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PubMed1990

Effects of acetazolamide on medullary extracellular pH and PCO2 and on ventilation in peripherally chemodenervated cats.

The responses of ventilation and of medullary extracellular fluid (ECF) pH and PCO2, to an intravenous (i.v.) infusion of 50 mg/kg acetazolamide (an inhibitor of carbonic anhydrase), were measured in cats anaesthetized with chloralose and urethane, in which both bilateral vagotomy and carotid nerve section had been performed. After 2 h, it was observed that: acetazolamide caused an acidosis in medullary ECF which was still developing after 2 h, reflected by a progressive fall in pH (mean = 0.215 pH units in 2 h), while ECF PCO2 showed an insignificant rise of about 1 kPa; acetazolamide caused a considerable rise in ventilation, which largely developed in the first 15 min after drug infusion; the direction of the ECF acid-base responses in the first 15 min varied, whereas that of the ventilatory response did not. Furthermore, the time course of the former developed quite differently from the latter. It was therefore concluded that the observed changes in medullary ECF pH and PCO2 can not explain the large and fast ventilatory response of acetazolamide.

Acetazolamide↗
PubMed2005

Effects of tissue heterogeneity on cerebral vascular response to acetazolamide stress measured by an I-123-IMP autoradiographic method with single-photon emission computed tomography.

OBJECTIVES: Single-photon emission computed tomography (SPECT) with iodine-123 (123I)-labeled N-isopropyl-p-iodoamphetamine (IMP) is widely used in measuring the cerebral blood flow (CBF) response to acetazolamide stress for assessment of cerebral vascular reserve. To quantitate CBF by means of SPECT with IMP, an autoradiographic (ARG) method has been developed and is widely used. Because the relation between the brain counts on the SPECT scan and CBF is not linear in the ARG method, a mixture of gray and white matter in a pixel causes errors in the calculation of CBF. In the present study, errors in the calculation of CBF and vascular response to acetazolamide stress by the ARG method due to tissue heterogeneity were estimated by simulation study. Correction for effects of tissue heterogeneity in SPECT data was also attempted. METHODS: Images of gray and white matter fraction were obtained by voxel-based morphometry analysis of magnetic resonance (MR) imaging data set. Ideal CBF images, which were generated from gray and white matter fraction images with assumed blood flow values for gray and white matter, were compared to CBF images generated by the ARG method. Correction for effects of tissue heterogeneity in SPECT data was performed with gray and white matter fraction data obtained from MR images. RESULTS: Systematic underestimation of CBF due to tissue heterogeneity was observed in all brain regions. In the neocortical regions, underestimation by -21% to -16%, -26% to -20%, -31% to -24%, and -35% to -27% was observed for gray and white matter blood flow of 80 and 20, 100 and 25, 120 and 30, and 140 and 35 ml/100 ml/min, respectively. Vascular response was also systematically underestimated in most brain regions. Vascular responses in the neocortical regions ranged from 17% to 20%, from 31% to 37%, and from 42% to 52% when ideal vascular responses were 25%, 50%, and 75%, respectively. After correction for the effects of tissue heterogeneity, values of vascular response to acetazolamide stress ranged from 64% to 116% in the neocortical regions, whereas values obtained by the ARG method ranged from 48% to 52%. CONCLUSION: Underestimation of the vascular response to acetazolamide stress due to tissue heterogeneity should be considered in the estimation of cerebral vascular reserve.

Acetazolamide↗
PubMed1982

Effects of sodium valproate and acetazolamide on cerebral respiration.

The effects of sodium valproate and acetazolamide on the oxygen uptake of guinea pig brain cortex slices were investigated. In calcium-free medium, sodium valproate inhibited the oxygen uptake appreciably in the presence of glucose and glutamic acid. Acetazolamide, on the other hand, was more effective in inhibiting oxygen uptake in the presence of glucose than in the presence of glutamic acid. Addition of 0.2 mM CaCl2 in the medium containing 5 mM KCl could appreciably reverse the inhibition of oxygen uptake by acetazolamide in the presence of glucose. The inhibition of oxygen uptake by these drugs in the presence of glucose, however, could be completely reversed by increasing the dose of K+ ions (100 mM) in the medium which had no effect on the inhibition of oxygen uptake in the presence of glutamic acid. When the concentration of Ca2+ ions in the medium was elevated to 0.75 mM, the inhibitory effects of these drugs on the oxygen uptake in the presence of both glucose and glutamic acid could be completely abolished. Sodium valproate also inhibited the endogenous respiration of guinea pig brain cortex slices, whereas acetazolamide was almost without any effect. Increase in the concentration of Ca2+ ions in the medium failed to counteract the inhibition of endogenous respiration of guinea pig brain cortex slices by sodium valproate.

Acetazolamide↗
PubMed1980

Effect of acetazolamide on rate of CO2 uptake in the perfused rat brain.

The accumulation of acid-labile CO2 was measured in the rat brain at early times after exposure to 30% CO2 in oxygen. In particular, the effect on CO2 accumulation of inhibiting brain carbonic anhydrase with acetazolamide was studied. For 57 rats, a rat head perfusion technique was used which permits control and rapid alteration of arterial acid-base conditions. At a paCO2 of 35 mm Hg, total carbon dioxide of the whole brain remained at a normal mean value of 13.4 +/- 0.6 (S.E.) mM/kg during perfusions 209-160 min long. On 30% CO2, brain CO2 increased rapidly to a mean of 24 mM/kg at 5 min and then much more slowly. The latter curve agreed well with values obtained in intact animals. Pretreatment with acetazolamide had no inhibitory effect on CO2 accumulation at 1-5 min. At 5 min, control brain CO2 was 23.9 +/- 0.6 (n = 10) and acetazolamide-pretreated brain CO2 was 24.4 +/- 0.7 (n = 9). Terminal venous pCO2s were 164-180 and 167-172 mm Hg, respectively. Thirty-one unperfused rats were also investigated with similar results. Acetazolamide-pretreated rats had the same CO2 uptake as controls after 15 min exposure to CO2, rather than lower uptake as would be expected if carbonic anhydrase were rate-limiting. The results suggest the need for reinterpretation of some concepts about the role of carbonic anhydrase in CO2 accumulation in the brain.

Acetazolamide↗
PubMed1987

Acetazolamide and cerebrospinal fluid ions in dogs with normal acid-base balance.

The purpose of these experiments was to study the effects of acetazolamide, a carbonic anhydrase inhibitor, on cisternal cerebrospinal fluid (CSF) ions during normal acid-base balance. We measured blood and CSF acid-base variables in two groups (n = 6 in each) of anesthetized, paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles. After baseline samples were obtained, acetazolamide was administered intravenously within 10 min (group II); group I received equal volume (20 ml) of half-normal saline. During the next 6 h, in both groups arterial blood acid-base variables and plasma strong ions remained relatively normal. In group I, mean values for cisternal CSF PCO2 were 45.3 and 49.3 mm Hg at 0 and 6 h; respective values for CSF [HCO-3] were 24.1 and 22.7 mEq/L. In group II, corresponding values for PCO2 and [HCO-3] were 46.4 and 51.9 mm Hg, and 23.8 and 23.7 mEq/L, respectively. Comparing the two groups, related mean values were not significantly different from each other. Furthermore, acetazolamide had no significant effect on CSF Na+, K+ and Cl- concentrations. Based on the results of this study and those reported previously, we conclude that under normal acid-base balance, acetazolamide does not change ionic composition of cisternal CSF, choroidal CSF or brain extracellular fluid.

Acetazolamide↗
PubMed1994

Calcium deficient diet, acetazolamide and gas exchange characteristics of avian eggshells.

The effects of calcium deficient diet and acetazolamide on the gas exchange characteristics of avian eggshells were independently investigated in two groups of unmated hens (Gallus domesticus). In one group, eggs were collected during both a normal diet (3.00% Ca) and a calcium deficient diet (0.34% Ca). In another group, eggs were collected both before and after acetazolamide administration (200 mg/kg) per os. Eggshell water vapor conductance (GH2O) increased 30% during the calcium deficient diet and was accompanied by a 21% decrease in eggshell thickness (L). Eggshell GH2O increased 200% one day after acetazolamide administration and was not only accompanied by a 36% decrease in L, but also by an 89% increase in total functional pore area (Ap). We conclude that a calcium deficient diet increases GH2O by eggshell thinning with little effect on Ap. On the other hand, acetazolamide profoundly increases GH2O, not only by eggshell thinning but also by a remarkable increase in Ap.

Acetazolamide↗
PubMed1990

Reduction of embryonic intracellular pH: a potential mechanism of acetazolamide-induced limb malformations.

The effects of acetazolamide on the developing rodent limb bud were postulated to result from a reduction of intracellular pH (pHi). Embryonic intracellular pH was calculated from transplacental distribution of the weak acid, 5,5'-dimethyloxazolidine-2,4-dione, in teratogenically sensitive (C57BL/6) and resistant (SWV) inbred mice. pHi was reduced by acetazolamide treatment in C57 embryos and limb buds but not in SWV samples. Acetazolamide teratogenesis can be exacerbated by coadministration of amiloride, presumably through inhibition of Na+/H+ exchange attributable to the latter agent. pHi reduction after such treatment was more profound than after acetazolamide alone, providing further support for the central hypothesis. pH was also reduced in other embryonic (embryo plasma) and extraembryonic compartments (exocoelomic fluid, amniotic fluid). pH changes in these compartments could also lead or contribute to abnormal development.

Abnormalities, Drug-Induced↗
PubMed1992

Dependence of acetazolamide teratogenesis on fetal and not maternal genotypes.

This study assesses the relative contributions of dam and conceptus to sensitivity to acetazolamide teratogenesis in an in vivo mouse model. Reciprocal F1 outcrosses were made between mice resistant to the teratogenic effects of acetazolamide (SWV) and the susceptible C57BL/6JBk line. Female F1 progeny were backcrossed either to C57BL or to SWV males. The F1 outcross resulted in identical fetuses developing in genetically different uterine environments. In the backcrosses, genetically identical hybrid dams were gestating genetically different populations of segregating fetuses. In both F1 outcrosses and backcrosses, as well as in pure-line controls, dams were treated on day 9 of gestation by subcutaneous injection of acetazolamide (ACZM) at a dose level of 1500 mg/kg, or identical volume of the vehicle. The principal abnormality seen was right front limb ectrodactyly. Among pure-line matings, SWV produced no ectrodactyly, but 68% of C57BL showed this defect. Only two cases were seen in outcross of C57BL females to SWV males, and one litter produced three ectrodactylous fetuses in the reciprocal cross. A highly significant increase in ectrodactyly was seen in treated backcrosses to C57BL relative to backcrosses to SWV. Thus, a litter in which most of the genes segregating are from a susceptible line will show major increases in susceptibility, despite being in a heterotic and somewhat resistant uterine environment, whereas the susceptible C57BL uterine environment does not result in significant abnormality in heterozygous resistant fetuses. These results unequivocally demonstrate that it is the genotype of the conceptus, and not the genotype of the dam, nor heterosis, that determines sensitivity to acetazolamide teratogenesis. They further suggest that this genetic approach may be useful in determining the relative contribution of dam and conceptus for other teratogens.

Abnormalities, Drug-Induced↗
PubMed1990

The effect of acetazolamide on hypercapnic and eucapnic/poikilocapnic hypoxic ventilatory responses in normal subjects.

We have studied the effect of acetazolamide 500 mg bd for three days on ventilatory response to CO2 (HCVR) and hypoxia under both isocapnic and poikilocapnic conditions (isocapnic and poikilocapnic HVR) in five normal subjects. Although acetazolamide reduced calculated arterial pH (7.41 [SEM] 0.01 to 7.37 [SEM] 0.01: p less than 0.01) there was no significant change in either isocapnic HVR (with PetCO2 held at the post-drug resting level) or poikilocapnic HVR in terms of slope and ventilation at SaO2 = 80%. HCVR slope rose slightly (+1.82 [SEM] 0.43 to +2.2 [SEM] 0.29 l/min/mmHg: NS) and there was a significant increase in ventilation at Pet-CO2 = 50 mmHg (9.42 [SEM] 3.3 to 31.4 [SEM] 6.31/min: p less than 0.01). These findings are consistent with the claim that acetazolamide stimulates central chemoreceptors and inhibits peripheral chemoreceptors. Increased sensitivity to CO2 would reverse the suppressive effect of respiratory alkalosis on hypoxic ventilatory drive following rapid ascent to high altitude, and this probably accounts for the efficacy of acetazolamide in the prophylaxis of acute mountain sickness. However, inhibition of peripheral chemoreceptors may also result in symptomatic benefit by reducing sleep disturbance due to periodic breathing.

Acetazolamide↗
PubMed2005

Preparation and evaluation of reverse-phase evaporation and multilamellar niosomes as ophthalmic carriers of acetazolamide.

Niosomes have been reported as a possible approach to improve the low corneal penetration and bioavailability characteristics shown by conventional ophthalmic vehicles. Niosomes formed from Span 40 or Span 60 and cholesterol in the molar ratios of 7:4, 7:6 and 7:7 were prepared using reverse-phase evaporation and thin film hydration methods. The prepared systems were characterized for entrapment efficiency, size, shape and in vitro drug release. Stability studies were carried out to investigate the leaching of drug from niosomes during storage. The intraocular pressure (IOP) lowering activity of acetazolamide niosomal formulations in rabbits was measured using ShiØtz tonometer. Histological examination for the corneal tissues of rabbits receiving niosomal formulations was carried out for assessment of the ocular irritancy of niosomes. The results showed that the type of surfactant, cholesterol content and the method of preparation altered the entrapment efficiency and drug release rate from niosomes. Higher entrapment efficiency was obtained with multilamellar niosomes prepared from Span 60 and cholesterol in a 7:6 molar ratio. Niosomal formulations have shown a fairly high retention of acetazolamide inside the vesicles (approximately 75%) at a refrigerated temperature up to a period of 3 months. Each of the tested acetazolamide niosomes prepared by either method produced a significant decrease in IOP compared to the solution of free drug and plain niosomes. Multilamellar acetazolamide niosomes formulated with Span 60 and cholesterol in a 7:4 molar ratio were found to be the most effective and showed prolonged decrease in IOP. Histological examination of corneal tissues after instillation of niosomal formulation for 40 days showed slight irritation in the substantia propria of the eye which is reversible and no major changes in tissues were observed.

Acetazolamide↗
PubMed2002

Acetazolamide for central serous retinopathy.

OBJECTIVE: To find out whether acetazolamide has a beneficial effect in the treatment of central serous retinopathy (CSR). DESIGN: Prospective, nonrandomized, comparative trial. PARTICIPANTS: Fifteen acetazolamide-treated and 7 untreated (control) CSR patients who completed at least 24 months of follow-up. METHODS: Patients in the treatment group were given systemic acetazolamide according to a standard protocol. Main outcome measures were compared between treatment and control groups using Student's t test and the Mann-Whitney U test for statistical analysis. MAIN OUTCOME MEASURES: Time until subjective visual improvement, time until full clinical resolution, and rate of recurrences. RESULTS: Mean times to both subjective visual improvement and clinical resolution of the attack were shorter in the study group than in the control group. Recurrence rate did not differ between the study and control groups. CONCLUSIONS: Acetazolamide treatment for CSR shortens the time for subjective and objective clinical resolution, but has no effect on either final visual acuity or recurrence rate of the disease.

Acetazolamide↗
PubMed1997

Additive ocular hypotensive effect of latanoprost and acetazolamide. A short-term study in patients with elevated intraocular pressure.

OBJECTIVE: To investigate the additive ocular hypotensive effect of latanoprost on the intraocular pressure (IOP) reduction induced by a suboptimal dose of acetazolamide, a carbonic anhydrase inhibitor. DESIGN: A short-term, randomized, placebo-controlled, double-masked study. PARTICIPANTS: Twenty-four patients with glaucoma with elevated IOPs. INTERVENTION: Acetazolamide 250 mg twice daily from day 1 to day 18. Topical 50 micrograms/ml latanoprost or placebo eye drops bilaterally instilled once daily from day 4 to day 18. MEAN OUTCOME MEASURES: IOP, conjunctival hyperemia. RESULTS: The mean IOP of 19.5 mmHg during acetazolamide treatment was further reduced to 16.8 mmHg after topical administration of latanoprost, i.e., a decrease of 2.9 +/- 2.8 mmHg (15%, P < 0.001). Administration of placebo to patients on acetazolamide resulted in an upward drift of 1.3 mmHg (6%, P = 0.03). A modest but statistically significant increase in conjunctival hyperemia was found in the latanoprost-treated group, but did not affect the masking. CONCLUSIONS: This short-term study indicates that the combination of topically applied latanoprost and a suboptimal dose of systemic carbonic anhydrase inhibitor is useful in the management of glaucoma.

Acetazolamide↗
PubMed2005

[Advantages of acetazolamide associated with anti-inflammatory medications in postoperative treatment of macular edema].

PURPOSE: To analyze the effectiveness of acetazolamide associated with topical nonsteroidal anti-inflammatory drugs (NSAIDs) and/or steroids in the treatment of postsurgical macular edema (ME). PATIENTS AND METHODS: Sixteen eyes of 15 consecutive patients presenting with clinical ME 1-120 months after ophthalmologic surgery were studied retrospectively. The mean duration of ME before treatment was 5 months. All patients were treated with 250-500 mg of acetazolamide per day, associated with topical NSAIDs and/or steroids for an average of 6.9 months. The main outcome measures were the best-corrected visual acuity expressed in Log MAR, and the retinal thickness evaluated with OCT. RESULTS: The mean initial visual acuity was 20/100 (0.7 +/- 0.28 Log MAR), with a macular thickness of 599.67 +/-174.17 microm (average +/- standard deviation). The mean final visual acuity was 20/40 (+0.3 +/- 0.2 Log MAR) with a macular thickness of 264.69 +/- 106.59 microm. Treatment was effective in 87.5% of overall cases. The effectiveness was 100% in the subgroup treated with acetazolamide, NSAIDs, and steroids. CONCLUSION: This study suggests that medical treatment with a combination of acetazolamide, topical NSAIDs and/or steroids may be beneficial for reducing retinal thickness and improving vision in postsurgical ME.

Acetazolamide↗
PubMed1992

Acetazolamide in hemodialysis patients: a rational use after ocular surgery.

Acetazolamide is a weak diuretic used to decrease production of aqueous humor in the eye. Hemodialysis patients undergoing ocular surgery may benefit from acetazolamide; however, no pharmacokinetic data are available for this group of patients. We report a patient who received acetazolamide 250 mg every 6 hours after ophthalmic surgery and developed reversible neurological side effects associated with very high plasma concentrations. Using pharmacokinetic analysis, we suggest an alternate administration of acetazolamide for end-stage renal patients.

Acetazolamide↗
PubMed1986

Solid-phase extraction of acetazolamide from biological fluids and subsequent analysis by high-performance liquid chromatography.

A sensitive, relatively fast and simple to operate high-performance liquid chromatographic method for the determination of acetazolamide in plasma and saliva is described. Quantitative extraction of the drug from both plasma and saliva was achieved using commercially available reversed-phase octadecylsilane-bonded silica column (Bond-Elut C18, 2.8 ml capacity). Acetazolamide and the internal standard are retained on the Bond-Elut C18 column and reproducibly recovered by elution with methanol. Liquid-liquid partition chromatography, carried out on a 30-cm mu Porasil column (10-microns porous silica) using a mobile phase consisting of dichloromethane-ethanol-water-glacial acetic acid (500:65:65:1), provided adequate separation with acceptable retention times. Acetazolamide levels in the region 50-100 ng/ml can be determined in 100 microliters of plasma or 200 microliters of saliva employing ultraviolet detection at 254 nm with a sensitivity of 0.005 absorbance units full scale. Although the method is primarily used to determine steady-state drug levels in paediatric patients, its general applicability is illustrated by the 24-h plasma and saliva concentration profiles obtained from a male volunteer following oral administration of acetazolamide.

Acetazolamide↗
PubMed2001

The spray drying of acetazolamide as method to modify crystal properties and to improve compression behaviour.

Acetazolamide shows a very poor compression ability and tablets must usually be produced through a wet granulation process. However, the possibility to obtain pure acetazolamide for direct compression could be interesting for industrial application. With the scope to obtain a material for direct compression, three different crystallisation methods were chosen, with respect to acetazolamide solvent solubility. (a) Acetazolamide was dissolved in an ammonia solution and then spray dried. It was possible to characterise the spherical particles as a mixture of two polymorphic forms, I and II by Powder X-ray diffraction study. (b) Pure form I was obtained by slowly cooling to room temperature a boiling water solution. (c) Pure form II, the marketed form, was obtained by neutralisation of an ammonia solution. Their compression behaviour was investigated firstly by a rotary press. Whilst pure polymorphic forms I and II could not be compressed, the spray dried particles showed very good compression properties. In fact, tablets were obtained only by spray dried particles, which show very good properties under compression and the absence of capping tendency. On the other hand, it was impossible to obtain tablets from polymorphic forms I and II, whatever compression pressures were used. In order to explain their densification mechanism, a single-punch tablet machine, equipped for the measurement of the upper punch displacement in the die, was used. From calculated Heckel's parameters, it was demonstrated that the spray dried material shows a greater particle rearrangement in the initial stage of compression due to its spherical habit and minor wrinkledness of particle surface. The crystalline structure due to the presence of polymorphic forms I and II concur to lowering the intrinsic elasticity of the material. This fact avoids the risk of the rupturing the interpaticulate bonds, which are formed during the compression, concurring to the consolidation of the tablet.

Acetazolamide↗
PubMed1995

Effectiveness of apraclonidine and acetazolamide in preventing postoperative intraocular pressure spikes after extracapsular cataract extraction.

We studied the effectiveness of two prophylactic agents in controlling early postoperative intraocular pressure (IOP) increases after cataract surgery. Fifty-four nonglaucomatous patients received either topical 1% apraclonidine, one drop before and after surgery, or sustained-release acetazolamide, 500 mg, or no medication at the completion of planned extracapsular cataract extraction (ECCE). Mean baseline IOPs were similar among patients randomized to the apraclonidine, acetazolamide, and control groups: 15.29 mm Hg, 15.33 mm Hg, and 14.26 mm Hg, respectively. At 3 hours postoperatively, IOPs were significantly lower in the apraclonidine group (11.13 mm Hg, P = .035), nonsignificantly lower in the acetazolamide group (13.3 mm Hg, P = .17), and significantly increased in the control group (21.32 mm Hg, P = .003). One eye in the apraclonidine group and six in the control group had IOPs greater than 30 mm Hg. At 24 hours, the only statistically significant difference was in the control group, whose mean IOPs remained elevated (21.83 mm Hg, P = .0008). One eye in the apraclonidine group, two in the acetazolamide group, and five in the control group had IOPs greater than 30 mm Hg. We found a significant early IOP reduction with apraclonidine given topically preoperatively and at the completion of planned ECCE.

Acetazolamide↗
PubMed2000

A comparison of topiramate and acetazolamide on seizure duration and paired-pulse inhibition in the dentate gyrus of the rat.

Topiramate is a relatively new antiepileptic drug with several putative anticonvulsant mechanisms. Among them is the ability to inhibit carbonic anhydrase, a property in common with the anticonvulsant acetazolamide. This study examined the effects of topiramate and acetazolamide on the duration of epileptiform activity and on paired-pulse inhibition in the dentate gyrus in urethane anesthetized adult Sprague-Dawley rats. Neither topiramate nor acetazolamide altered excitability in the dentate gyrus, as measured with input-output curves or induction of long-term potentiation. Topiramate increased paired-pulse inhibition, whereas acetazolamide had no effect. Both drugs dose-dependently blocked the lengthening of the duration of epileptiform activity compared to vehicle controls. These results indicate that topiramate has an anticonvulsant-related effect (increase in paired-pulse inhibition), which may contribute to its antiepileptic effect, that is not dependent on its ability to inhibit carbonic anhydrase.

Acetazolamide↗