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1   All patients had access to paracetamol and metoclopramide.
2 was well tolerated with superior efficacy to metoclopramide.
3 ergics reduce the incidence of PONV, whereas metoclopramide 10 mg does not appear to be effective for
4 ed at these times, we later treated her with metoclopramide (10 mg orally 3 times daily), a medicatio
5 6 attacks with aspirin, 800 to 1000 mg, plus metoclopramide, 10 mg, and patients with MIDAS grade III
6 tment was with aspirin, 800 to 1000 mg, plus metoclopramide, 10 mg.
7 tacks was with aspirin, 800 to 1000 mg, plus metoclopramide, 20 mg.
8 ence and presence of a pharmacologic dose of metoclopramide (3 mg/kg), with or without P-gp inhibitio
9                                              Metoclopramide, a drug frequently used for nausea and vo
10 on-pump inhibitors, nitroglycerin, diazepam, metoclopramide, acetylcysteine were associated with high
11                                              Metoclopramide and castor oil were most strongly associa
12 e conditional recommendations for the use of metoclopramide and erythromycin in patients with gastrop
13 ne RCT (n = 159) found no difference between metoclopramide and promethazine after 24 hours (episodes
14  mg/kg per dose over 3 days with concomitant metoclopramide and pyridoxine.
15                                        Using metoclopramide as a model of CNS drug, we demonstrated t
16 -21 mice aged 50 or 170 days underwent (11)C-metoclopramide baseline PET scans or scans after intrape
17 PS1-21 mice aged 50 or 170 d underwent (11)C-metoclopramide baseline PET scans or scans after intrape
18                                        (11)C-metoclopramide benefits from favorable pharmacokinetic p
19 ion, P-gp inhibition significantly increased metoclopramide brain distribution (VT = 6.28 +/- 0.48 mL
20                                    The (11)C-metoclopramide brain distribution (VT based on Logan plo
21 macologic dose did not affect baseline (11)C-metoclopramide brain kinetics (VT = 2.28 +/- 0.32 and 2.
22                   Previous data suggest that metoclopramide brain kinetics may nonetheless be control
23                                        (11)C-metoclopramide brain kinetics were compared using PET in
24 th two typical neuroleptics, haloperidol and metoclopramide, but not with the atypical neuroleptic cl
25 h the weak ABCB1 substrate radiotracer (11)C-metoclopramide can measure ABCB1 induction at the BBB in
26                            Conclusion: (11)C-metoclopramide can measure ABCB1 induction in the mouse
27                            Conclusion: (11)C-metoclopramide can measure ABCB1 induction in the mouse
28         In this situation, only parent (11)C-metoclopramide could be detected in the brains of P-gp-i
29 iemetics, antivertiginosa or antihistamines, metoclopramide, domperidone, anticholinergics, loop diur
30 gents effective in pseudoobstruction include metoclopramide, domperidone, cisapride, octreotide, and
31                   In addition, sulpiride and metoclopramide, drugs with high affinity for D2-dopamine
32      From a cohort of 1,222,503 pregnancies, metoclopramide-exposed and unexposed women were matched
33 3.5 {95% CI, 2.9-4.1} per 1000] among 40,306 metoclopramide-exposed women and 634 cases [3.9 {95% CI,
34 0 {95% CI, 18.5-21.4} per 1000] among 37,946 metoclopramide-exposed women and 9414 cases [62.1 {95% C
35 he kinetic impact of transporter function on metoclopramide exposure to the brain.
36  the efficacy and safety of Itopride against metoclopramide for EFI in critically ill patients.
37 ted that ginger, vitamin B6, antihistamines, metoclopramide (for mild symptoms), pyridoxine-doxylamin
38  therapy in the itopride group more than the metoclopramide group (p = 0.001), (p = 0.002), (p = 0.01
39 de significantly decreased GRV compared with metoclopramide group (p = 0.001).
40 were randomly assigned to either Itopride or metoclopramide group.
41 50 = 103 pM) and by the non-selective agents metoclopramide (IC50 = 69 nM), cocaine (IC50 = 459 nM) a
42 y in the brain comprised unmetabolized (11)C-metoclopramide in all animal groups.
43 he brain was composed of unmetabolized (11)C-metoclopramide in all animal groups.
44 rmed PET with the weak ABCB1 substrate (11)C-metoclopramide in humans to elucidate the impact of ABCB
45                Among 28,486 women exposed to metoclopramide in the first trimester, 721 had an infant
46 ticosteroids with placebo or promethazine or metoclopramide in women with severe symptoms.
47 ze the likelihood of a complete examination, metoclopramide is a well-supported option.
48 p inform decision making when treatment with metoclopramide is considered in pregnancy.
49 iated with lower nausea scores on day 4 than metoclopramide (mean visual analog scale [VAS] score, 4.
50                               The effects of metoclopramide on the central nervous system (CNS) in pa
51                                              Metoclopramide or erythromycin is appropriate for initia
52 esser QT-prolonging potential (promethazine, metoclopramide, or prochlorperazine) and the 10-day risk
53 D, 2.9] for ondansetron vs 5.7 [SD, 2.3] for metoclopramide [P = .023]) but not episodes of emesis (5
54                                We used (11)C-metoclopramide PET imaging to elucidate the kinetic impa
55  male subjects underwent 2 consecutive (11)C-metoclopramide PET scans without and with ABCB1 inhibiti
56 ration, and adequate nutrition; ondansetron, metoclopramide, promethazine, and intravenous glucocorti
57 heart rate-corrected QT interval response to metoclopramide ( QTc of 160 ms).
58                For individual symptoms, oral metoclopramide ranked first for nausea (RR 0.46; 95% CI,
59    Regarding individual agents and response, metoclopramide (RR = 3.11, 95% C.I. = 1.39-6.98), cyproh
60            Results: In baseline scans, (11)C-metoclopramide showed appreciable brain distribution (V
61 by treatment with the widely used prokinetic Metoclopramide, suggesting a potential of this drug to a
62 observation, a pilot study was undertaken of metoclopramide therapy in patients with Diamond-Blackfan
63 nt for the following agents, decreasing from metoclopramide through cyproheptadine, sulpiride, propan
64                                        (11)C-metoclopramide transport by P-glycoprotein (P-gp; ABCB1)
65                                        (11)C-metoclopramide transport was selective for P-gp over BCR
66 ere were no significant associations between metoclopramide use and malformations overall (prevalence
67                                              Metoclopramide use in pregnancy was not associated with
68 ours (episodes of vomiting, 1 [IQR, 0-5] for metoclopramide vs 2 [IQR, 0-3] for promethazine [P = .81
69 uidar significantly enhanced microdose (11)C-metoclopramide VT (7.80 +/- 1.43 mLcm(-3)) with a 4.4-fo
70                                              Metoclopramide was not associated with increased risk of
71 ficant difference between corticosteroids vs metoclopramide was reported (emesis reduction, 40.9% vs
72                           Furthermore, (11)C-metoclopramide washout from the brain was estimated by d
73 ncy, ginger, pyridoxine, antihistamines, and metoclopramide were associated with greater benefit than
74 ms, pyridoxine-doxylamine, promethazine, and metoclopramide were associated with greater benefit than
75 s of mice, radiolabeled metabolites of (11)C-metoclopramide were determined in plasma and brain at 15
76 gs tested, but not by chronic treatment with metoclopramide, which has low antipsychotic efficacy but