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PubMed1990

Refined structure of the acetazolamide complex of human carbonic anhydrase II at 1.9 A.

The binding of acetazolamide to human carbonic anhydrase II (HCA II) has been investigated by X-ray crystallography. The atomic positions of the enzyme inhibitor complex have been refined at 1.9 A resolution using the least squares refinement program package PROLSQ. The crystallographic R-factor is 17.6%. The bound inhibitor is clearly resolved in the active site of the enzyme. The acetazolamide amine group is bound as a fourth ligand to the zinc ion, the other three are all histidine residues. In addition to van der Waals' interactions and the previously described binding of the sulphonamide group, the inhibitor forms a hydrogen bond from the carbonyl oxygen of the acetylamido group to the amino group of Gln 92.

Acetazolamide↗
PubMed1993

Localization of acetazolamide-resistant carbonic anhydrase III in human and rat choroid plexus by immunocytochemistry and in situ hybridisation.

Carbonic anhydrase is an essential metabolic enzyme of the central nervous system and has an important role in the production and regulation of cerebrospinal fluid. Although it has been known for over 30 years that inhibition of the enzyme with acetazolamide dramatically but not completely reduces the production of cerebrospinal fluid, the precise mechanism of the inhibitory action has been only recently revealed. In this study we present evidence that apart from carbonic anhydrase II, the catalytically highly active isozyme, carbonic anhydrase III, an acetazolamide-resistant and kinetically different isozyme could be demonstrated in the epithelial cells of the developing and mature rodent and human choroid plexuses. Both isozymes express intense immunostaining revealed with specific antisera, and by using in situ hybridisation histochemistry, carbonic anhydrase III mRNA was also observed. Since the kinetic properties and proportion of brain carbonic anhydrase III in the human choroid plexus are not revealed the function of this isozyme in choroid plexus is still to be determined.

Acetazolamide↗
PubMed1992

Determination of acetazolamide in human urine samples by reversed-phase high-performance liquid chromatography in the presence of xanthines.

A simple, rapid and selective high-performance liquid chromatographic assay for the determination of acetazolamide in urine samples is described. After extraction with ethyl acetate, the drug is chromatographed on an HP-Hypersil ODS-C18 column with a mobile phase of acetonitrile-phosphate buffer (pH 3) and ultraviolet detection at 275 nm. The efficiency of the extraction, the linearity and the reproducibility of the method permit the evaluation of acetazolamide urinary excretion a long time after its administration.

Acetazolamide↗
PubMed1994

Application of column-switching techniques to the determination of medium polarity drugs: determination of acetazolamide in urine.

A column-switching system for the determination of the medium polarity diuretic acetazolamide in urine, has been designed. An Hypersil ODS C18, 30 microns (20 x 2.1 mm I.D.) pre-column was used for the pre-concentration and separation of acetazolamide from the biological matrix. The most polar urinary compounds were removed by washing the pre-column with a phosphate buffer solution (pH 3), and the fraction of eluate containing the analyte was switched to a LiChrospher RP C18, 5 microns (125 x 4 mm I.D.) analytical column, where it was chromatographed using gradient elution with acetonitrile-water, and detected at 275 nm. The most apolar urinary compounds were directly discarded by means of a second switching valve. Under these conditions the recovery of drug was 96 +/- 5% in the 0.50-100.0 micrograms/ml concentration range. The limit of detection was 10 ng/ml, the total analysis time being less than 8 min.

Acetazolamide↗
PubMed2006

Renal circulatory effects of acetazolamide in patients with essential hypertension.

BACKGROUND: Reports indicate that acetazolamide (ACZ) induces the vasodilation of all vessels in animal models, as well as in small and medium kidney vessels in animal models. However, the effect of ACZ on the renal circulation of patients with essential hypertension remains unknown. In this study we examined the effects of a carbonic anhydrase inhibitor, acetazolamide (ACZ), on the renal circulation of patients with essential hypertension. METHODS: We directly infused 1000 mg of ACZ into the main renal arteries of 10 patients with essential hypertension who had undergone cardiac catheterization. We then evaluated the effects of ACZ upon heart rate, renal artery blood pressure (BP), renal artery cross-sectional area, renal Doppler blood flow velocity, renal blood flow (RBF), and renal vascular resistance (RVR). RESULTS: The infusion of ACZ was not associated with any significant changes in heart rate or in systolic or diastolic BP. However, the velocity-time integral was increased by 11.1% +/- 7.2%, from 17.6 +/- 1.8 to 20.0 +/- 3.7 cm (P = .009); RBF was increased by 39% +/- 21%, from 300 +/- 43 to 422 +/- 96 mL/min/m(2) (P = .002); and RVR was reduced by 38% +/- 20% from 24,351 +/- 2,291 to 17,651 +/- 2,731 dynes.sec.cm(-5) (P < .01). In contrast the cross-sectional area of the renal artery did not change. CONCLUSIONS: The results of the present study demonstrated that ACZ has a potent vasodilatory effect on the renal circulation of patients with essential hypertension, leading to an obvious decrease in RVR and an increase in RBF.

Acetazolamide↗
PubMed2006

Comparative efficacy of HgCl2 with candidate aquaporin-1 inhibitors DMSO, gold, TEA+ and acetazolamide.

Aquaporin-1 (AQP1) inhibitors are predicted to have multiple clinical applications. Hg(++) is a non-specific and toxic AQP1 blocker. We compared compounds with reported AQP1 inhibition activity, including DMSO, Au(+++), Ag(+), tetraethylammonium and acetazolamide. Water permeability was measured by stopped-flow light scattering in erythrocytes and volume marker dilution in epithelial cells. Au(+++) inhibited AQP1 with IC50 approximately 14 microM, similar to 10 microM for Hg(++). DMSO slowed osmotic equilibration; however, the apparent inhibition was due to 'osmotic clamp' rather than AQP1 inhibition. Neither tetraethylammonium nor acetazolamide (to 10 mM) inhibited AQP1. Our data indicate the need to identify new AQP1 inhibitors.

Acetazolamide↗
PubMed2004

Preparation and in vitro evaluation of Eudragit microspheres containing acetazolamide.

The aim of this study was to prepare and evaluate Eudragit (RS and RL) microspheres containing acetazolamide. Microspheres were prepared by solvent evaporation method using acetone/liquid paraffin system. The influence of formulation factors (stirring speed, polymer:drug ratio, type of polymer, ratio of the combination of polymers) on particle size, encapsulation efficiency and in vitro release characteristics of the microspheres were investigated. The yields of preparation and the encapsulation efficiencies were high for all formulations the microspheres were obtained. Mean particle size changed by changing the polymer:drug ratio or the stirring speed of the system. Although acetazolamide release rates from Eudragit RS microspheres were very slow and incomplete for all formulations, they were fast from Eudragit RL microspheres. When Eudragit RS was added to Eudragit RL microsphere formulations, release rates slowed down and achieved the release profile suitable for peroral administration.

Acetazolamide↗
PubMed2006

Preparation of acetazolamide composite microparticles by supercritical anti-solvent techniques.

The possibility of preparation of ophthalmic drug delivery systems using compressed anti-solvent technology was evaluated. Eudragit RS 100 and RL 100 were used as drug carriers, acetazolamide was the model drug processed. Compressed anti-solvent experiments were carried out as a semi-continuous or a batch operation from a liquid solution of polymer(s)+solute dissolved in acetone. Both techniques allowed the recovery of composite particles, but the semi-continuous operation yielded smaller and less aggregated populations than the batch operation. The release behaviour of acetazolamide from the prepared microparticles was studied and most products exhibited a slower release than the single drug. Moreover, the release could be controlled to some extent by varying the ratio of the two Eudragit used in the formulation and by selecting one or the other anti-solvent technique. Simple diffusion models satisfactorily described the release profiles. Composites specifically produced by semi-continuous technique have a drug release rate controlled by a diffusion mechanism, whereas for composites produced by the batch operation, the polymer swelling also contributes to the overall transport mechanism.

Acetazolamide↗
PubMed1991

Acetazolamide in the treatment of abnormal oculovestibular response.

We treated seven patients with incapacitating vertigo elicited by walking down a grocery store aisle or driving a car. Results of neurologic, neuro-ophthalmic, and neuroradiologic examinations were normal. Episodic vertigo secondary to an abnormal oculovestibular response was diagnosed. Each patient was given a trial of 250 to 500 mg of acetazolamide daily. Symptoms resolved completely in four patients, two patients had near resolution of symptoms, and one patient had no relief. Carbonic anhydrase activity has been demonstrated in the inner ear, and acetazolamide has been shown to affect the ion balance of the inner ear fluids.

Acetazolamide↗
PubMed1997

Acetazolamide therapy improves action myoclonus in Ramsay Hunt Syndrome.

Acetazolamide treatment significantly improves action myoclonus in Ramsay Hunt Syndrome. A family with two brothers and a sister, and a sporadic case with Ramsay Hunt Syndrome and uncontrollable action myoclonus, are described where addition of oral acetazolamide lead to marked improvement in their action myoclonus.

Acetazolamide↗
PubMed1975

Acetazolamide-induced renal calculi.

The occurrence of urinary calculi associated with acetazolamide therapy is described. Patients with a history of urinary stones or surgery are a significant risk for further calculus formation when treated with acetazolamide. The concurrent use of sodium bicarbonate further potentiates this risk.

Acetazolamide↗
PubMed1986

Effect of acetazolamide on exercise performance and muscle mass at high altitude.

The effect of acetazolamide (Az) on exercise performance and muscle mass in acclimatised subjects at an altitude of 4846 m was assessed in 11 subjects and compared with the effect of placebo on 10 other subjects. Exercise performance at 85% maximum heart rate fell by 37% in the Az group and by 45% in controls (p less than 0.05). Weight loss was greater in the placebo group at high altitude (p less than 0.01) and this correlated with the fall in exercise performance (p less than 0.001). During the expedition anterior quadriceps muscle thickness fell by 12.9% in the control group and 8.5% in the Az group (p less than 0.001), while biceps muscle thickness fell by 8.6% in controls and 2.3% in the Az group (p less than 0.001). Measurements of skin-fold thickness indicated a loss of 18% of total body fat in the placebo group and 5% in the Az group by the end of the expedition (p less than 0.001). Calorie intakes at altitudes above 3000 m were low and similar for the two groups. The Az group had fewer symptoms of acute mountain sickness but differences between the two groups were not statistically significant. Acetazolamide is therefore useful for climbers and trekkers who are acclimatised to high altitudes. It could be most useful at extreme altitudes, where maintenance of exercise performance and muscle mass are important.

Acetazolamide↗
PubMed1981

The effect of timolol and acetazolamide on transient intraocular pressure elevation following cataract extraction with alpha-chymotrypsin.

Elevated intraocular pressure (IOP) early after cataract extraction with alpha-chymotrypsin is a well-described, common occurrence. To study the incidence of pressure increase and the efficacy of medical therapy, IOP was monitored every 12 hours beginning on the first postoperative day in 68 patients after otherwise uncomplicated intracapsular cataract extraction performed with one milliliter of alpha-chymotrypsin and wound closure with multiple sutures. Patients were randomly assigned to one of three groups: treatment with oral acetazolamide, treatment with topical timolol, or no treatment. Without prophylactic treatment, the prevalence of pressure elevation at 24 hours postoperatively was 69% with IOP greater than or equal to 25 mm Hg; 29% with IOP greater than or equal to 40 mm Hg. This was independent of the type of sutures used (10--0 nylon or 9--0 silk). The patients of four different surgeons had similar rates of occurrence of postoperative glaucoma. Both timolol and acetazolamide were essentially equally effective in lowering IOP in these patients. No adverse side effects were observed. With these effective treatments available if needed, we believe that routine monitoring of the IOP by applanation tonometry during the early postoperative course provides a good opportunity for reducing the risk of complications from excessive intraocular pressure.

Acetazolamide↗
PubMed1994

Joint determination of todralazine and acetazolamide in human serum by differential pulse polarography.

Differential pulse polarography (DPP) is proposed as a direct method for the quantitation of todralazine and acetazolamide in human serum. The method was applied to the determination of these drugs in human serum, after a liquid-liquid extraction process. This extraction process together with the use of the standard additions method is essential for the elimination of the matrix effect. The proposed method enables detection limits of 0.107 microgram ml-1 for acetazolamide and 0.111 microgram ml-1 for todralazine to be achieved at reduction potentials of -0.59 and -0.86 V, respectively, using Britton-Robinson buffer (pH 1.65) as the supporting electrolyte.

Acetazolamide↗
PubMed1996

EEG findings in acetazolamide-responsive hereditary paroxysmal ataxia.

EEG studies were performed in six family members affected by acetazolamide-responsive paroxysmal ataxia. Intermittent rhythmic delta activity was found at rest in five of them; low amplitude spikes were associated with delta waves in two cases, resulting in irregular spike and wave patterns. Slowing of background activity was present in three patients. EEG abnormalities were activated by hyperventilation and modified neither by intermittent photic stimulation, nor by acetazolamide therapy. Our results suggest that EEG may be helpful to recognize this rare, but well defined, treatable disorder.

Acetazolamide↗
PubMed2002

Acetazolamide and respiratory chemosensitivity to CO(2) in the neonatal rat transverse medullary slice.

Hypoglossal nerve rootlets in the transverse medullary slice prepared from neonatal rats exhibit a bursting 'respiratory' rhythm that increases in frequency with CO(2), presumably due to activation of chemosensitive cells such as the central chemoreceptors. Carbonic anhydrase is associated with areas of central chemoreception and we propose a hypothesis for its involvement in the chemoreception process. We tested this hypothesis by blocking its activity with acetazolamide in six slice preparations. However, the addition of 1 mM acetazolamide dissolved in dimethyl sulphoxide to the superfusing bathing solution produced no alteration in the bursting frequency response of the slice to CO(2). We concluded that the chemoreception process producing the CO(2) response of the superfused, transverse medullary slice does not involve carbonic anhydrase.

Acetazolamide↗
PubMed2004

[Acute confusional syndrome associated with obstructive sleep apnea aggravated by acidosis secondary to oral acetazolamide treatment].

Acute confusional syndrome, or delirium, is a transitory mental state characterized by the fluctuating alteration of awareness and attention levels. We present the case of a patient with acute confusional syndrome associated with obstructive sleep apnea syndrome (OSAS) aggravated by metabolic acidosis induced by oral acetazolamide treatment.A 70-year-old man with no history of neurological disease was referred with a clinical picture consistent with acute confusional syndrome presenting between midnight and dawn. During the admission examination infectious, toxic, and neurologic causes, or those related to metabolic or heart disease were ruled out. Arterial blood gases measured during one of the nighttime episodes of acute confusional syndrome showed mild hypoxia and hypercapnia with mixed acidosis. Signs and symptoms suggestive of OSAS had been developing over the months prior to admission, with snoring, sleep apnea, and moderate daytime drowsiness. Polysomnography demonstrated severe OSAS with an apnea-hypopnea index of 38. Mean arterial oxygen saturation was 83%; time oxygen saturation remained below 90% was 44%. The attending physician ordered the withdrawal of oral acetazolamide, which was considered the cause of the metabolic component of acidosis. Treatment with continuous positive airway pressure was initiated at 9 cm H2O, after a titration polysomnographic study. The patient continued to improve.OSAS, for which very effective treatment is available, should be included among diseases that may trigger acute confusional syndrome.

Acetazolamide↗