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PubMed1998

The separation of ipratropium bromide and its related compounds.

Ipratropium bromide, the active component in ipratropium bromide metered dose inhalers (MDI), is used as a bronchodilator for the maintenance and treatment of bronchospasms associated with chronic obstructive pulmonary disease (COPD). The separation of ipratropium bromide, tropic acid, N-isopropyl-nor-atropine (NINA), 8-s ipratropium bromide, apo-ipratropium bromide and the excipients found in the formulation is important for analyzing raw materials and stability samples. We now report a reversed-phase HPLC method that can be used for separating ipratropium bromide and its related compounds, using an acetonitrile/potassium phosphate buffer (100 mM, pH 4.0) gradient mobile phase. Previous methods used for separating ipratropium bromide from its related compounds involved reversed-phase ion-pairing HPLC with UV detection. These methods exhibited less reproducibility, less ruggedness and required a high flow rate. The reported method is linear from 10 to 1000 micrograms ml-1 with a limit of detection of 60 ng ml-1. In addition, analysis of samples subjected to accelerated stability conditions showed that all degradants are resolved from the active component, resulting in stability-indicating assay. This assay also saved mobile phase and eliminated problems associated with ion-pairing reagents.

Bronchodilator Agents↗
PubMed2002

Derivation of an occupational exposure limit (OEL) for n-propyl bromide using an improved methodology.

n-Propyl bromide is an industrial solvent with increasing production volume due to its use as a replacement for fluorohydrocarbons. Therefore, the number of occupationally exposed workers is growing accordingly. This manuscript presents a thorough evaluation of available animal and human data to derive an occupational exposure limit (OEL) for n-propyl bromide. In addition, structure activity relationship within the homologous series of methyl, ethyl, and n-propyl bromide and an identical spectrum of effects caused by similar doses of 2-propyl bromide are used to increase the confidence of the analysis. The structure activity relationship was entirely consistent for acute and subchronic (neurologic, reproductive, and hematopoietic) toxicities and for mutagenic potency in that CH3Br was more toxic than CH3CH2Br, which in turn was more toxic than CH3CH2CH2Br in every case in all species studied, including humans. Animals appeared to be similarly susceptible as, or slightly more susceptible than, humans to n-propyl bromide's toxicity. An OEL (60-90 ppm) was derived from a limited human study and supported by an across-the-toxic-spectrum comparison of animal and human data for both n-propyl and 2-propyl bromide. A carcinogenic classification was not deemed necessary at the recommended OEL based on very low mutagenic potency and the consistent structure activity relationship across the homologous series of these alkyl bromides.

Carcinogens↗
PubMed2002

Cimetropium bromide in the treatment of crisis in infantile colic.

BACKGROUND: Treatment of infantile colic remains an open issue. In Italy, cimetropium bromide is used extensively to treat infantile colic. The aim of this randomized, double-blind, placebo-controlled clinical trial was to investigate the effectiveness and side effects of cimetropium bromide in the treatment of infants with colic crisis. METHODS: Ninety-seven infants with colic were enrolled. The diagnosis of infantile colic in healthy infants with regular growth, aged 15 to 60 days was made according to the criteria of Wessel. The infants were divided into two groups, one treated with cimetropium bromide (1.2 mg/kg) and the other treated with placebo at onset of each crisis for 3 days. Duration of crying and side effects were recorded daily in a structured diary for the 3 days of therapy. Statistical analysis was performed using the chi-square and t tests. RESULTS: Eighty-six infants completed the trial. The average duration of crying for each crisis was 17.3 +/- 12.6 minutes in the cimetropium bromide group and 47.5 +/- 28.5 minutes in the placebo group (P < 0.005). Response to cimetropium bromide was 74%. Response to placebo was 33% (P < 0.05). Side effects did not differ significantly between the two groups, except sleepiness, which increased in the infants treated with cimetropium bromide. CONCLUSION: Cimetropium bromide was more effective than placebo in reducing the duration of crying in children with infantile colic. The use of the anticholinergic drugs, aside from the dicyclomine because of its dangerous side effects, should be revaluated for treating infantile colic.

Colic↗
PubMed1982

Use of ipratropium bromide in patients with severe airways obstruction.

In ten adult patients with severe, partially reversible airflow obstruction due to asthma, with or without co-existent chronic bronchitis, the acute bronchodilator responses of ipratropium bromide (40 micrograms) and terbutaline (500 micrograms) from metered-dose inhalers, atropine methonitrate (2 mg) as a wet aerosol and placebo were compared in a double blind trial. Also the combination of ipratropium bromide and terbutaline aerosols was compared with both ipratropium and terbutaline alone in short-term and long-term studies. In the short-term study, all the drugs produced significant bronchodilatation compared with placebo. The responses to ipratropium bromide and terbutaline alone were not significantly different. The combination of ipratropium bromide with terbutaline did not produce significantly greater changes in the FEV1, SGaw or static lung volume than terbutaline alone. Atropine methonitrate however, produced significantly greater changes of the airway conductance (SGaw) and static lung volumes (TLC and RV) but not FEV1, when compared to ipratropium bromide. When administered over randomised periods of one month each there were no significant differences between the combination of ipratropium bromide and terbutaline and each drug alone in daily airflometer recordings, daily symptom scores or fortnightly spirometry and clinical assessment. It is concluded that ipratropium bromide, in the conventional dose of 40 microgramm by metered-dose inhaler produces safe, effective bronchodilatation. Its effect, however, did not significantly augment that of the beta adrenergic stimulant, terbutaline and was less than that of atropine methonitrate 2 mg by wet aerosol.

Aerosols↗
PubMed1985

Mechanism of the Heat Sensitization of Bacillus subtilis Spores by Ethidium Bromide.

Pretreatment with ethidium bromide (5 mug/ml) followed by a water wash had no effect on unheated Bacillus subtilis spores, but the viability of these spores after heating was much lower than that of similarly heated spores exposed to water alone. The fate of water- or ethidium bromide-treated spores, unheated or heated, was followed by allowing them to germinate and outgrow in a minimal or a complex liquid medium. Spores exposed to ethidium bromide and then heated (85 degrees C, 10 min) exhibited a developmental block during germination and outgrowth. Many of them were blocked at the stage when the bacterium emerged from the germinated spore. When 0.35 mug of ethidium bromide per ml was added to heated spores in the germination-growth medium, the outgrowth of heated spores was inhibited to the same extent as were pretreated spores. Ethidium bromide acted in the first hour of germination of heated spores since addition after this time was ineffective in inhibiting recovery events. Repair of heat-damaged spore DNA was detected during the first 2 h of germination. The addition of ethidium bromide (final concentration, 0.35 mug/ml) inhibited DNA repair during early outgrowth. Increased sensitivity of spores to heat after pretreatment with sublethal concentrations of ethidium bromide was due to the inhibition of the repair of heat-damaged DNA.

Journal Article↗
PubMed1996

Glutathione transferase activity and formation of macromolecular adducts in two cases of acute methyl bromide poisoning.

OBJECTIVES: To determine the activity of glutathione transferase and to measure the S-methylcysteine adducts in blood proteins, after acute inhalation exposure to methyl bromide. To examine the influence of the polymorphism of glutathione-S-transferase theta (GSTT1) on the neurotoxicity of methyl bromide. METHODS: Two workers acutely exposed to methyl bromide with inadequate respiratory protective devices were poisoned. Seven weeks after the accident, blood samples were drawn from both patients, for measurement of glutathione transferase activity in erythrocytes (conjugator status--that is, GSTT1 phenotype) and measurement of binding products of methyl bromide with blood proteins. Conjugator status was determined by a standard procedure. The binding product of methyl bromide, S-methylcysteine, was measured in globin and albumin. RESULTS: Duration and intensity of exposure were identical for both patients as they worked together with the same protective devices and with similar physical effort. However, one patient had very severe poisoning, whereas the other only developed mild neurotoxic symptoms. The first patient was a "conjugator" with normal glutathone transferase activity, whereas this activity was undetectable in the erythrocytes of the second patient, who consequently had higher concentrations of S-methylcysteine adduct in albumin (149 v 91 nmol/g protein) and in globin (77 v 30 nmol/g protein). CONCLUSIONS: Methyl bromide is genotoxic and neurotoxic. Its genotoxicity seems to be the consequence of the alkylating activity of the parent compound, and conjugation to glutathione has a protective effect. The data presented here suggest a different mechanism for methyl bromide neurotoxicity which could be related to the transformation of methylglutathione into toxic metabolites such as methanethiol and formaldehyde. If such metabolites are the ultimate toxic species, N-acetylcysteine treatment could have a toxifying rather than a detoxifying effect.

Acute Disease↗
PubMed1991

Effects of allergy and age on responses to salbutamol and ipratropium bromide in moderate asthma and chronic bronchitis.

The bronchodilating responses to 400 micrograms salbutamol and 80 micrograms ipratropium bromide were studied in 188 patients with chronic bronchitis (n = 113) or asthma (n = 75) and mild to moderate airflow obstruction (forced expiratory volume in one second (FEV1) above 50% but below 2 SD of predicted value) in a crossover study on two days a week apart. Both the patients with asthma and the patients with chronic bronchitis varied considerably in their responses to the salbutamol and the ipratropium bromide. The mean increase in FEV1 in the subjects with asthma was higher after salbutamol (0.371 or 18% of the prebronchodilator value) than after ipratropium bromide (0.26 1 or 13%). In chronic bronchitis there was no difference between the increase in FEV1 after salbutamol (0.161 or 7%) and after ipratropium bromide (0.191 or 8%). When patients were categorised into those with a better response to salbutamol 400 micrograms and those with a better response to ipratropium bromide 80 micrograms, patients with chronic bronchitis responded better in general to ipratropium bromide whereas asthmatic patients responded better to salbutamol. The response pattern was also related to allergy and age, allergic patients and patients under 60 being more likely to respond better to salbutamol 400 micrograms than non-allergic patients and older patients, who benefited more from ipratropium bromide 80 micrograms. The response pattern was not related to sex, smoking habits, lung function, bronchial reactivity, respiratory symptoms, or number of exacerbations during the preceding year.

Age Factors↗
PubMed1999

Acute effect of pretreatment with single conventional dose of salmeterol on dose-response curve to oxitropium bromide in chronic obstructive pulmonary disease.

BACKGROUND: An earlier study documented that, in patients with chronic obstructive pulmonary disease (COPD), addition of ipratropium bromide at the clinically recommended dose (40 microg) does not produce any further bronchodilation than that achieved with salmeterol 50 microg alone. However, the dose of ipratropium bromide needed to produce near maximal bronchodilation is several times higher than the customary dosage. The full therapeutic potential of combined salmeterol plus an anticholinergic drug can therefore only be established using doses higher than those currently recommended in the marketing of these agents. A study was undertaken to examine the possible acute effects of higher than conventional doses of an anticholinergic agent on the single dose salmeterol induced bronchodilation in patients with stable and partially reversible COPD. METHODS: Thirty two outpatients received 50 microg salmeterol or placebo. Two hours after inhalation a dose-response curve to inhaled oxitropium bromide (100 microg/puff) or placebo was constructed using one puff, one puff, two puffs, and two puffs-that is, a total cumulative dose of 600 microg oxitropium bromide. Dose increments were given at 20 minute intervals with measurements being made 15 minutes after each dose. On four separate days all patients received one of the following: (1) 50 microg salmeterol + 600 microg oxitropium bromide; (2) 50 microg salmeterol + placebo; (3) placebo + 600 microg oxitropium bromide; (4) placebo + placebo. RESULTS: Salmeterol induced a good bronchodilation (mean increase 0.272 l; 95% CI 0.207 to 0.337) two hours after its inhalation. Oxitropium bromide elicited an evident dose-dependent increase in forced expiratory volume in one second (FEV(1)) and this occurred also after pretreatment with salmeterol with a further mean maximum increase of 0.152 l (95% CI of differences 0.124 to 0.180). CONCLUSIONS: This study shows that acute pretreatment with 50 microg salmeterol does not block the possibility of inducing more bronchodilation with an anticholinergic agent when a higher than normal dosage of the muscarinic antagonist is used.

Administration, Inhalation↗
PubMed1986

Treatment of asthma bronchiale with a combination of ipratropium bromide and fenoterol.

The efficacies of inhaled doses of fenoterol 200 micrograms, ipratropium bromide 40 micrograms and their combination (200 + 40 micrograms) were compared in a double-blind, placebo-controlled cross-over study in 24 adult patients with stable asthma bronchiale. The tests were performed during 4 consecutive days. The change in bronchial obstruction was assessed by means of spirometry [forced expiratory volume in 1 s (FEV 1.0), forced vital capacity (FVC), peak expiratory flow (PEF)] and body plethysmography [thoracic gas volume (TGV), airway resistance (Raw)] measurements. The values of FEV% and specific airway conductance (SGaw) were calculated. The frequency of side-effects was recorded. During the treatment with the combination of ipratropium bromide and fenoterol the change in the mean SGaw differed highly significantly (p less than 0.001) from placebo in the initial bronchodilator response and at 3, 4 and 5 h. With fenoterol, compared to placebo, a highly significant difference in bronchodilator effect lasted for 4 h, with ipratropium bromide for 3 h. Similarly, a highly significant difference measured with FEV 1.0 during the medication with the combination of ipratropium bromide and fenoterol lasted for 4 h, with fenoterol alone for 2 h, and with ipratropium alone for 1 h. The most harmful side-effect in this group of asthmatics proved to be muscular tremor, caused most often by the combination of ipratropium bromide and fenoterol. The findings of this study suggest that the combination of ipratropium bromide and fenoterol gives a stronger bronchodilatation and a more prolonged effect in asthmatics than ipratropium bromide or fenoterol alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of inhaled ipratropium bromide on the airway response to methacholine, histamine, and exercise in patients with mild bronchial asthma.

We studied the bronchodilator and protective potency of inhaled ipratropium bromide in 33 patients with mild bronchial asthma. Patients were divided into 3 groups with similar baseline lung function and similar degrees of bronchial hyperresponsiveness to participate in the methacholine (study I, n = 9), histamine (study II, n = 9), or exercise challenge tests (study III, n = 18). At each session, 80 micrograms ipratropium bromide or placebo were inhaled in a double-blind randomized fashion. After ipratropium bromide, the mean specific airway resistance (SRaw) decreased from 10.4 to 4.9 (study I, p less than 0.01), 9.3 to 5.4 (study II, p less than 0.05), or 7.8 to 5.1 cm H2O.s (study III, p less than 0.01), respectively. Mean methacholine provocation concentrations necessary to increase SRaw by 100% were 0.43 after placebo and 8.60 mg/ml after ipratropium bromide (p less than 0.01), the respective values after histamine challenges were 1.32 mg/ml after placebo and 2.25 mg/ml after ipratropium bromide (p less than 0.01). In the exercise challenges, the individual responses varied largely with a mean maximum percent increase in SRaw of 231% after placebo and 173% after ipratropium bromide pretreatment (p less than 0.05). Therefore, ipratropium bromide offers bronchodilation and protection against a variety of stimuli and should more often be considered as an effective and safe drug for asthma treatment.

Adult↗
PubMed1998

Effects of formoterol, salmeterol or oxitropium bromide on airway responses to salbutamol in COPD.

We examined whether a pretreatment with formoterol, oxitropium bromide, or salmeterol might modify the dose-response curves to inhaled salbutamol in patients with stable and partially reversible chronic obstructive pulmonary disease (COPD). Sixteen outpatients with partially reversible, stable COPD received 24 microg formoterol, 50 microg salmeterol, 200 microg oxitropium bromide, or placebo on four non-consecutive days. Spirometric testing was performed immediately before inhalation of treatment and after 2 h. A dose-response curve to inhaled salbutamol was then constructed using doses of 100, 100, 200 microg and 400 microg--that is, a total cumulative dose of 800 microg. Dose increments were given at 20 min intervals with measurements being made 15 min after each dose. Formoterol, salmeterol, or oxitropium bromide elicited a significant increase in forced expiratory volume in one second (FEV1) compared with placebo (mean differences (L) = placebo 0.05; formoterol 0.34; salmeterol 0.27; oxitropium bromide 0.23). Dose-dependent increases in FEV1 were seen (mean values (L) before salbutamol and after a cumulative dose of 100, 200, 400, and 800 microg = placebo: 1.06, 1.28, 1.35, 1.39, 1.41; formoterol: 1.33, 1.37, 1.41, 1.44, 1.44; salmeterol: 1.30, 1.33, 1.36, 1.39, 1.42; oxitropium bromide: 1.27, 1.34, 1.37, 1.41, 1.40). Statistical analysis revealed no significant differences in FEV1 and forced vital capacity (FVC) responses to salbutamol after therapy with formoterol, salmeterol, or oxitropium bromide compared with placebo. This study clearly shows that a pretreatment with a conventional dose of formoterol, salmeterol, or oxitropium bromide does not preclude the possibility of inducing a further bronchodilation with salbutamol in patients suffering from partially reversible chronic obstructive pulmonary disease.

Adrenergic beta-Agonists↗
PubMed1982

[Determination of bromine contents in the blood and hair of workers exposed to methyl bromide by radioactivation analysis method].

The bromine contained in blood and hair samples obtained from workers exposed to methyl bromide was analyzed by non-destructive activation analysis. The samples were irradiated for 1 min in pneumatic irradiation facility of Kyoto University research reactor with an estimated thermal neutron flux density at 2 X 10(13)n X cm-2 X sec-1. The irradiation was counted with Ge(Li) detector. The duration of measurement of radionuclide bromine in blood and hair was 200 sec within 2-10 min after irradiation. The bromine content of serum sample obtained from a worker suspected of methyl bromide poisoning was found to be 412 micrograms/g on 13 days apart from exposure to methyl bromide. The biological half-life of bromine in this case was found to be about 16 days. Then bromine contents in serum and hair samples obtained from workers exposed to methyl bromide were found to be 1.7 and 2.6 times higher respectively than those of nonexposed workers. Any correlations of bromine contents were not observed between serum and hair samples obtained from workers exposed to methyl bromide, nor between bromine amount in the serum of workers exposed to methyl bromide, and the terms exposed to it, but statistically significant positive correlation was observed between bromine amount in the hair of workers exposed to methyl bromide and the terms exposed to it.

Adult↗
PubMed1984

Effect of nolinium bromide on vascular smooth muscle.

Nolinium bromide inhibits gastric acid secretion and gastrointestinal smooth muscle contraction. While the compound's gastric antisecretory action has been attributed in part to inhibition of gastric adenylate cyclase and the gastric proton-transport ATPase, the mechanism of nolinium bromide's relaxant effect on smooth muscle has not been elucidated. We have determined that nolinium bromide inhibits contraction of vascular smooth muscle, using isolated rabbit aortic strips. This report characterizes the specificity of this inhibition (by using several agonists) and its Ca2+ dependence (by using contractile conditions of known dependence on various Ca2+ pools). Nolinium bromide (50-200 microM) was a reversible, insurmountable inhibitor of contractions induced by Ca2+ (in 40 mM KC1 depolarizing medium) and norepinephrine, with IC50 values of 96 and 118 microM, respectively, for suppression of maximum contractile force. Contractions in response to Asn1Val5-angiotensin II in both 2.5 mM Ca2+ and 0 mM Ca2+ medium were also inhibited (IC50 value = 110 microM under both conditions). Initial contraction rates for all these conditions were depressed by nolinium bromide. Nolinium bromide inhibited equally the phasic (internal Ca2+-dependent) and tonic (external Ca2+-dependent) components of norepinephrine-induced contractions. These results extend the muscle relaxant profile of nolinium bromide to include, albeit with low potency, vascular smooth muscle, and show that its potency is similar in inhibiting the contractile response to three different stimuli: angiotensin II, Ca2+, and norepinephrine.

Angiotensin II↗
PubMed1991

Modification of the ethidium bromide exclusion procedure for evaluation of turkey semen.

The objective of the present study was to modify the ethidium bromide exclusion procedure in order to detect dead and labile turkey spermatozoa after 24 h storage at 7 C. In Experiment 1, fresh and stored spermatozoa were suspended in phosphate-buffered saline (PBS) ranging in osmolarity from 296 to 3 mOsm/kg H2O, each solution containing the same concentration of the nuclear fluorochrome ethidium bromide. In the 3 mOsm/kg H2O PBS, nearly all the fresh (98.3%) and stored (96.7%) spermatozoa were stained with ethidium bromide, indicating they were nonviable. Fresh spermatozoa revealed minor variation in the percentage of nonviable spermatozoa in the ethidium bromide exclusion procedure (ethidium bromide in PBS at 296 mOsm/kg H2O) (20.9%) and the remaining hypotonic PBS solutions (range 20.4 to 18.9%). In the stored semen samples a previously undetected subpopulation of more labile spermatozoa became apparent in hypotonic solutions with osmolarities of 122 and 56 mOsm/kg H2O. In Experiment 2, hen fertility was determined using fresh and stored semen. All hens were inseminated with 100 x 10(6) viable spermatozoa. Viability of stored semen was determined either by the original ethidium bromide exclusion procedure or using the sperm-stress test (ethidium bromide in PBS at 56 mOsm/kg H2O). The observations showed that adjusting the number of viable spermatozoa inseminated based on the percentage of viable sperm estimated from the sperm-stress test did not improve hen fertility over a 15-wk egg production period.

Animals↗
PubMed1993

[Neurotoxicity of methyl bromide--neuropathologic evaluation--preliminary study].

Methyl bromide exposure produces disorders of the central and peripheral nervous system. In the literature, there are many neuropathologic studies on the nervous system, especially on the central nervous system, of experimental animals intoxicated with methyl bromide presented. However, in our opinion, a variety of lesions of the nervous system described in the human methyl bromide intoxication have not been well reproduced in the experimental animals. In this study, male Wistar rats were subjected to a 6-hour exposure a day to methyl bromide at a concentration of 500 or 290 ppm 3 days a week for 3 to 8 weeks. The systematic neuropathologic studies of their central and peripheral nervous systems were carried out to reproduce the nervous system lesions in the human methyl bromide intoxication hitherto not produced in the experimental animals. Among the rats exposed to methyl bromide at a concentration of 500 ppm for 10 to 18 days, the axonal degeneration of myelinated fibers at the cervical level of the fasciculus gracilis, which probably corresponds to the degeneration of the spinal posterior column in humans, and the necrosis of the caudate-putamen and atrophy of neurons and pallor of the neuropile in caudate-putamen, thalamus and cingulate cortex, which probably correspond to the degenerative findings of the cerebrum in humans, were found. The rats exposed to methyl bromide at a concentration of 290 ppm for 8 weeks (24 days) did not show any noticeable abnormalities histologically.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Methyl bromide decreases excitability without having immediate toxic effects in rat hippocampal CA1 neurons in vitro.

Methyl bromide, a disinfectant gas amply used worldwide, is neurotoxic in humans and other mammals. To study its short-term effects on neurons, it was applied in aqueous solution to hippocampal slices of young rats (1.4 and 0.7 mM; for 8 minutes). Extracellular field recordings and intracellular microelectrode recordings from CA1 pyramidal neurons showed that the neurons stay viable for at least one hour after application of the mono-halomethane. However, a moderate, but consistent, irreversible decrease in synaptic excitability was observed. The intracellular recordings indicate that this may be attributed to a decrease in excitatory postsynaptic potentials. No effects were observed at 0.7 mM methyl bromide. Bromide, in a dose-dependent, partly reversible manner (during one hour), produced a similar decrease in excitability. Quantitatively, the action of bromide at 0.5 mM resembled the one seen with methyl bromide at the concentration of 1.4 mM. Since methyl bromide did not induce electrophysiologic changes consistent with evidence of neurotoxicity during one hour of observation it is concluded that it lacks immediate toxic effects on hippocampal rat neurons. Its neurotoxicity may be entirely due to metabolites or other indirect effects. The slight decrease in excitability may be due to the effect of bromide that is set free as tissue proteins and other cell molecules are methylated.

Animals↗
PubMed2004

[A case of acute distigmine bromide intoxication in the therapeutic dosage for treatment of underactive neurogenic bladder].

Distigmine bromide (Ubretid) is a long-acting anti-cholinesterase, widely used for the treatment of underactive neurogenic bladder and myasthenia gravis. Our study concerns a 73-year-old man treated with a potentially life-threatening cholinergic state due to distigmine bromide. He had been administered distigmine bromide orally for over two years at a daily dosage of 10 mg as a treatment for underactive neurogenic bladder. He suddenly developed diarrhea and consciousness disturbance during treatment of his urinary tract infection. Bradycardia and miosis were noted. Blood examination revealed extremely low levels of the plasma cholinesterase activity. The condition was diagnosed as distigmine bromide intoxication. All cholinergic symptoms disappeared in several days after the administration of distigmine bromide was terminated. Cholinergic crisis due to overdosage with anticholinesterases is well known, and the myasthenic patients are usually supervised in the early stages of dosage regulation to guard against the possibility of cholinergic crisis. However the use of oral distigmine bromide, even in therapeutic doses for urinary retention, could result in cholinergic crisis. We therefore conclude that extreme caution must be used in administering distigmine bromide.

Aged↗
PubMed1996

Selective determination of chloride and bromide ions in serum by cyclic voltammetry.

Voltammetric determination of chloride and bromide ions in serum was made using a one-body type Ag electrode, whose surface was covered with a dialysis membrane for preventing interference from proteins. This determination was based on measurement of the charge of the reduction wave of silver halide formed on the Ag electrode surface in a halide ion solution during a cathodic potential sweep. In this method, depending on the potential sweep range, the charge of the reduction wave of AgI, AgI + AgBr, or AgI + AgBr + AgCl can be measured. Here, the method was used to determine the chloride and bromide ions in artificial serum. Linear concentration ranges were 1.0 x 10(-2)-2.4 x 10(-1) M for chloride ions and 5.0 x 10(-3)-1.8 x 10(-2) M for bromide ions. The correlation coefficient was 0.999 in each case. The relative standard deviation for chloride ion (1.0 x 10(-1) M) was 1.9% (n = 10), and that for bromide ion (1.5 x 10(-2) M) was 2.5% (n = 10). Bromide ions at a relatively high concentration as the component of serum had no effect on the determination of the chloride ion in the serum. This method is thus useful for the selective determination of chloride and bromide ions in serum.

Blood Substitutes↗