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PubMed1977

Uptake of acetazolamide by human erythrocytes in vitro.

The binding of acetazolamide to human erythrocytes was studied in vitro. Blood and plasma samples were analyzed by electron-capture GLC. At 37 degrees, drug equilibrated between plasma and erythrocytes in approximately 40 min. The effect of plasma concentration on the steady-state level of drug within the erythrocytes was examined. Erythrocyte accumulation of acetazolamide appeared to be a composite of two processes: a nonlinear, saturable process and a linear, diffusion-controlled process. By appropriate linear transformation of the data, estimates of the data, estimates of the erythrocyte binding capacity and the dissociation constant for the drug were obtained.

Acetazolamide↗
PubMed1980

Quantitation of acetazolamide in plasma by high-performance liquid chromatography.

A method for estimating acetazolamide concentrations in human plasma is described. Buffered plasma (pH 4.8) containing chlorothiazide as an internal standard is extracted twice with ethyl acetate. The extract is evaporated, redissolved, and chromatographed on silica gel with hexane-chloroform-methanol-acetic acid (65:25:10:0.25) as the mobile phase. The extraction efficiencies were greater than 90%, the coefficients of variation at 1 and 30 micrograms/ml of plasma were 3.5 and 2.0%, respectively, and the calibration curves were linear and had an intercept of essentially zero. The suitability of the method for pharmacokinetic studies was verified in a normal volunteer dosed with 250-mg (solution) and 500-mg (sustained-release tablet) acetazolamide formulations.

Acetazolamide↗
PubMed1989

Preformulation studies of acetazolamide: effect of pH, two buffer species, ionic strength, and temperature on its stability.

Using an HPLC method, the effect of pH, two buffer species (phosphate and citrate), ionic strength, and temperature on the stability of acetozolamide has been studied. The optimum pH of stability appears to be 4. The buffers and ionic strength did not affect the decomposition constant. There was a direct relationship between the activation energies and pH values, with an energy of activation (Ea) value of 16.61 kcal/mol at pH 4. The un-ionized acetazolamide is subject to specific acid-base catalysis. The KH and KOH values have been estimated to be 0.23 and 1.56 d-1, respectively. These preformulation studies can be used to develop a stable oral liquid dosage form of acetazolamide.

Acetazolamide↗
PubMed1987

Acetazolamide responsive hereditary paroxysmal ataxia.

The fourteenth family with an apparently autosomal dominant paroxysmal ataxia is described. As in the seven families described since 1978, acetazolamide completely cured the attacks. A possible mechanism of action of acetazolamide is discussed.

Acetazolamide↗
PubMed1994

BOLD MRI monitoring of changes in cerebral perfusion induced by acetazolamide and hypercarbia in the rat.

To evaluate MRI methods for estimating cerebrovascular reserve, we computed changes in the R2* and R2 transverse relaxation rate and apparent diffusion coefficient (ADC) at 2.0 Tesla in five rats after administration of 30 mg of acetazolamide and in four rats during inhalation of 20% carbon dioxide gas. Significant decreases in R2*, corresponding to increases in gradient echo MRI signals, occurred in both the acetazolamide (average change -8.3%, P = 0.005) and the carbon dioxide (-2.7%, P = 0.009) treated animals. The computed values for R2 and ADC were unchanged. The magnitude of the gradient echo MRI changes observed should permit anatomic mapping of blood flow reactivity patterns in normal human subjects and in patients at risk for cerebrovascular disease.

Acetazolamide↗
PubMed1975

Teratogenesis of acetazolamide in the CBA/J and SWV strains of mice. I. Teratology.

SWV mice were totally resistant to the teratogenic and embryolethal actions of acetazolamide. The time of maximal sensitivity to acetazolamide-induced ectrodactyly in the CBA/J strain was the middle of day 10; the dose response at this time was studied. Comparison of the responses of the two strains and reciprocal hybrids indicated that sensitivity is a property of the embryo and is not maternally mediated. SWV mice were also resistant to dichlorphenamide which suggests they may be resistant to many or even all teratogenic carbonic anhydrase inhibitors.

Abnormalities, Drug-Induced↗
PubMed1975

Teratogenesis of acetazolamide in the CBA/J and SWV strains of mice. II. Genetic control of the teratogenic response.

Three independently segregating loci appear to control the difference in response of CBA and SWV mouse embryos to the ectrodactyly-inducing effect of acetazolamide. Response of the CBA embryo appears to depend on recessive genes for sensitivity being present in the homozygous condition at all 3 loci, and resistance to be conferred by the presence of a dominant allele at any one of the 3 loci. The genetic variability for the ectrodactyly response of the mouse is discussed in the light of the reported physiological factors necessary for acetazolamide-induced ectrodactyly in the rat.

Abnormalities, Drug-Induced↗
PubMed1984

Potentiation of acetazolamide induced ectrodactyly in SWV and C57BL/6J mice by cadmium sulfate.

CdSO4 and acetazolamide each induce postaxial ectrodactyly in rodents when administered at a critical time in forelimb development. C57BL/6J mice are extremely sensitive to the teratogenic action of both agents, whereas SWV mice are relatively resistant. Additionally, both of these agents can inhibit carbonic anhydrase. In the present study administration of CdSO4 and acetazolamide in combination to either strain of mice potentiates the incidence of forelimb ectrodactyly. These results, in combination with the aforementioned similarities of teratogenesis, suggest a common mechanism of teratogenesis.

Abnormalities, Drug-Induced↗
PubMed1984

Acetazolamide teratogenesis: association of maternal respiratory acidosis and ectrodactyly in C57BL/6J mice.

Exposure of C57BL/6J mice to CO2 during a critical period of gestation results in predominantly right-sided, postaxial, forelimb ectrodactyly in the offspring. The incidence and severity of CO2-induced limb malformations has been shown to be dependent on the concentration of inspired CO2, the developmental age of the embryo at exposure and the duration of CO2 exposure. Offspring of acetazolamide-treated C57BL/6J mice also display this highly specific form of ectrodactyly (Green et al., '73). Since the drug has been shown to elevate tissue CO2 tension (Mithoefer and Davis, '58), the teratogenic effect of acetazolamide may be related to induction of a hypercapnic embryonic environment.

Abnormalities, Drug-Induced↗
PubMed1985

Histological changes induced in developing limb buds of C57BL mouse embryos submitted in utero to the combined influence of acetazolamide and cadmium sulphate.

Microscopic defects in limb buds of C57BL mouse embryos after the combined teratogenic action of acetazolamide plus cadmium sulphate administered on day 9 of gestation were studied in serial sections. Postaxial deficiencies observed in 12-15-day embryos and affecting preferentially the right forelimbs were classified in nine morphological types according to increasing amounts of missing parts. Type X defect consists of a nearly complete amelia in which all four limbs are represented only by the girdle and proximal end of the stylopod. Type XI abnormality appears as an intermediate reduction affecting the area of digit IV. In addition to modifications of the forelimb bud shape detected from the 10-day stage onwards, observations made 24 and 48 hr after treatment confirmed that the postaxial defects result from an absolute lack of postaxial mesoderm occurring without cell necrosis as a consequence of a postaxial shortening of the apical ectodermal ridge (aer). In 10-day embryos, the latter appears shortened and hypertrophied; it is later fragmented into alternate thick and thin portions in 11-day affected limb buds. These ectodermal changes might account for the genesis of all types of defects observed. Untreated 9-day embryos with 12-25 pairs of somites display a number of asymmetries between their right and left forelimb territories: Until the 19-somite stage, the vascular supply to that area is provided exclusively by the umbilical vein, which is larger on the right side; the initial amount of somatopleural limb mesoderm is greater in the right rudiment and the genesis of its aer is slightly protracted as compared to the left one. These asymmetries might contribute to the right side predominance of the forelimb defects induced by acetazolamide and cadmium.

Abnormalities, Drug-Induced↗
PubMed1988

Acetazolamide: maternal toxicity, pattern of malformations, and litter effect.

Thirty litters of C57BL 6J mice were administered intraperitoneally one of four doses (0, 500, 750, and 1,000 mg/kg maternal weight) of acetazolamide on day 9 of gestation. The fetuses were removed on day 18 and fixed, stained, cleared, and examined for the pattern of malformations. The forelimb postaxial limb deficiency was the most common abnormality, but forelimb postaxial polydactyly and a postaxial deficiency in the hindlimb were also observed. Males were significantly more likely to be malformed than females at all doses, in contrast to the predominance of females observed in rat fetuses exposed to acetazolamide (Scott et al.: Teratology 6:239-240, '73). The occurrence of limb malformations did not correlate with maternal weight loss, the birth weight of the fetus, or the position of the fetus in the uterus. A "litter effect" was demonstrated in that there was a nonuniform distribution of litters with different proportions of malformed fetuses.

Abnormalities, Drug-Induced↗
PubMed1990

Genetically determined transient edema found in the WB/ReJ mouse strain in a teratogenic survey with acetazolamide.

A continuing survey of the genetic variability of different mouse strains to acetazolamide teratogenesis demonstrated the WB/ReJ strain expresses a high frequency of induced subcutaneous edema in day 15 fetuses. In treated WB/ReJ fetuses, the probability of expression of edema is independent of the expression of forelimb ectrodactyly and, with the dosage regime, there is no significant increase in acetazolamide-induced resorption. It was surprising to find a high frequency of spontaneous edema on day 15 in untreated WB/ReJ fetuses. The spontaneous edema is a transient trait with maximum expression (56%) on day 14, and it is resolved by day 17 without apparent consequence to the survival of previously affected fetuses. There is no sex dimorphism in the liability to express the transient edema. Preliminary genetic crosses to investigate the spontaneous edema were made between WB/ReJ and the C57BL/6J strain, which historically had not be observed to express spontaneous edema. A low frequency of spontaneous edema was observed on day 14 in both C57BL/6J and the reciprocal F1 fetuses. The trait is not additive because there is dominance deviation of the BC1 fetuses in the direction of the F1 fetuses. The data were fitted to a threshold model suggesting that the developmental liability to express the difference in transient edema is determined by more than one gene, but the data can be interpreted by a minimum of two loci with duplicate epistasis. The observed differences in frequencies of edema suggest the genetic model can be tested with relatively few test crosses.

Acetazolamide↗
PubMed1992

Abnormalities in ureter and kidney development in mice given acetazolamide-amiloride or dimethadione (DMO) during embryogenesis.

These experiments more accurately define the effects of the combination acetazolamide-amiloride or a single dose of dimethadione (DMO), the active metabolite of trimethadione, on the development of the ureter. When acetazolamide-amiloride was administered in C57BL/6NCrlBR mice on day 9, 9.5, or 10 of gestation (plug = day 0) a second ureter was formed, anterior to the original ureter, inducing a second kidney. The second ureter then fails to make a connection with the developing bladder and remains attached to the mesonephric duct. The mesonephric duct becomes the vas deferens in the male and deteriorates completely in the female leading to either a restricted ureter or a blocked ureter depending on the sex of the fetus. Administration of a single dose of DMO between gestational day 9 and 10.3 produced both renal agenesis and ureters of varying lengths. Some ureters were of normal length with a tuft of one or two nephrons at their tip, while others were one half or one quarter of their normal length. In some instances the ureter was completely absent. The reason for this strong effect on the ureter is unknown.

Abnormalities, Drug-Induced↗
PubMed1985

Effect of acetazolamide (Diamox) on tear secretion.

The side effects of acetazolamide (Diamox) on lacrimation were measured in rats by means of the cotton-thread tear test. After a daily oral 1-mg dose (administered for five days), comparable to the dose used for adult humans on a drug-to-bodyweight basis, tear production remained unaffected but the lacrimal peroxidase secretion decreased by 60% of the baseline level. After withdrawal of acetazolamide the peroxidase secretion returned to the baseline level.

Acetazolamide↗
PubMed1986

Prevention of IOP-rise following Nd-YAG laser capsulotomy with pre-operative timolol eye-drops and 1 tablet acetazolamide 250 mg systematically.

Short-term observation following Nd-YAG laser capsulotomy indicates that serious elevation of intra-ocular pressure may occur, unrelated to the amount of energy used. In this study the IOP in 3 groups of 10 pseudophakic patients undergoing Nd-YAG laser posterior capsulotomy was measured before capsulotomy and 2 and 4 hours afterwards, using the fellow-eye as control. The first group received no medication, the second received timolol 1/2% eyedrops preoperatively, the third group a combination of timolol 1/2% and 1 tablet of acetazolamide 250 mg systemically. Pretreatment with timolol 0.5% minimizes IOP-rise but does not give complete protection. The combination of timolol 0.5% with 1 tablet of acetazolamide 250 mg proves to be a safe procedure for the prevention of IOP-rise after YAG laser capsulotomy. To prevent other complications it is advisable to make a small capsulotomy of 2-3 mm diameter using as little energy as possible. Also a defocussing system in the laser is a great advantage. Indomethacin drops during a period of 6 weeks after Nd-YAG laser capsulotomy should prevent cystoid macular edema.

Acetazolamide↗
PubMedDate not supplied

Acetazolamide-induced nephrocalcinosis.

Nephrocalcinosis has been reported in patients treated with acetazolamide and other agents, such as furosemide or bicarbonate. We present a case of nephrocalcinosis induced solely by acetazolamide and diagnosed radiographically. Possible mechanisms of pathogenesis are reviewed.

Acetazolamide↗
PubMed1988

Effects of acetazolamide on kidney function in type 1 (insulin-dependent) diabetic patients with diabetic nephropathy.

We investigated the effects of 3 days treatment with acetazolamide 250 mg three times daily on kidney function in 8 Type 1 (insulin-dependent) diabetic patients with nephropathy, and in 7 healthy subjects in a double-blind placebo controlled cross-over study. Glomerular filtration rate and extracellular fluid volume were measured with the single injection 51Cr-EDTA technique and fluid flow rate from the proximal tubules was determined by measurement of the renal lithium clearance. A 24% decline in glomerular filtration rate was observed in both groups during acetazolamide treatment (control subjects: 108 +/- 11 vs 82 +/- 9 ml/min, p less than 0.02, diabetic patients: 71 +/- 19 vs 54 +/- 14 ml/min, p less than 0.01). The renal lithium clearance (ml/min) remained about the same (control subjects: 22 +/- 6 vs 27 +/- 8, NS, diabetic patients: 14 +/- 5 vs 15 +/- 4, NS). Absolute proximal tubular reabsorption of water (ml/min) was reduced by about one-third (control subjects: 85 +/- 11 vs 56 +/- 7, p less than 0.02, diabetic patients: 55 +/- 17 vs 37 +/- 6, p less than 0.02), and fractional proximal reabsorption of water and sodium (%) declined (control subjects: 79 +/- 5 vs 67 +/- 8, p less than 0.02, diabetic patients: 79 +/- 5 vs 72 +/- 6, p less than 0.02). Renal sodium clearance and distal fractional reabsorption of sodium was unchanged. Extracellular fluid volume declined by 10% in both groups (p less than 0.02). Albuminuria and fractional albumin clearance decreased significantly in the nephropathic patients (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1980

Treatment of myotonic dystrophy with acetazolamide.

This report describes a patient with myotonic dystrophy who had severe action and percussion myotonia. The patient was unresponsive to diphenylhydantoin therapy. Treatment with acetazolamide, 250 mg daily, decreased the myotonia markedly. A possible mechanism of the favorable effect of acetazolamide in myotonia is discussed.

Acetazolamide↗