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PubMed1994

Acetazolamide challenge for three-dimensional time-of-flight MR angiography of the brain.

PURPOSE: We compared three-dimensional time-of-flight MR angiograms obtained before and after acetazolamide administration to evaluate whether use of this drug could improve visualization of small peripheral intracranial arteries and atherosclerotic stenosis. METHODS: For evaluation of small peripheral arteries, 10 patients with clinical diagnosis of ischemic cerebrovascular disease and 10 healthy volunteers were investigated, and for evaluation of stenosis, another 6 patients were investigated. Vascular images were obtained by three-dimensional time-of-flight MR angiography. After a baseline scan, 17 mg/kg acetazolamide was injected intravenously and the second scan was performed 20 minutes later. RESULTS: Several small peripheral arteries that had not been seen on the baseline images were visible on the acetazolamide images without any augmentation of the background signals. Stenotic lesions in the main trunks of the major cerebral arteries were detected more clearly on acetazolamide images. CONCLUSIONS: Acetazolamide improves visualization of small peripheral intracranial arteries and sensitivity in detecting atherosclerotic stenosis in the main trunk of major cerebral artery by three-dimensional time-of-flight MR angiography without changing MR apparatus and software.

Acetazolamide↗

PubMed1996

Susceptibility-weighted MR for evaluation of vasodilatory capacity with acetazolamide challenge.

PURPOSE: To investigate cerebral vasodilatory capacity by acetazolamide challenge in healthy subjects and in patients with chronic occlusive cerebrovascular disease by using susceptibility-weighted gradient-echo MR imaging. METHODS: Eight patients with chronic occlusive cerebrovascular disease and four healthy volunteers were studied with susceptibility-weighted MR imaging before and after intravenous administration of 1000 mg of acetazolamide. Signal intensities were measured as a function of time in several regions of interest defined on anatomic images. In all patients with chronic occlusive cerebrovascular disease, acetazolamide challenge and resting regional cerebral blood flow were also evaluated with single-photon emission CT (SPECT). RESULTS: In healthy volunteers, signal intensities began to increase 3 to 4 minutes after acetazolamide administration, with a continuous increase during the subsequent 10 minutes. The effect lasted for approximately 45 minutes after administration. In patients with chronic occlusive cerebrovascular disease, signal changes on susceptibility-weighted MR images of occluded areas with normal vasodilatory capacity on SPECT images did not differ from signal changes of nonocclusive areas. In those patients with changes that reflected diminished vasodilatory capacity, the MR images showed a lower percentage of signal changes after acetazolamide administration than those in normally perfused areas. CONCLUSION: Susceptibility-weighted MR imaging offers an alternative method for estimating vasodilatory capacity.

Acetazolamide↗

PubMed1977

Therapeutic testing by acetazolamide in the differentiation of a benign from a malignant niche.

Recognising the inhibitory activity of acetazolamide upon acid gastric secretion and its favorable effects in the treatment of gastric ulcer which we have described (see reference) - we applied the therapeutical testing by acetazolamide in the differentiation of benign from malignant niches of the stomach. Acetazolamide was administered orally at doses of 25-30 mg per kilogram body weight in a long term trial, together with 3 gr sodium bicarbonate, 1 gr potassium bicarbonate, 1.5 gr magnesium oxide per day and an increased quantity of liquids, to 741 patients with radiologically demonstrated ulcer craters. The fundamental criterion was the size of the niche as established by radiologic examination. In all gastric ulcers the size of the niche was considerably reduced after 7-9 days of treatment with acetazolamide; the niche disappeared in 2-3 weeks. This favorable result was obtained without diet and rest. In 38 cases in which there was no significant radiologic change of the niche after 7-9 days of treatment with acetazolamide - the malignancy of the niche was confirmed. The simplicity and the effectiveness of this rapid therapeutic test, makes it useful in the differentiation of benign from a malignant ulcer craters.

Acetazolamide↗

PubMed1997

Comparison of topical timolol gel to oral acetazolamide in the prophylaxis of viscoelastic-induced ocular hypertension after penetrating keratoplasty.

PURPOSE: Viscoelastic-induced ocular hypertension following penetrating keratoplasty (PK) may result in endothelial cell loss and optic nerve damage. METHODS: In a prospective, randomized, masked trial, two doses of oral sustained-release acetazolamide were compared to a single dose of topical 0.5% timolol gel after 40 PKs. RESULTS: The mean preoperative intraocular pressure (IOP) was 17.4 mm Hg for the oral acetazolamide group and 16.7 mm Hg for the timolol gel group. The mean IOP on the first postoperative day was 17.9 mm Hg with oral acetazolamide and 12.9 mm Hg with timolol gel. One patient developed significant adverse reactions with oral acetazolamide; there were no adverse reactions with timolol gel. CONCLUSION: Prophylactic use of timolol gel for viscoelastic-induced ocular hypertension after PK appears to offer better IOP control than oral acetazolamide, with potentially fewer adverse systemic effects.

Acetazolamide↗

PubMed1998

Age-related vasodilatory response to acetazolamide challenge in healthy adults: a dynamic contrast-enhanced MR study.

PURPOSE: We examined age-related changes in baseline regional cerebral blood volume (rCBV) and response to acetazolamide stimulation by using dynamic contrast-enhanced MR imaging. METHODS: Thirty healthy volunteers ranging widely in age (23 to 82 years) were examined before and after intravenous injection of acetazolamide with dynamic susceptibility contrast-enhanced MR imaging. rCBV values were normalized for intersubject and intrasubject comparison by estimating an arterial input function directly from the imaging data. Preacetazolamide baseline rCBV and the percentage volume change index (PVCI) of the postacetazolamide to preacetazolamide state were calculated and examined as a function of age. RESULTS: Older adults (>50 years) had lower baseline rCBV per unit tissue than did younger adults (<50 years), but higher rCBV after acetazolamide stimulation. Baseline rCBV tended to decrease with age in the medial frontal and frontoparietal gray matter regions. Response to acetazolamide stimulation, measured by PVCI, showed a significant age-related increase in gray matter, approximately 0.5% per year. CONCLUSION: rCBV can be significantly increased after acetazolamide stimulation in the healthy aged. These results support the notion that age-related decreases in rCBV measured at rest reflect reduced regional metabolic requirements rather than reduced capacity for regional substrate delivery. These data serve as a normative baseline for comparison studies of rCBV vascular reserve in aging persons with various cerebrovascular disorders.

Acetazolamide↗

PubMed1978

Gastrointestinal therapeutic system for acetazolamide. Efficacy and side effects.

Acetazolamide has been formulated in a new gastrointestinal therapeutic system that delivers the drug at an essentially constant rate of 15 mg/hr (GITS 15/125). We compared the therapeutic effect, magnitude of plasma concentration fluctuations, and incidence of side effects produced by the GITS 15/125 with conventional 250-mg acetazolamide tablets on eight glaucomatous patients randomly assigned to a different regimen each week. One or two GITS 15/125 twice a day (bid) were found as effective in reducing intraocular pressure as one 250-mg acetazolamide tablet. Plasma concentration fluctuations with the GITS 15/125 were decreased, compared with acetazolamide tablets, and, as a result, the incidence of drowsiness, tingling feet, tingling hands, and confusion was substantially reduced.

Acetazolamide↗

PubMed1983

Acetazolamide teratology and its association with carbonic anhydrase inhibition in the mouse.

Acetazolamide, an inhibitor of the enzyme carbonic anhydrase (E.C. 4.2.1.1.), causes a unique congenital anomaly characterized by postaxial reduction of the distal portion of the right forelimb. To gain an understanding of the mechanism of teratogenesis, the activity of carbonic anhydrase in sensitive and resistant mouse strains, and its inhibition by acetazolamide, were examined. Differences in teratologic sensitivity were found not to be attributable to differences in maternal or embryonic drug levels. Enzyme inhibition at acetazolamide concentrations ranging between 10(-11) and 10(-5) M did not differ between the mouse strains when adult erythrocytes or day 12 embryos were assayed. However, in day 10 embryos, the period of maximum teratologic susceptibility, a small strain difference was found which suggested that the form of carbonic anhydrase in the susceptible CBA/J strain at this time is somewhat more sensitive to inhibition by acetazolamide than the form found in the resistant SWV strain. The results suggest further that more than one isozyme of carbonic anhydrase may be present in all three samples.

Acetazolamide↗

PubMed1975

Binding-site interaction of chlorthalidone and acetazolamide, two drugs transported by red blood cells.

When 14C-chlorthalidone was administered orally to 2 healthy volunteers, the total recovery of radioactivity in urine (about 75 percent) and feces was close to 100 percent. Most of the label recovered in the blood was bound to the blood cells. When the procedure was repeated while the 2 subjects were receiving acetazolamide, the excretion of labeled material in urine and feces was essentially unchanged, but the blood cells contained less and the plasma more of the blood radioactivity. The half-life of the radioactivity in plasma and blood cells had decreased by about 65 percent. Intravenous administration of acetazolamide (single dose) to 2 other subjects who had received 14C-chlorthalidone orally resulted in a marked drop in the blood cell radioactivity, whereas that in plasma increased. The affinity of chlorthalidone for red blood cells was further evidenced on incubation of 14C-chlorthalidone with human blood. Of the incubated radioactivity, 94 percent to 99 percent was recovered in the erythrocytes. Preincubation of the blood samples with acetazolamide prior to the addition of 14C-chlorthalidone, as well as incubation of acetozolamide in blood samples previously incubated with 14C-chlorthalidone, demonstrated that acetazolamide is able to inhibit and to displace chlorthalidone from blood cells. There are several lines of evidence indicating that chlorthalidone is transported attached to the erythrocyte carbonic anhydrase.

Acetazolamide↗

PubMed1988

Characterization of isolated and cultured chick osteoclasts: the effects of acetazolamide, calcitonin, and parathyroid hormone on acid production.

The effects of acetazolamide, calcitonin (CT), and parathyroid hormone (PTH) on acid production in isolated osteoclasts has been investigated. Osteoclasts were isolated from the endosteum of 3-week chick tibias and were maintained under culture conditions for 5 days. The cells were treated with acetazolamide (10 x 4 M and 10(-7) M), CT (1 mU/ml and 0.31 mU/ml) and PTH (6.5 U/ml and 0.40 U/ml) for 1, 3, 6, and 18 hr. The cells were stained with acridine orange and the intensity of fluorescence measured by a light microscope photometer. Acetazolamide treatment resulted in a steady decline in intracellular acidity, suggesting that carbonic anhydrase plays a major role in acid production in isolated osteoclasts. Treatment with PTH produced a decline in acidity at 1 hr, followed by a peak at 3 hr and then a decline at 6 and 18 hr. The transient increase in acidity may be due to activation of carbonic anhydrase by PTH. Calcitonin treatment also resulted in a decline in cell acidity which was similar, but less pronounced than that resulting from acetazolamide treatment. These results indicate that calcitonin may mediate osteoclast activity by alterations in intracellular acid production.

Acetazolamide↗

PubMed1984

Determination of acetazolamide in biological fluids by reverse-phase high-performance liquid chromatography.

A high-performance liquid chromatographic method for the determination of acetazolamide in whole blood, plasma, and urine was developed. Samples of biological fluids containing various concentrations of acetazolamide were spiked with the internal standard, sulfadiazine. Samples were then mixed with a 50% ammonium sulfamate solution. Whole blood samples were heated for 25 s in boiling water. All samples were extracted with ethyl acetate; a phosphate buffer (pH 8.0) was used to wash the extracts. Acetazolamide was back-extracted into a glycine buffer (pH 10.0), which was then washed with ether. Separation of acetazolamide and internal standard from other biological constituents was achieved on a 10-micron C18 reverse-phase column using an acetonitrile-methanol-acetate buffer (pH 4.0). The eluant was monitored at 254 nm. All calibration curves were linear, and the results from reproducibility studies were excellent. Application of the method to human pharmacokinetic studies was demonstrated.

Acetazolamide↗

PubMed1988

Effect of salicylate on serum protein binding and red blood cell uptake of acetazolamide in vitro.

The diffusion of acetazolamide from buffered saline and buffered albumin solutions into human erythrocytes has been characterized. A model was developed for describing the effects of both intra- and extracellular binding on the approach to distributional equilibrium. Unbound acetazolamide entered the cells via an apparent first-order process at a rate that was unaffected by salicylate at a therapeutic concentration of 200 micrograms/mL. Salicylate concentrations ranging from approximately 100 to 400 micrograms/mL, were, however, extremely effective in displacing acetazolamide from its serum protein binding sites. Free fractions of acetazolamide in human serum were found to increase by an order of magnitude as salicylate concentrations approached 400 micrograms/mL, thereby greatly increasing the concentration of unbound drug available for passive diffusion into cells. The results indicate that while competitive binding effects, which may alter unbound drug concentration-time profiles and potentially impact on toxicity, do occur, alterations in red cell membrane permeability, which could adversely affect carbon dioxide transport, are not of significance.

Acetazolamide↗

PubMed2002

Test-retest reproducibility of quantitative CBF measurements using FAIR perfusion MRI and acetazolamide challenge.

The reproducibility of quantitative cerebral blood flow (CBF) measurements using MRI with arterial spin labeling and acetazolamide challenge was assessed in 12 normal subjects, each undergoing the identical experimental procedure on two separate days. CBF was measured on a 1.5T scanner using a flow-sensitive alternating inversion recovery (FAIR) pulse sequence, performed both at baseline and 12 min after intravenous administration of acetazolamide. T(1) was measured in conjunction with the FAIR scan in order to calculate quantitative CBF. The CBF maps were segmented to separate gray matter (GM) from white matter (WM) for region-of-interest (ROI) analyses. Post- acetazolamide CBF values (ml/100 g/min, mean +/- SD) of 87.5 +/- 12.5 (GM) and 46.1 +/- 10.8 (WM) represented percent increases of 37.7% +/- 24.4% (GM) and 40.1% +/- 24.4% (WM). Day-to-day differences in baseline CBF were -1.7 +/- 6.9 (GM) and -1.4 +/- 4.7 (WM) or, relative to the mean CBF over both days for each subject, -2.5% +/- 11.7% (GM) and -3.8% +/- 13.6% (WM) Day- to-day differences in absolute post-ACZ CBF increase were -2.5 +/- 6.8 (GM) and 2.7 +/- 9.4 (WM) or, relative to the mean CBF increase over both days for each subject, -4.7% +/- 13.3% (GM) and 9.1% +/- 26.2% (WM). Thus, FAIR- based CBF measurements show satisfactory reproducibility from day to day, but with sufficient variation to warrant caution in interpreting longitudinal data. The hemispheric asymmetry of baseline CBF and post-acetazolamide CBF increases varied within a narrower range and should be sensitive to small changes related to disease or treatment.

Acetazolamide↗

PubMed1986

Acetazolamide teratogenesis in Wistar rats: potentiation and antagonism by adrenergic agents.

Acetazolamide, a carbonic anhydrase inhibitor, induced right forelimb ectrodactyly in rat fetuses when the mothers were treated on late day 10 and early day 11 of gestation. Coadministration of the selective alpha-1-adrenergic agonist phenylephrine significantly increased the incidence of acetazolamide-induced right forelimb ectrodactyly while failing to induce the lesion when administered alone. Pretreatment with the alpha-adrenergic antagonists phenoxybenzamine and prazosin prevented the phenylephrine-induced increase in right forelimb ectrodactyly. In addition, treatment with either phenoxybenzamine or prazosin in the absence of stimulation with phenylephrine significantly decreased the incidence of acetazolamide-induced ectrodactyly. The results suggest an adrenergic component in acetazolamide teratogenesis. Alterations in uterine blood flow are discussed as a plausible mechanism for the modification of the incidence of ectrodactyly by these adrenergic agents.

Abnormalities, Drug-Induced↗

PubMed1988

Genetic differences in the frequency of acetazolamide-induced ectrodactyly in the mouse exhibit directional dominance of relative embryonic resistance.

Eleven of the common inbred strains of the mouse were surveyed for their teratogenic response to acetazolamide that was administered three times per os at 1,000 mg/kg (9 A.M. and 4 P.M. on day 9 and 9 A.M. on day 10). The products of conception were examined for gross malformations on day 15. One strain, SJL/J, exhibited maternal toxicity to the dosage regime and was excluded from the survey. Five strains exhibited significantly increased resorption rates after treatment. All strains responded with the expected malformation of postaxial forelimb ectrodactyly with a right-sided predominance. Nine of the strains could be assigned to one of four mutually exclusive classes of frequency of ectrodactyly and the tenth strain (BALB/cByJ) showed overlap between the two intermediate classes. The data suggest major genes determine the difference in sensitivity to ectrodactyly rather than a polygenic mode of inheritance. Induced cleft lip was found in four strains and one of these strains, SWR/J, exhibited a significantly higher frequency. The strain differences in sensitivity to induced resorption, forelimb ectrodactyly, and cleft lip were genetically independent. A reciprocal cross study was conducted with five of the strains from the four classes of frequency of ectrodactyly response in order to determine gene action. A significant maternal effect on the ectrodactyly response was found only with one of the strain pairs in the ten sets of reciprocal crosses with the five strains. When there was a significant difference between two strains, the F1 embryos exhibited dominance of relative resistance to ectrodactyly. The directional dominance of relative resistance to acetazolamide-induced ectrodactyly suggests that regulatory genes control the embryonic differences in frequency of ectrodactyly response to acetazolamide. By analogy with other metric traits of development that exhibit directional dominance, the genetic variation in ectrodactyly response that has been observed so far in the mouse embryo may not be involved with the primary target of acetazolamide teratogenesis.

Abnormalities, Drug-Induced↗

PubMed1992

Differential inhibition by acetazolamide on carbonic anhydrase distribution in the quail kidney: a proposal for a membrane-bound isoenzyme.

The effects of different concentrations of acetazolamide, a specific carbonic anhydrase inhibitor, have been investigated in the quail kidney. The histochemical patterns, interpreted by means of quantitative analyses proved that 0.1 microM acetazolamide inhibited the enzyme activity in all the reactive tubular segments except for distal tubules. At this site, the reaction product disappeared from the cytoplasm but strong positivity persisted at the apical surface. The luminal staining was still present at higher inhibitor concentrations up to 0.8 microM acetazolamide. Under histophotometric analyses, the residual reactivity proved to be nearly the same at the increasing inhibitor concentrations assayed. The validity of the results was checked by similar investigations in other control tissues. On the basis of the properties known for carbonic anhydrase in mammalian kidney, we conclude that the luminal membrane staining in the quail distal tubules might be due to a carbonic anhydrase isoenzyme that is similar, both in affinity for acetazolamide and in intracellular localization, to the membrane-bound enzyme purified from mammalian proximal convoluted tubules.

Acetazolamide↗

PubMed1986

Mechanisms of protective activity of 16,16-dimethyl PGE2 and acetazolamide on gastric and duodenal lesions in rats.

16,16-Dimethyl PGE2 (16,16-dmPGE2), given orally at 10-30 micrograms/kg, had no effects on gastric acid secretion, or carbonic anhydrase activity, but did increase HCO3- secretion in both the stomach and duodenum of rats. 16,16-dmPGE2, at nonantisecretory doses, potently inhibited indomethacin- and water-immersion stress-induced gastric lesions and mepirizole-induced duodenal lesions in rats. Acetazolamide, given orally at 50 mg/kg, markedly inhibited carbonic anhydrase activity, but had no effects on gastric acid secretion and the basal and 16,16-dmPGE2-stimulated HCO3- secretion. Acetazolamide, at a nonantisecretory dose, had no effects on indomethacin-induced gastric lesions and mepirizole-induced duodenal lesions, but significantly inhibited water-immersion stress-induced gastric lesions. Combined administration of 16,16-dmPGE2 and acetazolamide did not influence the protective activity of 16,16-dmPGE2 on these lesions. The mechanism of the cytoprotective activity of 16,16-dmPGE2 may involve an increase in HCO3- secretion (nonmediated by carbonic anhydrase), while mechanisms involved in the effects of acetazolamide are apparently different.

16,16-Dimethylprostaglandin E2↗

PubMed1996

Acetazolamide produced blood flow velocity changes measured by laser Doppler in gerbils with reduced CBF.

The effect of acetazolamide on the cerebral blood flow was studied in gerbils with unilateral carotid ligation. According to the effect of ligation the animals were divided into three groups: first group-the reduction more than 70%, second-CBF reduction 30-70% and the third group-CBF reduction less than 30%. The effect of acetazolamide administration was closely related to the effect of carotid ligation. More reduction of CBF was produced by carotid ligation, less increase of CBF after acetazolamide injection was noticed. The acetazolamide vascular reserve test was found a sensitive and useful method for detecting even modest reduction of vascular reserve in animals with slight - less than 30% CBF decrease following carotid ligation.

Acetazolamide↗

PubMed1985

Role of carbonic anhydrase in bone: partial inhibition of disuse atrophy of bone by parenteral acetazolamide.

Carbonic anhydrase inhibitor acetazolamide blocks the hypercalcemic response to parathyroid hormone (PTH) and to dibutyryl 3',5'-cyclic AMP in the nephrectomized-parathyroidectomized rat. In addition, we have reported that acetazolamide, when incorporated in the diet, partially prevents denervation-induced bone loss in a rat model of disuse osteoporosis. The present study compares the effectiveness of orally and subcutaneously administered acetazolamide in preventing denervation-induced bone loss in the rat model. The rats were treated with acetazolamide either orally, by incorporation in the diet of concentrations of 0.2, 0.5, or 1.5% for 15 days, or parenterally by two different subcutaneous methods of administration. The latter included either injection twice daily for 15 days or continuous infusion for 8 days using an osmotic minipump. It was found that parenteral administration was as effective in partially preventing denervation-induced bone mass changes as oral administration. In addition, protection by the parenteral route could be accomplished with much smaller daily doses; continuous infusion required the least daily dose. Approximately 50% protection was observed to occur with daily doses of 1,094, 129, and 8 mg/kg body weight for the oral, subcutaneous injection, and subcutaneous infusion routes respectively. These findings are consistent with our concept that carbonic anhydrase plays a significant role in bone metabolism.

Acetazolamide↗