Fatal cold medication intoxication in an infant. (1/10)

The case history and toxicological findings of an infant fatality involving pseudoephedrine, brompheniramine, and dextromethorphan are presented. Concentrations of brompheniramine and dextromethorphan were measured in both postmortem blood and liver specimens using a gas chromatograph equipped with a nitrogen-phosphorus detector. Brompheniramine and dextromethorphan were 0.40 mg/L and 0.50 mg/L, respectively, in the blood sample and 0.16 mg/kg and 0.57 mg/kg in the liver sample. The concentration of pseudoephedrine in blood and liver specimens was measured using gas chromatography-mass spectrometry and was determined to be 14.4 mg/L in the blood and 16 mg/kg in the liver. Additionally, a baby bottle allegedly administered to the infant was collected as evidence and sent to the Medical Examiner's Office for evaluation. The amounts of total brompheniramine, dextromethorphan, and pseudoephedrine remaining in the baby bottle were 1.4 mg, 9.4 mg, and 40 mg, respectively.  (+info)

Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema. (2/10)

Acute ultraviolet light B (UVB) injury is associated with dermal mast cell histamine release. The possibility that histamine-stimulated prostaglandin (PG) synthesis could be a mechanism for irradiation erythema was therefore examined using human skin explants. Explants responded to UV irradiation (120 mJ/cm2) with a fivefold increase in synthesis of prostaglandins E2, F2 alpha and 6-keto PGF1 alpha. Incubating explants with the H1 antihistamines brompheniramine (50 microM) or pyrilamine (30 microM) inhibited PG release from irradiated explants 63 +/- 4.9% (mean +/- SEM) 6 h after UV exposure. Antihistamines did not affect PG synthesis in control explants. Irradiation increased the histamine concentration in explant conditioned medium only 50% over basal values, suggesting that irradiation enhanced histamine responsiveness. Explants were therefore incubated with exogenous histamine. In irradiated explants, PG synthesis was stimulated threefold by 3 microM histamine. Unirradiated explants' PG synthesis was unaffected by histamine. Enhanced histamine sensitivity was also examined in epidermal cell cultures. In irradiated cultures, histamine sensitivity was again markedly potentiated: as little as 1 microM histamine stimulated significant PGE2 release and the response to 10-30 microM histamine was increased six to eight times compared with that of unirradiated cultures. These studies demonstrate that endogenous histamine stimulates PG synthesis in human skin after UV injury by potentiation of histamine-induced prostaglandin release. Potentiated agonist responses induced by UV exposure may contribute to the effects of UVB irradiation injury and in particular to irradiation erythema.  (+info)

Surface degradation of composite resins by acidic medicines and pH-cycling. (3/10)

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Muscarinic cholinergic binding in rat brain. (4/10)

Binding sites with high affinity and specificity for [(3)H]quinuclidinyl benzilate (QNB) are present in homogenates of rat brain. The characteristics of the binding sites resemble those of muscarinic cholinergic receptors. Specific binding is saturable with respect to [(3)H]QNB and tissue concentration and is time-, temperature-, and pH-dependent. The bimolecular rate of association (2.0 x 10(8) M(-1) min(-1)) and dissociation (1.2 x 10(-2) min(-1)) at 35 degrees indicate a dissociation constant of 60 pM and a density of 65 pmol/g of brain. Muscarinic antagonists and agonists displace specific [(3)H]QNB binding, while nicotinic and non-cholinergic drugs possess little affinity for [(3)H]QNB-binding sites.  (+info)

Effect of the antihistamines, brompheniramine maleate and triprolidine hydrochloride, on performance in man. (5/10)

1 Effects of brompheniramine maleate (4 and 12 mg) and triprolidine hydrochloride (2.5 and 10 mg) on visuo-motor coordination, and on subjective assessments of performance, well-being and sleep were each studied in six subjects at 0.5, 1.5, 3.0, 5.0 and 7.0 h after ingestion. The doses refer to immediate and sustained release preparations respectively. 2. Triprolidine hydrochloride (2.5 mg) had an immediate effect on performance which persisted to 3.0 h, and the sustained release preparation (10 mg) impaired performance from 1.5 to 5.0 h. Brompheniramine maleate (4 mg) impaired performance from 1.5 to 3.0 h, and the sustained release preparation (12 mg) impaired performance at 1.5 h. There were no consistent changes in the subjective assessments of performance, or of well-being and sleep. 3. The studies emphasize the variable effects of antihistamines on performance, and suggest that effects on performance of sustained release preparations may be similar to those of the usual form. Sustained release preparations may provide an advantage in clinical practice if the antihistaminic activity is prolonged.  (+info)

Event recording in a clinical trial of a new medicine. (6/10)

In a double-blind trial of the effect of zimelidine on weight and appetite 24 obese patients were allocated at random to receive either zimelidine or placebo for eight weeks followed by the alternative treatment for eight weeks. Possible adverse effects were elicited by asking patients at weekly intervals whether they had experienced any symptoms or ailments and recording all such "events" on a special form. A conventional checklist of symptoms was also used. Among 19 patients who completed the trial the two methods of recording yielded similar patterns of events. Of symptoms not on the checklist, insomnia was more common during treatment with zimelidine. Event recording was found to be a practicable and convenient method of detecting possible adverse effects.  (+info)

Attenuation of pethidine-induced antinociception by zimelidine, an inhibitor of 5-hydroxytryptamine reuptake. (7/10)

1 The effect of selective inhibition of 5-hydroxytryptamine (5-HT) re-uptake by fluoxetine and zimelidine on morphine- and pethidine-induced antinociception was studied in rats. The hot plate (55 degrees C) and tail flick test procedures for measurement of analgesia were employed to assess antinociception. 2 Pretreatment with fluoxetine and zimelidine potentiated the antinociceptive effect of morphine (4.5 mg/kg, as base); zimelidine was without effect on a lesser dose of morphine (3.0 mg/kg, as base). 3 Pretreatment with zimelidine but not fluoxetine, significantly attenuated pethidine-induced antinociception (24 mg/kg, as base) and prevented the expression of pethidine-induced antinociception at a lesser 10 mg/kg (as base) dose of pethidine. 4 These and other results support (a) a role for 5-HT in the expression of morphine-induced antinociception, and (b) a different mode of antinociceptive action of morphine and pethidine. The role of 5-HT in pethidine-induced antinociception remains unclear.  (+info)

Differences in performance impairment due to brompheniramine maleate as a function of the sustained-release system. (8/10)

1 study examined whether different sustained release systems would cause variation in the effect of an antihistamine, brompheniramine maleate 10 mg, upon mood and psychomotor performance. Two commercial preparations were examined, one giving linear release (LR) of the drug over time, the other releasing the drug in a non-linear fashion (NLR). 2 Thirty-six males were allocated to four separate groups receiving either the drug with LR, drug with NLR, placebo or drug-free control. Single dosage of the drug occurred at 08.30 h and subjects completed mood inventories and performed serial choice reaction time and visual search tasks at 1 h, 2.75 h, 5.5 h and 7.25 h post dosage. 3 The NLR system significantly increased feelings of unco-ordination at 2.75 h and significantly slowed reaction time at both 2.75 and 5.5 h post dosage. The LR system significantly slowed reaction time only at 5.5 h but increased pausing in serial choice performance at that time. Neither system impaired visual search. 4 Results suggest that two preparations having identical active constituents may vary in their effects on psychomotor performance and mood as a function of their sustained release systems. A system giving linear release of the drug can reduce the early post-dosage performance decrement associated with a non-linear release system.  (+info)

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