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A survey by Coates and co-workers in 1983 revealed that patients ranked nausea and vomiting as the most distressing side effects of chemotherapy. In the last decade the use of high-dose metoclopramide and, especially, the introduction of the 5-HT3 receptor antagonists, have been major leaps forward in the control of chemotherapy-induced emesis. Nevertheless, since patients still consider nausea and vomiting to be the most distressing side effect of their chemotherapy there is clearly a need for further improvements. Acute emesis, which is the topic of this review, can now be controlled in the majority of patients during their first course of chemotherapy. Future focus should be on better control of emesis during subsequent courses of chemotherapy as well as on better control of delayed emesis.
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The effect of an erythromycin derivative, EM-523, on gastrointestinal motility was investigated in conscious dogs and compared with that of motilin cisapride, trimebutine and metoclopramide. In the fasting state, EM-523 given i.v. or i.d. at 3 micrograms/kg or more induced contractions in the stomach that migrated along the small intestine. The pattern of the contractions was very similar to that induced by motilin. In the digestive state, EM-523 increased the amplitude of gastric contractions. Cisapride and metoclopramide increased gastrointestinal motility both in the fasting and digestive states; however, their contractile pattern was different from that of EM-523. Trimebutine did not induce gastric motility in the fasting state but rather decreased gastric motility in the digestive state. The contractions induced by EM-523 and motilin were inhibited by atropine but were not affected by naloxone, suggesting that the cholinergic pathway is important in the exertion of their action. These results indicate that EM-523 mimics motilin in stimulating gastrointestinal motility and that this agent may be useful treat gastrointestinal disorders such as gastric stasis, gastroesophageal reflux, and postoperative ileus, and so forth.
This study is performed with 50 female patients who had APFEL score 3-4 after ethics committee approval and informed consent was taken from patients. The patients were divided into 2 groups: group 1 (P1): propofol + preoperative hydration and group 2 (P2): propofol + no preoperative hydration.
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In dogs with gastric fistulas, intragastric pressure was measured with a flaccid ballon containing 500 ml of water. Graded doses of dopamine caused graded decreases in intragastric pressure. The effect was blocked by pimozide or by metoclopramide but was not significantly affected by phenoxybenzamine, propranolol, guanethidine, or FLA-63 (a beta-hydroxylase inhibitor). Pretreatment with metoclopramide or with pimozide shifted the volume-pressure diagram of the stomach to the left; that is, at any given volume the pressure was greater after than before these drugs. In dogs with vagally innervated gastric pouches and gastric fistulas, feeding for 1 min (while allowing the food to leave the stomach through the gastric fistula) caused a prompt decrease in pressure in the pouch that lasted for about 5 min. Pretreatment with metoclopramide decreased the magnitude and duration of this receptive relaxation. It is concluded that these findings are consistent with (but do not establish) the hypothesis that dopamine is the neurotransmitter for receptive relaxation of the stomach, because dopamine mimics receptive relaxation, and dopamine antagonists partially block reflexly induced receptive relaxation.
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Our combined therapy is safe and highly efficacious but caution must be exercised because intestinal obstruction can occur if large fragments pass through the pylorus. A more extensive study is required to assess these clinical observations.
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The effect of different opioids on postoperative nausea and vomiting (PONV) has not been conclusively determined yet, thus the aim of this study was to compare the incidence of PONV in propofol-anaesthetized patients receiving either fentanyl or remifentanil as opioid supplement.
Metoclopramide, a dopaminergic inhibitor, injected in 9 normal volunteers, was followed by a prompt decrease of serum potassium (10--20 min; p less than 0.01) and by an increase of plasma aldosterone (p less than 0.01). Renin slightly increased at 45 min (p less than 0.05); insulin and cortisol did not show any significant increase. The urinary excretion of potassium rose after metoclopramide (p less than 0.05). A bolus of aldosterone (250 micrograms i.v.) in 4 normal subjects was not followed by any modification of serum potassium, but increased urinary potassium excretion (p less than 0.05); the injection of metoclopramide in two patients with an aldosterone-secreting adenoma of the adrenal and in one patient with Addison's disease induced a decrease of serum potassium in absence of any modification of plasma aldosterone. The decrease of serum potassium after metoclopramide is not explained by changes of aldosterone or insulin, considered the most important hormonal controls of potassium. The rapidity of potassium decrease implies a change of distribution of potassium between extra- and intracellular compartments, which, in turn, may stimulate aldosterone secretion. It is conceivable that the dopaminergic system has a role in the control of serum potassium.
The actions of metoclopramide and ergotamine, drugs which are used as a combined migraine medication, on human (h)5-HT3A receptors and 5-HT reuptake carriers, stably expressed in HEK-293 cells, were studied with patch-clamp- and ([3H]5-HT)-uptake techniques. At clinical concentrations, metoclopramide inhibited peak and integrated currents through h5-HT3A receptors concentration-dependently (IC50 = 0.064 and 0.076 microM, respectively) when it was applied in equilibrium (60 s before and during 5-HT (30 microM) exposure). The onset and offset time constants of metoclopramide action were 1.3 and 2.1 s, respectively. The potency of metoclopramide when exclusively applied during the agonist pulse decreased more than 200-fold (IC50 = 19.0 microM, peak current suppression). Metoclopramide (0.10 microM) did not alter the EC50 of 5-HT-induced peak currents. In contrast to the lack of competitive interaction between metoclopramide and 5-HT in this functional assay, metoclopramide inhibited specific [3H]GR65630 binding to human h5-HT3A receptors in a surmountable manner. This seeming discrepancy between functional studies and radioligand binding experiments may be accounted for by (1) the slow kinetics of inhibition of peak currents by metoclopramide compared with the fast onset and offset kinetics of 5-HT-induced currents and (2) the low efficacy of metoclopramide in inhibiting radioligand binding (e.g. only 20% binding inhibition compared to 79% peak current suppression by 200 nM metoclopramide). At low concentrations (1-10 nM), ergotamine had no effect on 5-HT (30 microM)-induced peak currents. Above clinical concentrations, ergotamine (>3 microM) inhibited them. When both drugs were applied together (0.10 microM metoclopramide +0.001 to 0.01 microM ergotamine), an inhibition of both, peak and integrated current responses was observed. Neither metoclopramide (< or =30 microM) nor ergotamine (< or =30 microM) had an effect on the 5-HT reuptake carrier as they did not alter the citalopram-sensitive [3H]5-HT uptake.
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Pretreatment with ondansetron or metoclopramide does not reduce oral contrast solution ingestion time.
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Gastrointestinal promotility agents may improve tolerance to enteral nutrition, reduce gastroesophageal reflux and pulmonary aspiration, and therefore have the potential to improve outcomes of critically ill patients.
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The presence of dopamine (DA) receptors in feline kidneys is a matter of contention. Radioligand binding and Western blotting studies were employed to determine whether DA receptors are present in feline kidneys. The pharmacologic profile of the selective D1-receptor antagonist [3H]-SCH 23390 was studied in renal cortical membrane preparations from cats by conducting saturation binding isotherm and competitive binding experiments. [3H]-SCH 23390 bound to feline renal cortical membranes in a manner consistent with labeling of a D1-like receptor. The binding profile revealed a single site D1-like or D1 receptor in the feline renal cortex with a Kd = 7.8 +/- 1.0 nmol/L and Bmax = 76.5 +/- 19.5 fmol/mg. Competitive binding studies for [3H]-SCH 23390 against unlabeled agonists yielded the following Ki values and rank order of competition: SKF38393 (Ki = 0.47 +/- 0.26 micro m) > fenoldopam (Ki = 3.12 +/- 1.1 micro m) > DA (Ki = 933.1 +/- 1.6 micro m). Competitive binding studies for [3H]-SCH-23390 against unlabeled antagonists yielded the following rank order of competition: SCH 23390 (Ki = 1.97 +/- 0.81 micro m) > spiperone (Ki = 3.79 +/- 0.79) > metoclopramide (Ki = 4.26 +/- 2.4 micro m). Western blot analysis with anti-DA D1 receptor antibodies detected a single band with Mr of 74 kDa corresponding to a D1 DA receptor. These results suggest that a putative D1-like or D1 receptor exists in feline kidneys different from those previously identified in rat, dog or human kidneys.
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A retrospective study is reported carried out on a group of 166 patients affected by dyspeptic syndrome who presented at least 3 of the 9 symptoms which characterise this pathology. One hundred and twenty-eight patients underwent prokinetic drug therapy and 38 received placebo. Clinical parameters were evaluated following one month of therapy all patients in order to compare them to basal values. The results obtained confirm a satisfactory efficacy of the prokinetic treatment in improving dyspeptic symptoms. Although administered to a smaller number of patients, placebo was also found to play an important role in the multifactorial etiopathogenesis of the dyspeptic syndrome on a functional basis.
In this review, no evidence of a relationship between SI and GE was identified for different drugs used for the treatment of gastroparesis. This finding questions the use of GE measurement to direct drug development for gastroparesis.
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A retrospective analysis was carried out in 104 patients with peptic oesophagitis treated with Pyrogastrone (carbenoxolone with alginate-antacid) during a 3 1/2-year period. There wer 3 treatment groups: one had Pyrogastrone alone, another pyrogastrone with metoclopramide and in the third, both agents were given together with cimetidine. Highly significant symptomatic improvement was achieved in 85% of 96 patients treated between 4 and 8 weeks and equally significant endoscopic healing was noted in 76% of 55 patients for the same period. Best results were seen in those given Pyrogastrone alone; the concurrent use of metoclopramide and cimetidine did not enhance healing or symptom relief. 40% of patients received multiple courses, 22% were treated for at least six months and 16% for one year or longer continuously; 3 patients for over 3 years. The only noteworthy side effects were due to the tablet flavour and chewing property. These results confirm clinical trial experience that Pyrogastrone is highly effective in healing peptic esophagitis.
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In a randomised, double-blind manner, 120 patients, 60 younger (aged 20-40 years) and 60 older (aged 60-80 years) adults, received placebo (saline) or metoclopramide intravenously at two different doses (2.5mg and 5 mg) [younger group n = 20 each, older group n = 20 each], with venous occlusion for 1 minute, followed by administration of propofol 0.5 mg/kg into a dorsal hand vein. A blinded researcher asked the patient to assess the pain according to a pain score (0 = none, 1 = mild, 2 = moderate, 3 = severe) during injection of propofol.
Nineteen mechanically ventilated medical patients intolerant of enteral nutrition and receiving metoclopramide underwent bilateral celiac plexus block. The anterior procedure was accomplished under sonographic guidance with the injection of either 25 mL bupivacaine 0.25% (celiac group, n = 10) or saline (control group, n = 9) bilaterally. Gastric emptying was assessed by the acetaminophen absorption method. After the block, nasogastric feeding was commenced, and nasogastric aspirates were collected once every 24 hours. Successful feeding was defined as 24-hourly gastric residual volume <250 mL with a feeding rate > or = 40 mL/h.
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A new sensitive and selective liquid chromatography coupled with mass spectrometry (LC/MS/MS) method for quantification of loratadine (LOR) and its active metabolite descarboethoxyloratadine (DSL) in human plasma was validated. After addition of the internal standard, metoclopramide, the human plasma samples (0.3 ml) were precipitated using acetonitrile (0.75 ml) and the centrifuged supernatants were partially evaporated under nitrogen at 37 degrees C at approximately 0.3 ml volume. The LOR, DSL and internal standard were separated on a reversed phase column (Zorbax SB-C18, 100 mmx3.0 mm i.d., 3.5 microm) under isocratic conditions using a mobile phase of an 8:92(v/v) mixture of acetonitrile and 0.4% (v/v) formic acid in water. The flow rate was 1 ml/min and the column temperature 45 degrees C. The detection of LOR, DSL and internal standard was in MRM mode using an ion trap mass spectrometer with electrospray positive ionisation. The ion transitions were monitored as follows: 383-->337 for LOR, 311-->(259+294+282) for DSL and 300-->226.8 for internal standard. Calibration curves were generated over the range of 0.52-52.3 ng/ml for both LOR and DSL with values for coefficient of determination greater than 0.994 by using a weighted (1/y) quadratic regression. The lower limits of quantification were established at 0.52 ng/ml LOR and DSL, respectively, with an accuracy and precision less than 20%. Both analytes demonstrated good short-term, long-term, post-preparative and freeze-thaw stability. Besides its simplicity, the sample treatment allows obtaining a very good recovery of both analytes, around 100%. The validated LC/MS/MS method has been applied to a pharmacokinetic study of loratadine tablets on healthy volunteers.
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This article discusses the studies on functional and motor gastrointestinal disorders presented at the 2014 Digestive Diseases Week conference that are of greatest interest to us. New data have been provided on the clinical importance of functional gastrointestinal disorders, with recent prevalence data for irritable bowel syndrome and fecal incontinence. We know more about the pathophysiological mechanisms of the various functional disorders, especially irritable bowel syndrome, which has had the largest number of studies. Thus, we have gained new data on microinflammation, genetics, microbiota, psychological aspects, etc. Symptoms such as abdominal distension have gained interest in the scientific community, both in terms of patients with irritable bowel syndrome and those with constipation. From the diagnostic point of view, the search continues for a biomarker for functional gastrointestinal disorders, especially for irritable bowel syndrome. In the therapeutic area, the importance of diet for these patients (FODMAP, fructans, etc.) is once again confirmed, and data is provided that backs the efficacy of already marketed drugs such as linaclotide, which rule out the use of other drugs such as mesalazine for patients with irritable bowel syndrome. This year, new forms of drug administration have been presented, including metoclopramide nasal sprays and granisetron transdermal patches for patients with gastroparesis. Lastly, a curiosity that caught our attention was the use of a vibrating capsule to stimulate gastrointestinal transit in patients with constipation.
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We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of treatment for nausea and vomiting in early pregnancy? What are the effects of treatments for hyperemesis gravidarum? We searched: Medline, Embase, The Cochrane Library, and other important databases up to May 2008 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
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The behavioural responses to RU 24213 (D2 agonist) and SKF 38393 (D1 agonist) were studied in the morphine cataleptic rat. D2 stimulation evoked slow forward walking coupled with head-down sniffing that was blocked both by SCH 23390 (D1 antagonist) and metoclopramide (D2 antagonist). D1 stimulation was without effect by itself, but when administered together with RU 24213 it reversed the direction of walking and initiated licking and chewing. Backward walking was attenuated by metoclopramide and restored to forward locomotion by SCH 23390. These data further show that D1 receptors exert an important modulatory influence on motor behaviours mediated by the D2 site.
Experiments were performed with fenoldopam (SKF-82526), a selective DA1 receptor agonist, and quinpirole (LY-171555), a selective DA2 receptor agonist, to determine their actions on ganglionic transmission. Fenoldopam caused significant inhibition of the tachycardia elicited during preganglionic stellate stimulation; however, it did not alter the positive chronotropic responses to postganglionic stellate stimulation, suggesting that the compound exerts its inhibitory action at the ganglia. Electrophysiological experiments in the isolated stellate ganglia showed that fenoldopam produced inhibition of ganglionic transmission as indicated by a significant reduction in the magnitude of the compound postganglionic action potential elicited during preganglionic nerve stimulation. The inhibition of ganglionic transmission produced by fenoldopam both under in vivo and in vitro conditions was antagonized by R-sulpiride and metoclopramide, but not by SCH 23390, S-sulpiride or phentolamine. Quinpirole produced significant inhibition of the tachycardia elicited during both preganglionic as well as postganglionic cardiac sympathetic nerve stimulation. This action of quinpirole was antagonized by RS-sulpiride. In electrophysiological experiments it was discovered that quinpirole caused a significant reduction in the magnitude of the compound action potential elicited during stimulation of preganglionic stellate nerve fibers. This inhibition of ganglionic transmission produced by quinpirole was antagonized by S- but not by R-sulpiride. Although phentolamine antagonized the inhibitory action of quinpirole, it was much less effective than S-sulpiride. Norepinephrine also produced inhibition of ganglionic transmission in the isolated stellate ganglia which was antagonized by phentolamine but not by S-sulpiride. These results demonstrate the presence of two subtypes of specific dopamine receptors in the stellate ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)
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Sixty patients were studied in a randomized, double-blind manner to determine whether metoclopramide added to droperidol decreased further the incidence of emetic symptoms (nausea, retching, vomiting) in outpatients receiving alfentanil anaesthesia for nasal surgery. Group 1 (n = 30) received metoclopramide 0.15 mg.kg-1 and Group 2 (n = 30) received placebo. In addition, both groups received droperidol 0.02 mg.kg-1 immediately before anaesthesia which was supplemented by alfentanil 20 micrograms.kg-1 at induction followed by an infusion of 0.25-1 micrograms.kg-1.min-1. Emetic symptoms were assessed 0-3 hr, 3-6 hr and 6-24 hr after surgery. Both groups received similar doses of alfentanil (mean +/- SD; Group 1 4641 +/- 1894 micrograms, Group 2 4714 +/- 1640 micrograms). The percentage of patients who had either nausea or vomiting at 0-3, 3-6 or 6-24 hr was 23%, 14% and 13% in Group 1; and 20%, 17% and 10% in Group 2. The overall incidence for each group was 8/30 (27%). There was no difference in the incidence of emetic symptoms between the groups at any time interval or throughout the study. Metoclopramide did not improve upon the antiemesis of droperidol during alfentanil anaesthesia for outpatient nasal surgery.
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Metoclopramide was administered by continuous infusion to two groups each of 14 patients on chemotherapy, randomized to receive either doses adjusted to individual pharmacokinetic parameters or doses adjusted as usual to body weight. The mean plasma concentration at the end of the infusion in the adjusted group was 1.01 mg.l-1, close to that aimed for (1.20 mg.l-1). It was significantly different from that in the other group. v 0.54 mg.l-1. Antiemetic efficacy, defined as less than or equal to 2 emetic events in the 24 h following cisplatin, was similar in both groups (being found in 12/14 (86%) and 10/14 patients (71%), respectively). Analysis of the cumulative percentage of responders according to plasma concentration showed a clear plasma concentration-effect relationship. Routine MCP pharmacokinetic dosage adjustment is not indicated, but this therapeutic approach can be used to optimize antiemetic therapy in poor responder patients.