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PubMed1986

Effect of acute hypercapnia on renal and proximal tubular total carbon dioxide reabsorption in the acetazolamide-treated rat.

The present study evaluates the effect of acute hypercapnia on renal total CO2 (tCO2) reabsorption after inhibition of renal carbonic anhydrase. Simultaneous renal clearance studies and free-flow micropuncture studies of the superficial proximal tubule were performed on plasma-repleted Sprague-Dawley rats treated with acetazolamide, 50 mg/kg body weight. Acute hypercapnia (arterial PCO2, 120 mmHg; blood pH, 7.02) was induced by ventilation with a 10% CO2-90% O2 gas mixture. Control rats (PCO2, 49.5 mmHg, pH 7.34) were ventilated with room air. The renal fractional excretion of tCO2 was approximately 20% lower in the hypercapnic group compared with the rats given acetazolamide alone. Acute hypercapnia reduced the fractional delivery of tCO2 to the late proximal tubule by a comparable amount. The absolute proximal reabsorption of tCO2 was increased by hypercapnia to 410 +/- 47 vs. 170 +/- 74 pmol X min-1, P less than 0.05. The single nephron glomerular filtration rate was 32.6 +/- 0.7 nl X min-1 in the hypercapnic group and 43.8 +/- 1.7 nl X min-1 in the rats given acetazolamide only, P less than 0.01. Acute hypercapnia enhances renal sympathetic nerve activity. To eliminate this effect, additional experiments were performed in which the experimental kidney was denervated before study. Denervation prevented the change in the single nephron filtration rate during acute hypercapnia, but absolute and fractional proximal tCO2 reabsorption remained elevated in comparison to denervated controls. The concentration of H2CO3 in the late proximal tubule, calculated from the measured luminal pH and bicarbonate concentration and the estimated cortical PCO2, was higher in the hypercapnic group, which was a finding compatible with H2CO3 cycling from lumen into proximal tubular cell, which provided a source of hydrogen ions for secretion.

Absorption↗
PubMed1999

Localization of carbonic anhydrase in living osteoclasts with bodipy 558/568-modified acetazolamide, a thiadiazole carbonic anhydrase inhibitor.

We describe the synthesis of Bodipy 558/568-modified acetazolamide, a fluorescent inhibitor of carbonic anhydrase and its use to localize the enzyme in living cells. The modified acetazolamide, with its specific sulfonamide group intact, labeled cells at concentrations as low as 10(-9) M, with a minimal loading time of 5 min. The staining was decreased by 57.4% by preincubating cells with unaltered acetazolamide (1:100) or with trifluoromethane sulfonamide, 6-ethoxyzolamide, and 5-(3-hydroxybenzoyl)-thiophene-2-sulfonamide. The efficacy of the inhibitor was unchanged by the fluorescent label, as determined by an acridine orange assay that detects acidification of osteoclasts, the cell model used in this study. This compound should prove to be useful for studying carbonic anhydrase in many organisms because of the high degree of conservation of the active site of this enzyme. (J Histochem Cytochem 47:545-550, 1999)

Acetazolamide↗
PubMed1994

Childhood pseudotumor cerebri: clinical and intracranial pressure response to acetazolamide and furosemide treatment in a case series.

The purpose of this study was to investigate the efficacy of combined therapy with acetazolamide and furosemide in normalizing intracranial pressure in children with pseudotumor cerebri. The role of repeated lumbar cerebrospinal fluid pressure monitoring in evaluating the response to therapy is also demonstrated. Continuous 1-hour lumbar cerebrospinal fluid pressure monitoring was done in eight children with pseudotumor cerebri on admission and at weekly intervals until the baseline pressure had normalized. (One child had two episodes of pseudotumor cerebri). All patients were treated with oral acetazolamide and furosemide until papilledema had cleared. Raised intracranial pressure was present on admission in all nine episodes of pseudotumor cerebri. Six children had an increased baseline cerebrospinal fluid pressure, whereas raised intracranial pressure was diagnosed in three children on account of an abnormal pulse wave and/or pressure waves. The mean baseline pressure was significantly lower after the 1st week of treatment than on admission (P = .007) and normalized in all patients within 6 weeks of start of therapy. All children had a rapid clinical response. Combined therapy with acetazolamide and furosemide is an effective first-line method of treating raised intracranial pressure in children with pseudotumor cerebri. The good correlation found between the clinical response and normalization of baseline cerebrospinal fluid pressure suggests that clinical monitoring of treatment is adequate in most children with this condition.

Acetazolamide↗
PubMed1981

Acute effects of acetazolamide in hyperkalemic periodic paralysis.

We studied the effect of acetazolamide on plasma potassium in normals and in two patients with hyperkalemic periodic paralysis. Administration of acetazolamide for 48 hours lowered mean plasma potassium in normals from 4.01 to 3.56 mEq per liter (p less than 0.001) and in the patients from 4.55 to 4.00 mEq per liter (p less than 0.001). This kaliopenic effect of acetazolamide may account for its therapeutic action in hyperkalemic periodic paralysis.

Acetazolamide↗
PubMed1996

Video-imaging micro-fluorometric assessment of luminal chloride/bicarbonate exchange activity in Madin-Darby canine kidney cells: influence of cell density, 4,4'-diisothiocyano-2,2'-disulfonic stilbene and acetazolamide.

To investigate whether or not MDCK cells may be used as a model for beta-intercalated cells, we studied: (1) The effect of luminal [Cl-]0 changes on pHi measured by video-imaging micro-fluorometry, (2) the influence of the inhibitor 4,4'-diisothiocyano-2,2'-disulfonic stilbene (DIDS) on anion-exchange activity, and (3) the effect of acetazolamide on intracellular pH-indicator (c-SNAFL-2) accumulation and anion-exchange activity. At least three different modes of fluorescence accumulation were found in confluent monolayers: cells with high, low or undetectable fluorescence. Highly fluorescent cells responded to a rise of [Cl-]0 (30-140 mM) with a proportional decrease of pHi (7.6-6.4). Acetazolamide (10(-4) M) completely blocked the acidifying effects of the increased [Cl-]0, indicating that HCO3- is the intracellular ion exchanged for extra-cellular Cl-. Acetazolamide caused a reduction of SNAFL-2 fluorescence suggesting that carbonic anhydrase activity contributes to indicator accumulation. The high DIDS concentration (50 microM) required to prevent intracellular acidification suggests that the exchanger involved is identical to that present in beta-intercalated cells. All cells of non-confluent monolayers were highly fluorescent and expressed Cl-/ HCO3(-)-exchanger activity. In conclusion, highly fluorescent MDCK cells in confluent monolayers have a luminal DIDS inhibitable, carbonic anhydrase dependent Cl-/HCO3(-)-exchanger, and may therefore be used as a model for beta-intercalated cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2001

Randomized, controlled trial of acetazolamide and furosemide in posthemorrhagic ventricular dilation in infancy: follow-up at 1 year.

OBJECTIVE: Posthemorrhagic ventricular dilation (PHVD) is a complication of intraventricular hemorrhage in preterm infants and is associated with a high risk of long-term disability. Furosemide and acetazolamide are used widely in the treatment of PHVD in the hope of avoiding the need for placement of a ventriculoperitoneal shunt, but these drugs have not been evaluated in a controlled trial. This article reports a multicenter, randomized, controlled trial designed to test the hypothesis that these drugs would reduce the rate of shunt placement (or death) and increase survival to 1 year of age without disability. METHODS: Between 1992 and 1996, 177 infants who were less than 3 months past term and had ventricular width >4 mm above the 97th centile following intraventricular hemorrhage were assigned randomly to either standard therapy or standard therapy plus drug therapy with acetazolamide (100 mg/kg/d) plus furosemide (1 mg/kg/d). Infants who were enrolled in the trial had a median gestational age of 28.6 weeks and were enrolled at a mean postnatal age of 3.6 weeks. Forty-four percent were reported to have a cerebral parenchymal lesion on ultrasound scan at randomization. The primary outcome measure of death or shunt placement (known in all but 1 infant) occurred in 56 of 88 infants who were allocated to drug plus standard therapy compared with 46 of 88 who were allocated to standard therapy. The risk ratio was 1.23 (95% confidence interval: 0.95-1.59). Neurodevelopmental outcome information at a corrected age of 1 year (known in all but 3 of 149 surviving infants) included disability or neuromotor impairment in 54 of 67 infants (81%) who were allocated to drug plus standard therapy and 52 of 69 infants (66%) who were allocated to standard therapy. Seventy-two of 85 infants (85%) who were allocated to drug therapy either died or were disabled or impaired at 1 year compared with 62 of 89 infants (70%) who were treated with standard therapy (risk ratio: 1.22; 95% confidence interval: 1.03-1.4376). The excess risk of these adverse outcomes was greater among infants who did not have a cerebral parenchymal lesion seen on ultrasound examination at trial entry. CONCLUSIONS: These results suggest that the use of acetazolamide and furosemide in preterm infants with PHVD is ineffective in decreasing the rate of shunt placement and is associated with increased neurologic morbidity. This treatment therefore cannot be recommended.

Acetazolamide↗
PubMed1988

Effect of cisternal administration of acetazolamide on rapid excitation of central chemoreceptors.

We evaluated rapid and transient changes in phrenic (PN) and internal intercostal (IIC) activities when 0.5 ml of saline saturated with 100% CO2 was injected into the vertebral artery at the C1 level before and after cisternal administration of carbonic anhydrase inhibitor (acetazolamide) in decerebrated, spontaneously breathing cats. Before acetazolamide administration, the injections evoked an initial, transient inhibition of ongoing PN or IIC activity, followed by excitation of subsequent respiratory activities with a short onset latency of less than 3 sec. On the other hand, cisternal administration of acetazolamide abolished both the initial inhibition and the subsequent rapid excitation of respiratory activities, although there still existed a delayed, weak and prolonged excitation of respiration. These results indicated that hydration of CO2 accelerated by carbonic anhydrase within the brain would be essential for the rapid changes in respiratory activity mediated by the central chemoreceptors.

Acetazolamide↗
PubMed2004

Development of topically effective formulations of acetazolamide using HP-beta-CD-polymer co-complexes.

The myriad of side effects induced by acetazolamide (oral use), the introduction of newer topical carbonic anhydrase inhibitors (CAI's) and the advent of other antiglaucoma medications has led to a decreased interest in acetazolamide. The use of cyclodextrins to improve the solubility and bioavailability of poorly soluble drugs has however, rekindled an interest in acetazolamide (ACZ), because its poor solubility is one of the major factor responsible for its failure to show topical effectiveness. Since water soluble polymers have been reported to improve the complexing capabilities of beta-cyclodextrins, in the present study water soluble polymers like polyvinyl alcohol (PVA), polyvinylpyrrolidone (PVP), hydroxypropymethylcellulose (HPMC) and the mucoadhesive polymer Carbopol 934P were incorporated into aqueous 10% w/v 2HP-beta-CD solution to improve the solubility of ACZ. The effect of these polymers on the corneal transport of 5 mg/ml (0.5% w/v) solution of ACZ in aqueous 10% 2HP-beta-CD was evaluated. The inclusion of these polymers significantly increased the solubility of ACZ from 3.43 mg/ml in aqueous 10% 2HP-beta-CD to 5.1 mg/ml (48.6%) in 0.05% PVP; 6.80 mg/ml (98.3%) in 0.05% PVA; and 6.74 mg/ml (96.5%) in 0.2% Carbopol 934P. From amongst the various polymers assessed in the study, PVA was deemed the best, based on the premise of better apparent permeability coefficient (P(app)) upon in vitro corneal permeation studies. Inspite of a large enhancement in solubility produced by Carbopol 934P, surprisingly, it could not efficiently increase the Papp.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed1989

The acute effect of acetazolamide on glomerular filtration rate and proximal tubular reabsorption of sodium and water in normal man.

The acute effects on kidney function of acetazolamide (250 mg) given intravenously were evaluated in seven healthy subjects. Glomerular filtration rate was measured as the renal clearance of 51Cr-EDTA, and fluid flow rate out of the proximal tubules was assessed by measurement of the renal lithium clearance. An 18% decline in glomerular filtration rate (ml/min) was observed after acetazolamide administration (109 +/- 16 vs 89 +/- 14, p less than 0.02), while lithium clearance (ml/min) increased by 35% (30 +/- 5 vs 38 +/- 8, p less than 0.02). Absolute proximal tubular reabsorption of water (ml/min) was reduced by about one third (79 +/- 12 vs 51 +/- 9, p less than 0.02), and fractional proximal reabsorption of water and sodium (%) declined (73 +/- 2 vs 58 +/- 6, p less than 0.02). Renal sodium clearance and absolute distal reabsorption of sodium increased, while fractional distal reabsorption of sodium declined. Acetazolamide reduces absolute and fractional proximal tubular reabsorption of sodium and water, and glomerular filtration rate. Primarily, this induces an increase in the output of fluid from the proximal tubules accounting for the diuretic effect of the drug. The acute fall in glomerular filtration rate is probably mediated by a temporary increase in proximal intratubular pressure and activation of the tubuloglomerular feedback mechanism.

Acetazolamide↗
PubMed1980

Teratogenic activity in the mouse after oral administration of acetazolamide.

Acetazolamide was administered orally by gavage to pregnant mice twice a day on days six through 15 of gestation at a dose level of 300.0 mg/kg. This treatment produced maternal toxicity as evidenced by significantly reduced food consumption and body weight gain. Embryotoxicity demonstrated by significant reductions in fetal weight and crown-rump length was also observed. Resorption rates were considerably higher (77.9%) for the acetazolamide treated litters when compared to those from the control group (8.23%). A variety of malformations was observed in the acetazolamice-treated rats (rib and vertebral fusion, gastroschisis, tail defects, cleft palate and ectrodactyly). These results further establish acetazolamide as an acceptable positive teratogenic control by demonstration of species and strain susceptibility in the CD-1 mouse.

Abnormalities, Drug-Induced↗
PubMed1989

Intraocular pressure changes during hemodialysis: prevention of excessive dialytic rise and development of severe metabolic acidosis following acetazolamide therapy.

The response of intraocular pressure (IOP) to hemodialysis was investigated in 55 patients with end-stage kidney disease enrolled in a chronic dialysis program. The mean level of IOP, measured by the Goldman applanation tonometer, before dialysis was slightly lower than that of a control group of 50 healthy subjects (14.9 +/- 2 mm Hg vs 15.6 +/- 1.9 mm Hg. p = .07). During dialysis IOP underwent an excessive rise (7.8 to 12.5 mm Hg) in 10 patients (group 1), remained unchanged (variations below 2 mm Hg) in 41 patients (group 2), and decreased (3.1 to 5.1 mm Hg) in 4 patients (group 3). In group 1 patients, gonioscopy showed a narrow angle between iris and lateral cornea. Conversely, the anterior chamber angle was normal in patients of groups 2 and 3. The effect of a 7-day course of acetazolamide therapy (500 mg per day orally) on IOP was investigated in group 1 patients. Acetazolamide was capable of preventing the excessive IOP rise during dialysis. The mean reduction of such a dialytic rise was 8.1 mm Hg. However, despite this effect, in these patients the IOP level after dialysis still remained significantly higher than that of patients of group 2 (18.1 +/- 1 mm Hg vs 14.9 +/- 0.8 mm Hg. p less than .0001). Acetazolamide therapy precipitated in all patients a severe metabolic acidosis (blood pH fell from 7.38 +/- 0.02 to 7.24 +/- 0.03, p less than .0001; and bicarbonate concentration from 21 +/- 2.5 mmol/liter to 12.3 +/- 2.4 mmol/liter, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1975

Effect of parenteral acetazolamide on intestinal absorption of salt and water in man.

Acetazolamide was administered intravenously during jejunal perfusion of isotonic saline in six subjects. Bicarbonate was present in very low concentration intraluminally and there was net bicarbonate secretion during control and acetazolamide perfusions. Acetazolamide significantly inhibited sodium chloride, and water absorption. As this occurred in the absence of an effect on net bicarbonate secretion, it may have been due to an action other than carbonic anhydrase inhibition.

Acetazolamide↗
PubMed1999

[Reduction of renal uranium uptake by acetazolamide: the importance of urinary elimination of bicarbonate].

Acetazolamide was compared with bicarbonate for the treatment of contamination with uranium. Uranium was injected peritoneally in rats, and its distribution was investigated. Acetazolamide was three times more efficient than bicarbonate in reducing the renal content of uranium. On the other hand, it had no effect on hepatic or skeletal content. In this study, renal physiology provides the basis for understanding the mode of action of acetazolamide and bicarbonate. In this context, it is of interest to determine the alkalinity of the urine, with the aim of knowing whether bicarbonate is present to mobilize uranium.

Acetazolamide↗
PubMed2000

Acetazolamide stress brain-perfusion SPECT predicts the need for carotid shunting during carotid endarterectomy.

UNLABELLED: Although carotid shunting is occasionally necessary to prevent cerebral ischemia during carotid endarterectomy, there is no reliable indication for this procedure. The purpose of this study was to evaluate whether acetazolamide stress brain-perfusion SPECT can predict the need for carotid shunting during carotid endarterectomy. METHODS: Basal and acetazolamide stress brain-perfusion SPECT imaging was performed using a 1-d protocol and 99mTc-ethylcysteinate dimer (ECD) in 75 patients (12 women, 63 men; mean age, 64.8 y) before carotid endarterectomy. The need for carotid shunting during carotid endarterectomy was determined by the development of neurologic deterioration after carotid clamping under regional anesthesia. Regional cerebral blood flow, cerebrovascular reserve, the presence of contralateral carotid stenosis (> or =70%), and clinical risk factors, including age, sex, history of minor stroke or transient ischemic attack, diabetes mellitus, hypertension, and smoking, were assessed with regard to whether they could predict the need for shunting. RESULTS: Carotid endarterectomy was performed safely without carotid shunting in 61 of 75 patients (81.3%). Carotid shunting was required in 14 patients (18.7%). Seven of 21 patients with a contralateral carotid stenosis, 9 of 41 with a reduced regional cerebral blood flow, and 11 of 30 with a reduced regional cerebrovascular reserve underwent carotid shunting. Patients with a reduced cerebrovascular reserve had a significantly higher number of carotid shunts performed (P < 0.01) than did those with a normal reserve, whereas contralateral carotid stenosis (P = 0.054) showed borderline significance. Reduced cerebral blood flow and clinical risk factors did not predict the need for carotid shunting (P > 0.1). Multiple logistic regression analysis showed that reduced cerebrovascular reserve was the only reliable predictor of the need for carotid shunting (P < 0.01). When a severely reduced cerebrovascular reserve (8/8) or reduced cerebral blood flow and cerebrovascular reserve with contralateral carotid stenosis (6/7) were present, carotid shunting was necessary, with positive and negative predictive values of 91% (10/11) and 94% (60/64), respectively. CONCLUSION: A reduced cerebrovascular reserve can predict the development of cerebral ischemia during carotid clamping. Acetazolamide stress brain-perfusion SPECT may be useful as a complementary method in determining selective carotid shunting during carotid endarterectomy.

Acetazolamide↗
PubMed2001

[A case of potassium-sensitive periodic paralysis with cardiac dysrhythmia controlled with imipramine and acetazolamide].

We report a patient with potassium-sensitive periodic paralysis with cardiac dysrhythmia. The patient was a 16-year-old man. He presented with asymptomatic ventricular dysrhythmia and periodic paralysis when he was 6 and 12 years old, respectively. Physical examination revealed slight dysmorphic features such as hypoplastic mandible, low-set ears and clinodactyly. Through an exercise test, a potassium tolerance test and a muscle biopsy, his illness was diagnosed as potassium-sensitive periodic paralysis with cardiac dysrhythmia. For the treatment of his episodic paralysis, we started acetazolamide, which improved both the incidence and the severity of paralysis. However, the incidence of cardiac dysrhythmia was increased after the use of acetazolamide. Routine anti-arrhythmic drugs such as lidocaine failed to control his ventricular dysrhythmia. Only imipramine showed its efficacy by improving the degree and the incidence of cardiac dysrhythmia without aggravating periodic paralysis. This syndrome is relatively rare and there have been no standard protocols for the treatment. We propose the combination of acetazolamide and imipramine as the first choice for this clinical entity. We also discussed the efficacy of the exercise test. It enabled us to confirm the diagnosis of periodic paralysis safely and easily by recording the change of compound muscle action potential amplitudes.

Acetazolamide↗
PubMed2001

The efficacy of acetazolamide on visual functions in a patient with choroid metastasis of breast carcinoma.

Breast carcinoma is the most frequent cancer in women and is the second leading cause of death. Choroid metastasis of breast carcinoma can be found either at presentation or in remission. It is frequently encountered in disseminated breast cancer with multiple organ metastasis. It has been proposed that the oedema-reducing effect of acetazolamide is due to stimulated ion and fluid removal from the retina to the choroid. A 40-year-old female patient on adjuvant chemotherapy for breast cancer was found to have an isolated choroid metastasis. Clinical and radiological remission was achieved after orbital radiotherapy, chemotherapy and acetazolamide treatment. In this case report, we emphasise the possible beneficial effect of acetazolamide in patients with choroid metastasis.

Acetazolamide↗
PubMed1975

Changes in the surface features of choroid plexus of the rat following the administration of acetazolamide and other drugs which affect CSF secretion.

The surface of the choroid plexus of the rat was examined by scanning electron microscopy before and after administration of acetazolamide and other drugs (cardiac glycosides and pilocarpine) which affect the rate of secretion of the CSF. In control animals, bleb-covered cells were more common on the IVth ventricle choroid plexus than on the lateral ventricle choroid plexus (20 per specimen compared to 0-3 per specimen). Following administration of acetazolamide the number of bleb-covered cells was reduced significantly (P less than 0-001). The effects of the other drugs were less well defined. Since acetazolamide is known to interfere with the active transport of the extra chloride ions normally added to the CSF in the IVth ventricle, it is suggested that the bleb-covered cells of the IVth ventricle choroid plexus are the specific site for chloride secretion.

Acetazolamide↗
PubMed1976

The effect of acetazolamide on the movements of anions into the posterior chamber of the dog eye.

The rate of entry of bicarbonate and chloride ions the posterior chamber of the dog, a species that has both HCO3- and Cl- concentrations in excess of plasma in this chamber, was measured in order to clarify the mechanisms involved in the produciton of aqueous humor. Four animals were given H14CO3- and 36Cl- intravenously first in a control series and then after pretreatment with acetazolamide, (50 mg/kg), a carbonci anhydrase inhibitor. Samples were taken from arterial blood and the posterior chamber. Acetazolamide did not affect chloride entry into the posterior chamber but bicarbonate entry was decreased about 50%. It is concluded that in this species, bicarbonate is the key anion for the decrease of aqueous humor production caused by the administration of acetazolamide.

Acetazolamide↗