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At least 523 records · Page 29Linked to original sources
PubMed1993

Glycopyrronium bromide blocks differentially responses mediated by muscarinic receptor subtypes.

To analyse the potency of glycopyrronium bromide in blocking responses mediated via subtypes of muscarinic receptors in vitro, we tried to determine its equilibrium dissociation constants at prejunctional muscarinic receptors inhibiting the twitch response of rabbit vas deferens (presumed M1 type), at M2 (paced at left atria), M3 (guinea pig ileum) muscarinic receptor subtypes and at the muscarinic receptor of the rabbit iris sphincter (not M1-M4, not m5). Glycopyrronium bromide shifted to the right the curve for inhibition of the twitch response induced by the agonist McN-A-343, and the methacholine-induced curves for inhibition of rat atrial contraction, and for tonic contraction of guinea pig ileum and rabbit iris sphincter. Glycopyrronium bromide blocked with very high potency (> 11, apparent -log KB) the response in rabbit vas deferens. Its affinity was low (9.09) for the M2 subtype, and intermediate (10.31 or 10.13) for the ileal M3 and the atypical iris muscarinic receptor subtype, respectively. Except at the receptors in rabbit vas deferens, the blockade of agonist effect appeared to be of simple competitive type. In conclusion, glycopyrronium bromide is about 10 or 100 fold more potent in preventing a response to activation of the prejunctional receptor in rabbit vas deferens than in blocking an M3 or M2 muscarinic receptor subtype, respectively, in vitro. The low affinity for M2 receptors may, in part, explain the low incidence of unwanted tachycardia in therapy. The drug failed to discriminate between an M3 receptor and the atypical rabbit iris sphincter receptor.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1979

Alkylation of RNA by vinyl bromide metabolites in vitro and in vivo.

[1,2-14C]Vinyl bromide was incubated with rat liver microsomes, NADPH, and polyadenylic acid, polycytidylic acid, or RNA, respectively. Part of the adenosine moieties in RNA or in polyadenylic acid were alkylated and labelled 1,N6-ethenoadenosine structures were formed. Part of the cytidine moieties were converted into 3,N4-ethenocytidine. In addition, a further unidentified cytidine alkylation product was observed which was not seen in experiments using [1,2-14C]vinyl chloride. When rats were exposed to [1,2-14C]vinyl bromide, radioactive ethenoadenosine and ethenocytidine were present in hydrolysates of liver RNA. A further alkylation product was observed in the RNA hydrolysates which did not occur in experiments using [14C]vinyl chloride. The data show that vinyl bromide metabolites alkylate nucleic acids; although in general in this respect vinyl bromide and vinyl chloride behave similarly, some differences are observed in the alkylation behaviour of both compounds.

Alkylation↗
PubMed1975

Biogenesis of mitochondria. 43. A comparative study of petite induction and inhibition of mitochondrial DNA replication in yeast by ethidium bromide and berenil.

The action of ethidium bromide and berenil on the mitochondrial genome of Saccharomyces cerevisiae has been compared in three types of study: (i) early kinetics (up to 4 h) of petite induction by the drugs in the presence or absence of sodium dodecyl sulphate; (ii) genetic consequences of long-term (8 cell generations) exposure to the drugs; (iii) inhibition of mitochondrial DNA replication, both in whole cells and in isolated mitochondria. The results have been interpreted as follows. Firstly, the early events in petite induction differ markedly for the two drugs, as indicated by differences in the short-term kinetics. After some stage a common pathway is apparently followed because the composition of the population of petite cells induced after long-term exposure are very similar for both ethidium bromide and berenil. Secondly, both drugs probably act at the same site to inhibit mitochondrial DNA replication, in view of the fact that a petite strain known to be resistant to ethidium bromide inhibition of mitochondrial DNA replication was found to have simultaneously acquired resistance to berenil. From consideration of the drug concentrations needed to inhibit mitochondrial DNA replication in vivo and in vitro it is suggested that in vivo permeability barriers impede the access of ethidium bromide to the site of inhibition of mitochondrial DNA replication, whilst access of berenil to this site is facilitated. The site at which the drugs act to inhibit mitochondrial DNA replication may be different from the site(s) involved in early petite induction. Binding of the drugs at the latter site(s) is considered to initiate a series of events leading to the fragmentation of yeast mitochondrial DNA and petite induction.

Amidines↗
PubMed1988

Reduction by cimetropium bromide of the colonic motor response to eating in patients with the irritable bowel syndrome.

Cimetropium bromide is an antimuscarinic compound with antispasmodic properties. Its effect on meal-stimulated sigmoid motor activity in 30 patients with the irritable bowel syndrome, mainly with pain and constipation, has been evaluated. The mechanical activity of the sigmoid colon was recorded with a probe with three open-tipped tubes ending 45, 30, and 15 cm from the anal margin. After a recording period of 60 min, 5 mg cimetropium bromide or saline was given i.v., according to a randomized, double-blind design 5 min before a 1000 calorie meal, and motility was then recorded for 2 h. The meal caused a significant increase in motor activity for 90 min in the saline-treated group. Cimetropium bromide abolished the peak of motor activity 10-20 min after the meal and significantly inhibited postprandial colonic motility for at least 2 h (p less than 0.01). This effect provides a rationale for the use of cimetropium bromide in treatment of the irritable bowel syndrome.

Colon, Sigmoid↗
PubMed1993

Bronchodilator effects of oxitropium bromide, fenoterol, and their combination in normal subjects.

Oxitropium bromide is a quaternary anticholinergic compound based on the scopolamine molecule instead of atropine. The purpose of this study was to compare the bronchodilator effects of oxitropium, a beta 2-agonist fenoterol, and their combination, on basal bronchomotor tone in normal subjects. Partial flow-volume curve (PEF25), was measured as an index representing bronchomotor tone. The cumulative dose-response curve of oxitropium bromide inhaled from a metered-dose inhaler was determined in eleven normal subjects. Measurement of PEF25 was repeated every 1 h for 8 h after inhalation of oxitropium (200 micrograms), fenoterol (200 micrograms), their combination or placebo in six normal subjects in a randomized, single-blinded, placebo-controlled, cross-over manner. As the percentage increase in PEF25 by 200 micrograms of oxitropium (45 +/- 6%) was equivalent to nearly 80% of that by dose of 1,600 micrograms (58 +/- 8%), the dose of 200 micrograms is thought to be appropriate. The group mean percentage increase in the PEF25-time course curve was significantly greater after treatment with the combination than with placebo (p < 0.001) and fenoterol (p < 0.001) but not with oxitropium bromide, while the increase in PEF25 following the combination was significantly greater than that following oxitropium bromide after 2 and 3 h. These findings indicate that in normal subjects oxitropium has a powerful bronchodilator effect and that the addition of oxitropium to fenoterol caused greater bronchodilation in normal subjects.

Adult↗
PubMed1980

Plasma levels and urinary excretion of orally administered propantheline bromide in man.

After a single oral dose of 30 or 60 mg of propantheline bromide peak plasma levels of the drug were reached within 2 h in six healthy men. Mean peak plasma concentrations were 20.6 and 53.1 ng/ml after 30 mg and 60 mg respectively. The mean apparent absorption and elimination half-lives after 30 mg dose were 0.22 and 1.57 h respectively, and similar half-lives were found at the higher dose level. There was a dose related change in plasma levels and AUCinfinity of the drug, and some 3% to 4% of the administered dose of propantheline bromide was excreted unchanged in urine at each dose level. Comparison of the plasma levels and urinary excretion of the drug with those seen after i.v. administration in an earlier study indicated an apparently low systemic availability of orally administered propantheline bromide. There was tentative evidence of a qualitative relationship between the oral dose administered, plasma concentrations and the effects of propantheline bromide on salivary excretion.

Administration, Oral↗
PubMed2003

On-line speciation of bromine and bromide using sequential injection analysis with spectrophotometric detection.

An on-line procedure for the simultaneous determination of bromine and total bromine (bromine+bromide oxidised to bromine) is proposed, which lead to the determination of bromide by subtraction. Phenol red was used as chromogenic reagent for bromine and total bromine after bromide was oxidised to bromine by Chloramine T. The linear range found is 1-10 mg L(-1) with a detection limit of 0.6 mg L(-1) for bromine, and a linear range of 0.8-15 mg L(-1) with a detection limit of 0.4 mg L(-1) for total bromine. The calculated RSD for bromine is less than 0.8% and for total bromine less than 0.7%. The system is fully computerised and able to run 30 samples per hour with an automated rinsing step that eliminates sample carry-over. The results for both bromine and bromide from the proposed sequential injection analysis (SIA) system compare favourably with standard manual methods and statistical evaluation proves no significant difference between the results of the proposed SIA system and the standard method at the 95% confidence level. The presence of other halides was found not to interfere.

Journal Article↗
PubMed2004

Clinical efficacy of distigmine bromide in the treatment of patients with underactive detrusor.

PURPOSE: The aim of this study was to assess the clinical efficacy of distigmine bromide, an anticholinesterase agent, deemed to improve detrusor function thereby restoring normal voiding patterns in patients suffering from detrusor underactivity. MATERIALS AND METHODS: A total of 27 patients (11 men and 16 women) with poor detrusor function were included in the study. The diagnosis was established using pressure-flow studies. All patients received distigmine bromide at a dose of 5 mg three times daily for 4 weeks and re-attended for a follow-up urodynamic investigation. The results of baseline pressure-flow studies were compared to those after completion of treatment. RESULTS: Treatment with distigmine bromide resulted in a statistically significant reduction of residual volume and percent residual volume, obviating the need for intermittent self-catheterisation in 11 patients. In addition, maximum flow rate and detrusor pressure at maximum flow increased, although not significantly. The drug was generally well tolerated by the majority of patients. CONCLUSION: Distigmine bromide shows clinical efficacy in patients with poor detrusor function and may therefore be used alternatively in selected cases.

Adolescent↗
PubMed1987

Ethidium bromide: destruction and decontamination of solutions.

Ethidium bromide in water, TBE buffer, Mops buffer, and cesium chloride solution may be completely degraded by reaction with sodium nitrite and hypophosphorous acid. Only non-mutagenic reaction mixtures were produced. Destruction was greater than 99.8% in all cases; the limit of detection was 0.5 micrograms ethidium bromide per milliliter of solution. Ethidium bromide also may be removed completely from the above solutions by using Amberlite XAD-16 resin. The limit of detection was 0.05 micrograms ethidium bromide per milliliter of solution (0.27 micrograms/ml when cesium chloride solution was used).

Decontamination↗
PubMed1989

An ethidium bromide-agarose plate assay for the nonradioactive detection of cDNA synthesis.

Ethidium bromide was used to determine the success of cDNA synthesis reactions. Since ethidium bromide in agarose can be used to quantitate RNA and DNA, conditions under which the greater fluorescence of double-stranded DNA (dsDNA) is utilized were devised to assay dsDNA synthesis from mRNA. Ethidium bromide at 5 micrograms/ml in agarose allowed quantitative detection of cDNA in the range of 0.03 to 0.0015 microgram. Sodium dodecyl sulfate had an adverse effect on the measurement of cDNA. Subsequent cDNA analysis by alkaline gel electrophoresis and staining in 5 micrograms/ml ethidium bromide allowed accurate and rapid sizing of cDNA and required only 0.1-0.05 microgram cDNA.

DNA↗
PubMed1991

An assay for proteinases and their inhibitors based on DNA/ethidium bromide fluorescence.

Proteinases and their inhibitors have become the subject of intense research interest recently, since they control a multitude of very important biological processes, from the development of lambda phage to hypertension in humans. We have developed a simple and sensitive assay for detecting the activity of proteinases and of their proteinase inhibitors. The assay is based on ethidium bromide fluorescence, according to the following principles: (i) Ethidium bromide increases its fluorescence by 25-fold when it intercalates between base pairs of double-stranded DNA. (ii) Histones prevent this large increase in fluorescence by binding with high affinity to DNA thus blocking ethidium bromide intercalation. (iii) A proteinase that digests histones will make more DNA available for ethidium bromide intercalation, thereby producing an increase of fluorescence. Proteinase activity can easily be determined, in the presence of a DNA/histone complex, from the rate of ethidium fluorescence increase. In contrast, activity of a proteinase inhibitor is quantitated by the inhibition of fluorescence gain in the presence of a known amount of proteinase. This assay is rapid, simple, inexpensive, and, at the same time, accurate and sensitive enough to allow quantitation of nanogram amounts of various broad-specificity proteinases and their inhibitors. We show some possible applications of the assay (i) in testing column fractions during protein purifications, (ii) quantitation of alpha 1-antitrypsin in human serum, and (iii) detection of proteinase activity in cell extracts.

DNA↗
PubMed1978

Sidedness of inhibition of energy transduction in oxidative phosphorylation in rat liver mitochondria by ethidium bromide.

Ethidium bromide, a new type of inhibitor of energy transduction in oxidative phosphorylation, inhibited ATP synthesis in intact mitochondria but not in submitochondrial particles, the latter being inside-out relative to the membranes of intact mitochondria. Ethidium bromide incorporated inside the submitochondrial particles inhibited ATP synthesis in the particles. The decrease of the membrane potential by valinomycin (plus KCl) inhibited only slightly the energy-dependent binding of ethidium bromide to the mitochondria. The present results show clearly that ethidium bromide inhibited energy transduction in oxidative phosphorylation by acting on the outer side (C-side) of the inner mitochondrial membrane, perhaps by neutralizing negative charges created on the surface of the C-side, and that it had no inhibitory activity on the inner side (M-side) of the membrane. Th present results show also that the energy-dependent binding of ethidium is not due to electrophoretic transport down the membrane potential; ethidium may bind to negative charges on the surface of the C-side. The present study suggest that an anisotropic distribution of electric charge in the inner mitochondrial membrane is an intermediary high energy state of oxidatvie phosphorylation.

Adenosine Triphosphate↗
PubMed1980

Controlled trial of the effect of repeated administration of ipratropium bromide on ventilatory function of patients with severe chronic airways obstruction.

A trial was designed to assess whether repeated administration of ipratropium bromide for two weeks produced greater improvement than was obtained after a single dose. The effect of ipratropium bromide was compared with that of a placebo during a double-blind cross-over randomized trial in patients with advanced chronic airways disease in a stable state. Ipratropium bromide and placebo were both administered by metered dose inhaler for 14 days. There was a slight statistically significant improvement of conductance, thoracic gas volume, FEV1 and VC after inhalation of ipratropium bromide, but repeated doses of the drug did not produce progressive improvement.

Airway Obstruction↗
PubMed1979

Ethidium bromide enhancement of frameshift mutagenesis caused by photoactivatable ethidium analogs.

Ethidium azide analogs (3-amino-8-azido-ethidium monoazide and ethidium diazide) have been developed as photosensitive probes in order to analyze directly the reversible in vivo interactions of ethidium bromide. Our preliminary observations [11], relating the mutagenic potential of the monoazide analog of ethidium, have been extended and refined, using the highly purified ethidium azide analogs [5]. A number of physical-chemical studies indicate that the monoazide analog interaction with nucleic acids, prior to photolysis, resembles remarkably the interaction of the parent ethidium (unpublished). It was anticipated, therefore, that competition by ethidium for the ethidium monoazide mutagenic sites in Salmonella TA1538 would be observed when these drugs were used in combination. Previous results in fact showed a decreased production of frameshift mutants when ethidium bromide was added to the ethidium monoazide in the Ames assay [1]. However, more extensive investigations, reported here, have shown that this apparent competition was the result of neglecting the toxic effects of ethidium monoazide and its enhanced toxocity in the presence of ethidium bromide. Conversely, an enhancement of the azide mutagenesis and toxicity for both the mono- and diazide analogs was seen when ethidium bromide was used in combination with these analogs.

Azides↗
PubMed1989

Long-term effect of ipratropium bromide and fenoterol on the bronchial hyperresponsiveness to histamine in children with asthma.

We studied the effects of the anticholinergic ipratropium bromide (40 micrograms three times daily) and the beta-agonist, fenoterol (0.2 mg three times daily), both administered by powder inhaler, on bronchial hyperresponsiveness (BHR) to histamine in children, aged 7 to 15 years with mild stable asthma and limited bronchoconstriction who had a highly increased BHR. The double-blind, randomized, parallel study was conducted and performed in spring and early summer. BHR and FEV1 were measured on two occasions, before the start of treatment and monthly thereafter for 4 months. Symptoms, peak expiratory flow, and concomitant medication were registered daily. Nine of the 12 patients receiving ipratropium bromide and all eight patients receiving fenoterol completed the study. Patients completing treatment had few symptoms and were in a stable condition throughout the treatment period. Neither the administration of ipratropium bromide nor fenoterol resulted in a significant change of BHR. We concluded that long-term treatment with ipratropium bromide or fenoterol had no effect on BHR in children with mild stable asthma.

Adolescent↗
PubMed1992

Ipratropium bromide (Atrovent nasal spray) reduces the nasal response to methacholine.

We investigated the efficacy of local ipratropium bromide on methacholine-induced nasal secretions in a double-blind, placebo-controlled experiment. Twenty subjects with perennial rhinitis received a total intranasal dose of 21, 42, 84, and 168 micrograms of ipratropium bromide or placebo in each nostril. One hour later, filter paper disks were used to deliver increasing doses of methacholine and to collect secretions from the left septum. Concomitantly, symptoms of rhinorrhea and nasal congestion were scored. Compared with doses of placebo, all doses of ipratropium bromide significantly reduced the methacholine-induced increase in nasal secretion weights and symptoms of rhinorrhea (p less than 0.01). The highest dose was significantly more effective than the lower doses in reducing secretion weights (p = 0.01). We speculate that ipratropium bromide may prove beneficial for the treatment of rhinorrhea in perennial rhinitis. Furthermore, increasing the delivered dose to 168 micrograms may increase efficacy without augmenting side effects.

Adult↗
PubMed1987

Inhalation of methyl bromide gas induces mitotic recombination in somatic cells of Drosophila melanogaster.

The fumigant methyl bromide was evaluated for genotoxicity in the somatic wing-spot assay of Drosophila melanogaster. Third instar larvae trans-dihybrid for mwh and flr3 were exposed to varying concentrations (0-16 mg/l) of the gas for 1 h. Following this exposure via inhalation, the larvae were placed into vials containing Instant Medium. 7 days after the exposure, the adult flies in the vials were collected, and their wings were scored under 400X magnification for the presence of clones of cells possessing malformed wing-hairs. Such clones appeared as mwh-flr3 twin spots and single spots of either mwh or flr3 phenotype. Exposure to methyl bromide was found to result in the positive induction of both twin spots and large (greater than 2 cells) single spots. For each endpoint, a significant exponential association was obtained between concentration and frequency of spots per wing. Methyl bromide was found to be a negative inducer of small (1-2 cells) single spots at all concentrations except 16 mg/l where a positive effect was observed. Because twin spots arise exclusively from mitotic recombination, methyl bromide was identified as having recombinogenic activity in the somatic tissue of Drosophila larvae.

Animals↗
PubMed1996

Comparative evaluation of the prophylactic effect of slow release devices containing homidium bromide and isometamidium on Trypanosoma congolense in rabbits.

Two consecutive experiments were carried out to evaluate the prophylactic effect of biodegradable slow release devices (SRD), containing either isometamidium or homidium bromide. Rabbits subcutaneously implanted with SRD, were challenged with different Trypanosoma congolense stocks at regular intervals between 1 and 6.5 months after treatment. In a first experiment the efficacy of two types of isometamidium-SRD (poly(D,L-lactide) and poly(D,L-lactide-co-glycolide)) was compared with the classical intramuscular (i.m.) injection of the drug. Since the former polymer gave an average protection period, which was much longer than the other isometamidium formulation, a second experiment was carried out to evaluate the prophylactic effect of poly(D,L-lactide) SRD, containing either isometamidium or homidium bromide, with that of the i.m. injections of the same drugs at a dose of 1 mg kg-1. The average protection period of the homidium bromide SRD was significantly longer than that of the i.m. injected drug (112 vs. 49 days). No significant difference was obtained, however, when isometamidium was administered either as a SRD or as an i.m. injection. The average protection periods were, respectively, 106 +/- 37 days and 84 +/- 18 days. When breakthrough isolates derived from SRD-treated animals were compared with the original stocks of T. congolense, the former showed some loss of sensitivity to homidium bromide. No difference in sensitivity was observed, however, for isometamidium.

Animals↗