 10 mg/kg, s.c.) and morphine (1.3 and 10 mg/kg, s.c.) produced a dose-dependent decrease in gastrointestinal transit of charcoal dust in rats. The involvement of dopamine in such a constipatory effect was found to be mediated to a greater extent by DA2 than by DA1 receptors, using a specific DA1 antagonist (SCH 23390) and DA2 antagonists (alizapride, domperidone). The decrease in apomorphine (50 micrograms) and dopamine (100 and 200 micrograms)-induced gastrointestinal transit after intracisternal administration was antagonized by haloperidol. These results provide evidence for the involvement of dopamine receptors in the constipatory effects of apomorphine and morphine in rats.
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This case study presents a maternal-infant dyad, both of whom bring risk factors to the breastfeeding relationship. The mother had true glandular hypoplasia that was not detected in the antenatal period or during her hospital stay. In addition, the infant was a late preterm infant, bringing the risks of poor feeding behavior and ineffective removal of milk from the breast as well as limited body reserves. Through the use of breastfeeding technology, including test weights, use of a hospital grade double electric breast pump and use of a nipple shield, in addition to a pharmacologic intervention, in which Domperidone was administered, this mother was able to maximize her milk yield and the infant was able to receive human milk for 6 months. This case report highlights the need for a thorough assessment of the breasts as well as the breastfeeding process in all breastfeeding dyads.
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To retrospectively analyze the individual risk factors for radioactive iodine (RAI)-associated nausea and vomiting, and to examine the anti-emetic effect of ramosetron (5-hydroxytryptamine-3 receptor antagonist) in RAI therapy. Patients with differentiated thyroid carcinoma who underwent first-time RAI therapy at Nagasaki University Hospital between January 2009 and 2013 were included (N = 81). As a routine treatment, all patients were administered 30 mg of domperidone per day. Patients who underwent RAI therapy between April 2011 and January 2013 were also administered 0.1 mg of ramosetron per day in addition to domperidone. Nausea and vomiting were evaluated based on Common Terminology Criteria for Adverse Events version 4.0. RAI-associated nausea and vomiting of any grade were seen in 37.0 and 6.2 % of patients in total, respectively. Moderate to severe nausea (grade 2–3) was seen in 22.2 % of patients and associated with the dose of RAI per body weight (odds ratio = 1.046, p = 0.013), but not with the use of ramosetron, in multivariate logistic regression analysis. We have identified the dose of RAI per body weight to be an individual risk factor associated with moderate to severe RAI-associated nausea. This study failed to show that the combined use of ramosetron and domperidone reduced the frequency of RAI-associated nausea and vomiting.
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Domperidone has been widely used in children with gastroesophageal reflux disease (GERD). Studies on the effects of domperidone on corrected QT interval (QTc) in young children are limited. Our aim was to study the effect of domperidone on the repolarization abnormalities assessed by electrocardiogram (ECG) in young children.