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1 re on standard acid-suppressive therapy with ranitidine.
2 rmation yield of NDMA from chloramination of ranitidine.
3 e decomposition of the methylfuran moiety of ranitidine.
4 re chlorinated and hydroxylated analogues of ranitidine.
5 acid and 20 animals fed pH 7 formula without ranitidine.
6 e, and group 2 patients received intravenous ranitidine.
7 nytoin or carbamazepine), dexamethasone, and ranitidine.
8 Sucralfate was given to 47, and 49 received ranitidine.
9 d quinidine, drugs structurally unrelated to ranitidine.
10 mpromise or transfusion); all were receiving ranitidine.
11 e, patients received an intravenous bolus of ranitidine (0.5 mg/kg) followed by a continuous infusion
13 with omeprazole at bedtime (P = NS); 4 with ranitidine, 150 mg at bedtime; and 3 with ranitidine, 30
16 d, placebo-controlled, double-blind trial of ranitidine 300 mg (orally twice daily) in subjects with
17 th ranitidine, 150 mg at bedtime; and 3 with ranitidine, 300 mg at bedtime (P < 0.05, ranitidine vs.
19 The most commonly used agents for SUP were ranitidine (31%), famotidine (24%), sucralfate (24%), an
20 ell+/-SEM are reported: control 68.3+/-37.8; ranitidine 38.4 +/-94.2; lansoprazole 14.6+/-84.4; and o
21 nes that produce NDMA at high yields, namely ranitidine, 5-(dimethylaminomethyl)furfuryl alcohol, N,N
22 ated premedication regimen that consisted of ranitidine 50 mg, diphenhydramine 50 mg, and a single 20
24 etics of decomposition of the pharmaceutical ranitidine (a major precursor of NDMA) during chloramina
26 , and the H2 histaminergic receptor agonist, ranitidine, also hindered recognition of the familiar ju
27 nd the H2 histaminergic receptor antagonist, ranitidine, also hindered the recognition of the familia
28 animals, either alone or in combination with ranitidine (an alcohol dehydrogenase inhibitor) while th
29 ncluding histamine H(2) receptor antagonist (ranitidine), analgesic (paracetamol), opiate (codeine),
32 hloramine, nucleophilic substitution between ranitidine and monochloramine led to byproducts that are
34 ed with a minimum 3 mg/kg/day of intravenous ranitidine and the dose should be titrated to a gastric
35 gonists such as diphenhydramine, loratadine, ranitidine, and cimetidine, but has modest affinity for
36 fter exposure to the H2 receptor antagonist, ranitidine, and identified an antibody that reacted with
38 omeprazole at bedtime with that of a dose of ranitidine at bedtime on residual nocturnal acid secreti
41 niramine, but not the H2 receptor antagonist ranitidine, blocks the effects of histamine in this prep
42 fect of the histamine-2-receptor antagonist, ranitidine, both at the cellular and mediator levels in
43 269 pg/mL (p < .05) in patients treated with ranitidine, but not in patients treated with placebo.
47 e continuous infusion, the mean steady-state ranitidine concentration associated with gastric pH > or
48 he American population would need to consume ranitidine daily to match the NDMA loadings from laundry
49 antihistamine treatments with pyrilamine or ranitidine did not impair tolerance and neither did IgE-
50 in this study may used to design an initial ranitidine dosage regimen that targets a gastric pH > or
52 Gastric pH was determined at the end of the ranitidine dosing interval, 1 hr after the dose, and at
53 orothiazide (during the whole treatment) and ranitidine-fenofibrate (at short periods) in the BTV bio
56 24 hrs of scheduled intermittent intravenous ranitidine for stress ulcer prophylaxis were enrolled in
61 ent of patients who received <3 mg/kg/day of ranitidine had poor gastric pH control as compared with
63 patients, after treatment with cisapride or ranitidine in 2 patients, and after Nissen fundoplicatio
67 servation implies that the N(CH3)2-moiety of ranitidine is transferred to NDMA without being chemical
68 the delta(2)H value of the N(CH3)2-group of ranitidine measured by quantitative deuterium nuclear ma
69 line or an antisecretory dose of omeprazole, ranitidine, or cimetidine, were intragastrically adminis
70 nificant difference between lansoprazole vs. ranitidine (p< .01), and omeprazole vs. ranitidine (p< .
71 vs. ranitidine (p< .01), and omeprazole vs. ranitidine (p< .05), and no significant difference betwe
73 sess the impact of multiple risk factors and ranitidine prophylaxis on the development of stress-rela
74 doses of the histamine 2-receptor antagonist ranitidine (RAN) and bacterial lipopolysaccharide (LPS)
75 of the tertiary amines, mianserin (MIA) and ranitidine (RAN), exhibiting similar compound specificit
78 cokinetic variables, the dose of intravenous ranitidine required to target 373 ng/mL as the average s
79 1 and 2 receptor antagonists pyrilamine and ranitidine, respectively, did not significantly alter NT
83 ly the parietal cell signal was inhibited by ranitidine, showing the absence of PAC1 on parietal cell
84 onsumption of a standard dose of the antacid ranitidine substantially increased NDMA and its chlorami
86 Infectious complications totaled 128 in the ranitidine-treated group and 50 in the sucralfate-treate
87 of infectious complications associated with ranitidine use and total infectious complications were a
94 nts enrolled in a randomized trial comparing ranitidine with sucralfate for gastritis prophylaxis wer
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