Disease relevance of Dimedrol

• Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability [1].
• Pretreatment of the ileal segments with either benadryl + cimetidine, indomethacin, or methylprednisolone did not significantly alter the permeability increase induced by regional ischemia [2].
• Premedication with diphenhydramine did not decrease the incidence of infusion-related hypersensitivity reactions [3].
• Diphenhydramine in the differential diagnosis of neuroleptic-induced oral-facial dyskinesia [4].
• No animal pretreated with diphenhydramine exhibited thrombocytopenia or respiratory dysfunction [5].

Psychiatry related information on Dimedrol

• Initial and steady-state effects of diphenhydramine and loratadine on sedation, cognition, mood, and psychomotor performance [6].
• Drugs had no significant effects on the stimulus-locked P1 and N2 ERPs or on behavioral response latencies, but tended to affect post-error reaction time (RT) latencies in opposite ways (haloperidol decreased and diphenhydramine increased RTs) [7].
• We measured the initial and steady-state effects of diphenhydramine, a first-generation antihistamine, and loratadine, a second-generation antihistamine, by means of a comprehensive battery of psychometric tests that mirror real-world tasks [6].
• As in young adults, there was minimal psychomotor impairment after oral and after intravenous diphenhydramine [8].
• A chronic schizophrenic patient with a neuroleptic-induced dystonic reaction and akathisia, both of which were unresponsive to benztropine and diphenhydramine, derived rapid therapeutic benefit from diazepam [9].

High impact information on Dimedrol

• Acute dystonia. An unusal reaction to diphenhydramine [10].
• Diphenhydramine, an H1 receptor antagonist, had no effect [11].
• In tissues from +/+ mice, antigen caused increases in Isc which were significantly inhibited by antagonists to histamine (diphenhydramine) and serotonin (ketanserin), by a cyclooxygenase inhibitor (piroxicam) and by a neurotoxin (tetrodotoxin) [12].
• Histamine (5 X 10(-6)-10(-4) M) contracted mesangial cells, and the H1 antagonist diphenhydramine (10(-4) M) but not the H2 antagonist cimetidine (10(-4) M) prevented histamine (10(-4) M) induced contraction [13].
• We conclude that diphenhydramine can prevent histamine-induced pulmonary edema and can prevent and reverse increased lung vascular permeability caused by histamine, and that histamine effects on lung vascular permeability are H1 actions [1].

Chemical compound and disease context of Dimedrol

• Grade 3-4 hypersensitivity reactions occurred in 4 of 13 courses at the first 2 dose levels, but premedication with dexamethasone, diphenhydramine, and cimetidine resulted in only 3 additional Grade 2 reactions in the next 70 courses [14].
• In addition, our patient developed noncardiogenic pulmonary edema despite pretreatment with prednisone and diphenhydramine, administered because of a past history of a similar reaction [15].
• Pretreatment with pertussis toxin (0.25 microg/mouse i.c.v.) prevented pyrilamine, diphenhydramine and promethazine antinociception [16].
• When compared with placebo, caffeine significantly increased the number of correct responses and decreased response times, whereas diphenhydramine decreased the number of correct responses and increased response times [17].
• The effect of pretreatment with pertussis toxin at the doses of 0.25 and 0.50 microg per mouse ICV on the amnesic effect produced by baclofen (0.1 4 mg kg(-1) i.p.), diphenhydramine (15-30 mg kg(-1) i.p.) and scopolamine (0.5-5 mg kg(-1) i.p.) was investigated in the mouse passive avoidance test [18].

Biological context of Dimedrol

• Histamine-induced P-selectin upregulation was inhibited by the H1 receptor antagonist diphenhydramine, whereas the H2 receptor antagonist cimetidine had no effect [19].
• Diphenhydramine attenuated the coronary vasoconstriction but potentiated the positive inotropic response [20].
• The ratio of the change in oxygen extraction to the change in oxygen consumption caused by histamine was significantly increased by diphenhydramine [20].
• This inhibition of chemotaxis could be abolished by pretreatment with metiamide, an H-2 receptor antagonist, and levamisole, but not by diphenylhydramine, an H-1 receptor antagonist [21].
• The kinetics and psychomotor effects of diphenhydramine were investigated in Orientals and Caucasians [22].

Anatomical context of Dimedrol

• After the loading of the hypothalamus with [3H]histamine, release of label by K+ depolarization in vitro (an indirect index of release from the neuronal histamine pool) was readily obtained at all ages and was unaffected by diphenhydramine administration [23].
• The reduction in the flux of rolling leukocytes translated into fewer adherent leukocytes with diphenhydramine or PB1 [24].
• Initial incubation of the membranes in the presence of the H1 receptor antagonist diphenhydramine virtually abolished the DEAE-cellulose peak, while incubation with cimetidine, the H2 receptor antagonist, blocked the phosphocellulose peak [25].
• Lymphocytes incubated with histamine and diphenhydramine produced LCF but neither LyMIF, whereas cells incubated with histamine in the presence of cimetidine produced both LyMIF but not LCF [26].
• Intravenous administration of indomethacin, 2 mg/kg, or continuous intravenous infusion of prostacyclin, 50 ng/kg per min, failed to prevent histamine-induced coronary artery spasm (four of four and eight of eight cases, respectively), yet the spasm was all but prevented by intravenous pretreatment with diphenhydramine at a dose of 1 mg/kg [27].

Associations of Dimedrol with other chemical compounds

• They underwent active catecholamine depletion (via oral administration of 5 g alpha-methylparatyrosine) or sedation-controlled, sham catecholamine depletion (via oral administration of 250 mg diphenhydramine hydrochloride), during a 2-day observation [28].
• As a result, the time span of intravenous (IV) infusion of taxol was routinely prolonged to 6 hours or beyond, and premedication with diphenhydramine, dexamethasone, and cimetidine was initiated [29].
• These included diphenhydramine, catalase, heparin, hyaluronidase, hydrocortisone, cysteine, N-acetylcysteine, lidocaine, vitamin E, and superoxide dismutase [30].
• The increase in leukocyte flux associated with CMP 48/80 was blocked by diphenhydramine (H1-receptor antagonist) and an anti-P-selectin Ab (PB1.3), but not by the 5-lipoxygenase inhibitor, MK 886 [24].
• In the first, 12 subjects received single oral doses of phenindamine (25 mg), diphenhydramine (50 mg), terfenadine (60 mg), or placebo in a four-way crossover study [31].

Gene context of Dimedrol

• Clinically relevant drug interactions may occur between diphenhydramine and many CYP2D6 substrates, particularly those with a narrow therapeutic index [32].
• Therefore, P450 isozymes involved in N-demethylation, a main metabolic pathway of diphenhydramine, were identified by a liquid chromatography-mass spectrometry method developed in our laboratory [33].
• DPH inhibited the GH response to both GHRH (AUC: 453.9 +/- 104.7 vs 1223.7 +/- 202.6 micrograms*min/l, p < 0.05) and HEX (922.0 +/- 215.4 vs 1636.4 +/- 267.5 micrograms*min/l, p < 0.05), although the HEX-induced GH rise persisted higher than that induced by GHRH (p < 0.05) [34].
• Tripelennamine, chlorpheniramine, and diphenhydramine showed no inhibitory effects on CYP2C9 [35].
• Cimetidine, an H2 receptor antagonist, blocked chemoattractant production, whereas diphenhydramine, an H1 receptor antagonist, did not [36].

Analytical, diagnostic and therapeutic context of Dimedrol

• Premedication with diphenhydramine was instituted for the remainder [3].
• RESULTS: The patients with premenstrual dysphoric disorder experienced a return of symptoms 24 hours after treatment with metergoline but not diphenhydramine (active placebo) [37].
• RESULTS: Of the 426 patients, 114 (27%) received diphenhydramine during hospitalization and shared similar baseline characteristics including age, sex, delirium risk, and Mini-Mental State Examination scores compared with nonexposed patients [38].
• Measurements included baseline and daily assessments including Mini-Mental State Examination scores, Confusion Assessment Method ratings, direct observations for medical devices (urinary catheter or physical restraints), and blinded medical record extractions for diphenhydramine use [38].
• Subjects received single oral doses of diphenhydramine, 50 mg, and placebo in this double-blind crossover study [39].

References