Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACETAZOLAMIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed1990

Tissue electrical admittance (electrolyte concentration) in rat renal medulla: effects of furosemide and acetazolamide.

Fluctuations of total electrolyte concentration in the renal medulla were estimated from continuous measurement of tissue electrical admittance (reciprocal impedance) by means of needle electrodes placed in the kidney of anaesthetized rats. To compare effects of two diuretic agents with different sites of action, rats received either furosemide, 0.3 mg/kg i.v. followed by an infusion at 0.3 mg/kg.h, or acetazolamide, a single injection of 10 mg/kg. At this dosage similar increases in renal excretion were obtained with either drug. After furosemide (a loop diuretic) admittance fell sharp within first 10 min, then partly recovered and reached a plateau 35 min after injection. Acetazolamide (inhibitor of proximal reabsorption) caused no changes in admittance compared to the pattern observed in untreated control animals. We conclude that dissipation of tissue electrolytes from the renal medulla is not simply a consequence of diuresis and natriuresis but depends critically on the site of transport inhibition in the nephron.

Acetazolamide↗
PubMed1993

Acetazolamide in dominant cystoid macular dystrophy. A pilot study.

UNLABELLED: Eight patients (four men, four women), with low visual acuity caused by autosomal dominant cystoid macular dystrophy, were treated daily with oral 250 mg dose acetazolamide. Treatment ranged from two to 17 months. None of these eight patients had improvement of visual acuity of more than 0.1. CONCLUSION: Treatment with 250 mg acetazolamide appears not to be an effective therapy for cystoid macular oedema in dominant cystoid macular dystrophy. The electroretinography b-wave/a-wave ratio was normal. The primary lesion in dominant cystoid macular dystrophy remains obscure.

Acetazolamide↗
PubMed2002

Acetazolamide therapy for symptomatic plateau waves in patients with brain tumors. Report of three cases.

In this report, the authors describe three patients with malignant gliomas who experienced paroxysmal neurological symptoms triggered by standing. The symptoms were attributed to acute elevations of intracranial pressure, an uncommon phenomenon called "plateau waves." In each instance, the attacks occurred despite the fact that the patient was receiving dexamethasone therapy and stopped promptly with the addition of acetazolamide. Acetazolamide, an orally administered carbonic anhydrase inhibitor, appears to be a specific and effective therapy for this uncommon neurological disorder.

Acetazolamide↗
PubMed1998

Acetazolamide-responsive hereditary paroxysmal ataxia: report of a family.

Hereditary paroxysmal ataxia is a rare dominantly inherited disorder characterized by recurrent attacks of cerebellar ataxia, dysarthria, and nystagmus. Each attack lasts from several minutes to few hours or days. Usually there are no motor difficulties between attacks. We report a patient who had had recurrent ataxic episodes since early childhood. Four members of the family over two generations had similar attacks. There were no abnormalities in the laboratory studies including plasma amino acid, lactate, pyruvate, and EEG. Treatment with acetazolamide resulted in complete abolition of the attacks. Because of its dramatic response to acetazolamide, the recognition of this rare disorder is important.

Acetazolamide↗
PubMed1999

Effects of acetazolamide on passive and active transport of fluorescein across the normal BRB.

PURPOSE: To investigate the effect of the carbonic anhydrase inhibitor acetazolamide (AZM) on passive permeability and active transport of fluorescein across the blood-retina barrier in healthy subjects. The study may have implications for the understanding of the edema-reducing effect of AZM. METHODS: The effect of AZM on the blood-retina barrier function was assessed by differential vitreous spectrofluorometry using fluorescein as a tracer. The study included fourteen healthy subjects in a randomized double-masked crossover trial with 3 days' treatment with AZM (500 mg/d) and placebo, respectively. The two examinations were separated by at least 1 week. Fluorescein concentration was determined separately from its metabolite fluorescein glucuronide. The passive permeability of fluorescein was determined by computerized modeling and curve-fitting to the preretinal curve and the plasma concentration curve obtained at 30 to 60 minutes after the injection of fluorescein. The unidirectional permeability due to outward active transport from vitreous to blood was estimated from the preretinal gradient and the plasma concentration at 7 to 10 hours after injection. RESULTS: Treatment with AZM was associated with significant increases in passive permeability and unidirectional permeability of fluorescein. For the passive permeability the increase was on average 0.3+/-0.4 nm/s (mean+/-SD; range, -0.8-1.0 nm/s), and for the unidirectional permeability the increase was on average 7.4 nm/s+/-7.0 (mean+/-SD; range, -3.3-19.0 nm/s). CONCLUSIONS: Acetazolamide caused an increase in passive permeability. Unidirectional permeability was increased by AZM, indicating a stimulation of the outward active transport of fluorescein. It has been proposed that the edema-reducing effect of AZM is due to stimulated ion and fluid removal from the retina to the choroid. The results of this study are consistent with AZM affecting the blood-retina barrier with stimulation of at least one ion transport mechanism.

Acetazolamide↗
PubMedDate not supplied

Acetazolamide-induced Gerstmann syndrome.

Acute confusion induced by acetazolamide is a well known adverse drug reaction in patients with renal impairment. We report a case of acetazolamide-induced Gerstmann syndrome in a patient with normal renal function, to highlight predisposing factors that are frequently overlooked.

Acetazolamide↗
PubMed2000

[Fatal anaphylactic reaction after oral acetazolamide (diamox) for glaucoma].

A woman aged 66 was prescribed acetazolamide (Diamox) in the outpatient clinic because of glaucoma. She went into irreversible anaphylactic shock with massive pulmonary oedema, probably due to a cross reaction in sulphonamide allergy. Before prescribing acetazolamide, the physician should inquire about sulphonamide allergy because of the related chemical structure of the substances. Such an allergy should be regarded as a contraindication.

Acetazolamide↗
PubMed1975

The effect of acetazolamide and carbonic anhydrase inhibition on erythrocyte 2,3-diphosphoglycerate content and metabolism.

Experiments were designed to test the hypothesis that the change in erythrocyte 2,3-diphosphoglycerate (2,3-DPG) content which occurs when metabolic acidosis is induced by prolonged inhibition of carbonic anhydrase in vivo is the same as that which occurs with the induction of other types of metabolic acidosis states. 1) Thirteen-hour infusions of nondiuretic doses of a potent carbonic anhydrase inhibitor, acetazolamide (Diamox) did not alter erythrocyte 2,3-DPG levels in rats. 2) In vitro incubation of whole blood from rats for 10 days with high concentrations of two carbonic anhydrase inhibitors failed to alter the red cell content of 2,3-DPG. 3) Purified human carbonic anhydrase B had no phosphatase activity on 2,3-DPG and it appears unlikely that the enzyme hydrolyzes other phosphate esters of the erythrocyte which could indirectly alter 2,3-DPG content. 4) Acetazolamide administered in diuretic doses for 8 days to rats induced a metabolic acidosis which was accompanied by a decrease in erythrocyte 2,3-DPG. The change in 2,3-DPG content was similar to that produced by other methods of producing metabolic acidosis, namely NH4Cl treatment and nephrectomy. It appears that changes in 2,3-DPG content associated with effects of carbonic anhydrase inhibition can be ascribed to the metabolic acidosis resulting from the action of these drugs on the kidney.

Acetazolamide↗
PubMed1976

Studies of aqueous humor dynamics in man. V. Effects of acetazolamide and isoproterenol in young and old normal volunteers.

Young and old volunteers received acetazolamide systemically or isoproterenol topically. Although the responses of the two groups of volunteers were quite similar for acetazolamide, they differed significantly for isoproterenol. It is suggested that a normal aging change is altered responsiveness of the site of aqueous production and of the outflow pathways to topical isoproterenol. The site of aqueous production becomes less responsive; the outflow pathways become more responsive.

Acetazolamide↗
PubMed1976

The rates of movement of Na+, Cl-, and HCO-3 from plasma to posterior chamber: effect of acetazolamide and relation to the treatment of glaucoma.

The rates of accession of sodium and chloride, and the formation of bicarbonate into the posterior chamber have been studied in normal dogs, and following complete inhibition of carbonic anhydrase by acetazolamide, 50 mg. per kilogram. Sodium accession approximated fluid formation rate and was reduced 30 per cent by acetazolamide. Bicarbonate formation was reduced to one-third the control value by the inhibitor; chloride was unaffected. Reduction of accession was 1.9 mM per minute for sodium and 1.6 mM per minute for bicarbonate, showing that these are stoichiometrically linked. These results, together with other data in fish and rabbit, support the idea that bicarbonate formation is a general function of ciliary epithelia and, through its effect on sodium, is the basis for a considerable component of fluid movement into the eye. Inhibition of bicarbonate formation appears to be the pharmacological basis for the treatment of glaucoma by carbonic anhydrase inhibitors.

Acetazolamide↗
PubMedDate not supplied

Qualitative versus quantitative assessment of cerebrovascular reactivity to acetazolamide using iodine-123-N-isopropyl-p-iodoamphetamine SPECT in patients with unilateral major cerebral artery occlusive disease.

BACKGROUND AND PURPOSE: Qualitative measurement of regional cerebrovascular reactivity (rCVR) to acetazolamide with single-photon emission CT (SPECT) has been widely used to determine the severity of hemodynamic impairment. We attempted to validate the accuracy of qualitative assessment by using SPECT to detect reduced rCVR compared with rCVR determined quantitatively in patients with unilateral major cerebral artery occlusion. METHODS: Regional cerebral blood flow was assessed with iodine-123-N-isopropyl-p-iodoamphetamine ((123)I-IMP) at rest and after acetazolamide activation in 133 patients with previously symptomatic, unilateral internal carotid or middle cerebral artery occlusion. Quantitative values were calculated by using the (123)I-IMP autoradiographic method and analyzed for each cerebral hemisphere as the percentage change in rCBF between resting and activation studies (%(Hem)). Qualitative rCVR was determined for the target hemisphere distal to the occlusion as the cerebral-interhemispheric asymmetry index (AI(Hem)) and as an index of flow difference between the target cerebral and ipsilateral cerebellar hemispheres (FI(Hem-Cbl)). Values 2 SDs below the mean in healthy volunteers were defined as decreased. RESULTS: Fair agreement was observed between %(Hem) and both AI(Hem) change (resting vs activation, kappa = 0.409) and FI(Hem-Cbl) change (resting vs activation, kappa = 0.440). When %(Hem) was assumed to represent the true determinant of assessing rCVR, AI(Hem) change and FI(Hem-Cbl) change demonstrated sensitivities of 68% and 78%; specificities, 72% and 76%; positive predictive values, 48% and 56%; false-positive incidences, 28% and 24%; and false-negative incidences, 32% and 22% for detecting patients with reduced rCVR, respectively. CONCLUSION: Subgroups of patients with hemodynamic impairment cannot be accurately defined by using rCVR qualitatively measured with SPECT.

Acetazolamide↗
PubMed1992

[Serous retinal detachment. Value of acetazolamide].

The effect of acetazolamide in the treatment of chronic macular edema has been well established. The pharmacologic action of this product suggested possible efficacy in the treatment of serous retinal detachment. We studied 38 patients presenting with serous retinal detachments of various etiologies divided into four groups: age related macular degeneration, central serous chorioretinopathy or diffuse epithelial retinopathy, epiretinal membranes, and other causes. Treatment with acetazolamide, at a dosage of 0.375 g/day, in three divided doses was proposed for five weeks. We observed a reduction of metamorphopsia in all cases, a stability or even an improvement of visual acuity, and a resorption of serous retinal detachment confirmed by decreased pooling of fluorescein on the angiographic examination. Considering each etiology, clinical and angiographic findings demonstrated the value of this treatment, although this study was not prospective. The encouraging results observed in many cases, raise hopes concerning the treatment for these diseases, usually not amenable to treatment.

Acetazolamide↗
PubMed2003

In vitro study on sustained release capsule formulation of acetazolamide.

In the present study formulation of sustained release capsule of acetazolamide 250 mg was tried using nonpareil seeds. Nonpareil seeds were coated with drug, polyvinylpyrrolidone, glyceryl monostearate, microcrystalline wax, and glyceryl distearate either individually or in combination to achieve sustained release capsule 250 mg. In successful formulation 20% drug coated pellets and 80% wax coated pellets were taken. Wax coated pellets for successful formulation contained coating of microcrystalline wax and glyceryl distearate on drug coated pellets of the same concentration of 1.6% w/w. Successful formulated sustained release capsule 250 mg of acetazolamide was compared in in vitro study with theoretical sustained release formulation suggested by wagner and one marketed sustained release capsule 250 mg. Formulated capsule showed result superior to or on par with marketed capsule. For successful formulation pellets were filled in '1' size hard gelatin capsule and stability study was carried out in hot air over at room temperature and 45 degrees C for 5 weeks. The formulation was found stable in respect of drug content and release rate.

Acetazolamide↗
PubMed1990

Treatment of chronic macular oedema with low dosage acetazolamide.

In this study, 46 eyes of 40 patients exhibiting chronic macular oedema have been treated with 125 mg Acetazolamide. The eyes with pseudophakia and the eyes with retinitis pigmentosa obtained considerable beneficial help from this treatment. Our findings indicate that Acetazolamide may offer the clinician an alternative approach in the treatment of central vision threatening chronic macular oedema.

Acetazolamide↗
PubMed1990

[Use of acetazolamide in external hydrocephalus in infants].

External hydrocephalus is believed to be benign but published cases do not clearly establish this prognosis. Five children with typical external hydrocephalus were given acetazolamide. Head circumference measurements or other investigations demonstrated therapeutic effectiveness in four of the five patients. Although this series is too small to establish that acetazolamide avoided external hydrocephalus-related adverse events, the drug's outstanding tolerance and anatomic effectiveness justify widespread use in all patients with CSF resorption disorders.

Acetazolamide↗
PubMed1990

[Acetazolamide: an alternative to shunting in normal pressure hydrocephalus? Preliminary results].

From a series of 15 consecutive patients with a normal-pressure hydrocephalus examined over 2 years. 10 showed frank improvement with oral acetazolamide. The drug was a first-choice treatment in 5 cases and was given up after a spinal tap in 5 cases. Clinical response occurred even in the most severe cases, although it was slightly less impressive for intellectual impairment than for gait or bladder disturbances. Tolerance was excellent with a daily dose of 250 to 500 mg. The benefit remained stable on a more than 1 year follow-up in 8 cases. We suggest that acetazolamide should be tried in patients with normal pressure hydrocephalus prior to considering shunting.

Acetazolamide↗
PubMed1977

[Investigations on the effect of various doses of acetazolamide (Diamox) on intraocular pressure (author's transl)].

In the scope of a clinical-experimental study on 12 patients with chronic open-angle glaucoma we proved that a reduction in the individual doses of Acetazolamide (Diamox) brought no reduction in the effect on raised intraocular pressure when the frequency of application was the same. Daily doses of 3 X 125 mg were compared with those of 3-250 mg and 2 X 500 mg (Retardform). A additional trial on 6 patients with a daily dose of 3 X 62.5 mg also showed an obvious effect. The possibilities of long term treatment with acetazolamide are discussed.

Acetazolamide↗
PubMed1983

Methazolamide and acetazolamide in acute mountain sickness.

Methazolamide (150 mg/d) was as effective as acetazolamide (500 mg/d) in preventing the symptoms of acute mountain sickness in 20 subjects ascending to 4985 m. PaO2 and oxygen saturation levels were similar on the two drugs but the fall in PaCO2 was greater on acetazolamide. Paraesthesiae, a side-effect of carbonic anhydrase inhibitors, tended to be less at high altitude on methazolamide and was significantly less when taking 100 mg/d at low altitude. It is likely that paraesthesiae is similar on the two drugs when given in doses that affect blood gases equally.

Acetazolamide↗