Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACETAZOLAMIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1978

Effect of long-term subconjunctival administration of Diamox (acetazolamide) on the ocular tension in rabbit.

In eight normal rabbits, sodium acetazolamide (5.5 mg per kg of body weight) in 11% solution was injected subconjunctivally daily for about four weeks in the left eye of each rabbit, with the right eye serving as a control. Ocular tension in both eyes was measured by the Perkins hand-held applanation tonometer. Five of the eight rabbits showed a significant difference (P less than 0.05) in ocular tension between treated and untreated eyes, with a decrease in the treated left eye. The ocular tension decrease in the treated left eye began about one week after the beginning of the injections and lasted for about two weeks. Thereafter, ocular tension in the treated left eye returned to base-line levels, despite continued subconjuctival injection of sodium acetazolamide.

Acetazolamide↗
PubMed1979

Sodium reabsorption in the papillary collecting duct of rats. Effect of adrenalectomy, low Na+ diet, acetazolamide, HCO-3-free solutions and of amiloride.

Using the shrinking droplet method and simultaneous perfusion of the peritubular capillaries the isotonic reabsorption of Ringer's solution from the papillary collecting ducts was measured. Under control conditions the volume reabsorption from the papillary collecting ducts was Jv +/- SE = 2.6 +/- 0.1 . 10(-5) cm3 . cm-2 . s-1. In rats which were on low Na+ diet, Jv increased to 127%, and in adrenalectomized animals it decreased to 34% of the control value. Three hours after a;ocatopm pf a;dpsterpme om tje adrenalectomized animals Jv was partially restored to 63% of control rats. Amiloride 10(-4) M, added to the luminal perfusate, produced a strong inhibition of Jv (to 32% of control). Acetazolamide, 10(-4) M, added to both perfusates, reduced Jv very strongly (to 40% of control), while omission of bicarbonate reduced it only to 77% of control. Acetazolamide, added to bicarbonate-free perfusates, did not result in a significant further reduction of Jv. The data indicate that the Na+ reabsorption from the papillary collecting duct is controlled by mineralocorticoids. Furthermore, they suggest the existence of two transport mechanisms in the luminal cell membrane: 1. An amiloride-sensitive entry step and 2. an entry step via a Na+-H+-countertransport mechanism, the latter being less important.

Absorption↗
PubMed1991

Acetazolamide for alkalinisation of urine in patients receiving high-dose methotrexate.

Acetazolamide, 500 mg 6 hourly, has been used to alkalinise the urine in patients receiving high dose methotrexate. A urinary pH of greater than 7.5 was achieved in every cycle (13 cycles in 10 patients). In 6 cycles a single supplementary dose of sodium bicarbonate was necessary. Plasma methotrexate levels fell satisfactorily at 24 and 48 h. Acetazolamide is a simple and effective method of achieving urinary alkalinisation with advantages over oral and intravenous bicarbonate.

Acetazolamide↗
PubMed1995

18FDG PET and acetazolamide-enhanced 99mTc-HMPAO SPET in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), brain and kidney are the most frequently affected organs. Measurements of cerebral blood flow and metabolism by means of positron emission tomography (PET) and single-photon emission tomography (SPET) can contribute to the diagnostic assessment of the involvement of the central nervous system (CNS) in SLE. Functional imaging has been proven to be more sensitive than morphological imaging (magnetic resonance imaging and computed tomography). In this report, we present the case of a 70-year-old female patient, suffering from SLE without symptoms of CNS involvement. In addition to a SPET study using technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO) and a PET scan with fluorine-18 deoxyglucose (18FDG), a SPET study after acetazolamide injection was performed in order to assess the cerebral perfusion reserve. While the PET scan showed no major abnormalities, and the baseline SPET study revealed only minor changes, the acetazolamide-enhanced SPET study revealed a marked reduction of the cortical perfusion reserve, particularly in both frontal lobes. It is concluded that "preclinical" CNS involvement, mainly caused by pathological mechanisms involving the cerebral blood vessels, can be considered to exist in this patient with SLE.

Acetazolamide↗
PubMed1997

Comparison of changes in cerebral blood flow and cerebral oxygen saturation measured by near infrared spectroscopy (NIRS) after acetazolamide.

The present study compares the change of cerebral blood flow and HbO2 measured by near-infrared spectroscopy (NIRS) after administration of 1000 mg acetazolamide intravenously. CBF studies in 21 patients with ischaemic cerebrovascular disease were performed routinely with the 133Xenon technique. Additionally the local HbO2 was recorded by NIRS. A rest study was followed by a second study after the administration of 1000 mg acetazolamide. In 18 patients we observed an increase of 30.8% of CBF and 4.7% of HbO2, 3 patients showed a decrease of CBF and 2 patients a simultaneous decrease of HbO2. We did not find a correlation between the absolute values of CBF and HbO2 at rest or after stimulation. However, a positive correlation (r = 0.71, p < 0.05) between the change of CBF and HbO2 could be detected. Assuming a threshold value of normal CBF reactivity of 30% and 4% HbO2 reactivity we found for NIRS a sensitivity of 0.88 and a specificity of 0.75. The results demonstrate that changes of CBF can be detected with NIRS and the algorithm of the used monitor is able to calculate the intracranial part of the signal. So, NIRS can be used as non-invasive screening method to test the cerebrovascular reserve capacity.

Acetazolamide↗
PubMed1975

Inhibition of diuresis in the tsetse fly (Glossina morsitans) by ouabain and acetazolamide.

Acetazolamide and ouabain, metabolic inhibitors which interfere with certain membrane transport systems, reduce the rate of water elimination by male Glossina morsitans morsitans. The results suggest that water is transported across membranes during diuresis and that a ouabain sensitive Na+K+ATPase and an acetazolamide-sensitive carbonic anhydrase are involved in diuresis.

Acetazolamide↗
PubMed2000

The threshold of acetazolamide vasoreactivity as an indicator of maximum cerebral blood volume.

Using xenon-enhanced computed tomographic (Xe-CT) cerebral blood flow (CBF) measurement, we attempted to determine the extent of vasoreactivity indicating reserve autoregulatory potential by comparing maximal cerebral blood volume (CBV) induced by acetazolamide activation (activated CBV) and the resting CBV. We measured the activated and resting CBVs in two different groups by the subtraction technique using contrast-enhanced CT, and measured the resting and activated CBF in both groups to calculate the percentage increase (%deltaCBF). We extracted CBF and CBV in the territory of the middle cerebral artery on both sides separately for each patient, and treated them independently. We then divided the resting CBV values in group B (25 patients, n=50) into 6 subgroups according to their %deltaCBF (below 10%, n=13; 20%, n=7; 30%, n=8; 40%, n=6; 50%, n=6; and over 50%, n=10) and examined the differences from the activated CBVs in group A (12 patients, n=24) by Dunnett's multiple comparison test. Significant differences were seen in subgroups with %deltaCBF exceeding 20% but less than 30%, and in the subgroups with higher %deltaCBF. We consider that %deltaCBF of at least 20% induced by acetazolamide indicates nonmaximal vasodilation, i.e., reserve autoregulatory potential.

Acetazolamide↗
PubMed2000

Simplified quantitative determination of cerebral perfusion reserve with H2(15)O PET and acetazolamide.

The measurement of regional cerebral blood flow (rCBF) and perfusion reserve (PR) with H2(15)O positron emission tomography (PET) and acetazolamide challenge is of importance in evaluating patients with cerebrovascular disease and is thought to be useful in selecting patients for possible vascular surgery. Full quantitative assessment of rCBF with PET requires arterial blood sampling, which is inconvenient in a clinical setting. In this work, we present a simple non-invasive method with which to quantitatively evaluate PR in one PET session lasting no more than 30 min. In ten patients with cerebrovascular disease, rCBF was measured with H2(15)O PET under the baseline condition and after administration of 1 g acetazolamide using a standard technique involving arterial blood sampling. The activity accumulated over 60 s was normalized to injected activity per kilogram body weight (nAA) and compared with rCBF in eight different brain regions. A high linear correlation was found for PR based on nAA (PRnAA) and rCBF (PRrCBF) (PRnAA=0.843 PRrCBF + 0.092, r=-0.83, Pearson's correlation coefficient). Bland-Altman analyses further confirmed that PRnAA reflects PR in a quantitative manner. These results demonstrate that the method based on normalized counts allows the quantitative assessment of PR without blood sampling.

Acetazolamide↗
PubMed2001

Assessment of cerebral perfusion and cerebrovascular reserve in insulin-dependent diabetic patients without central neurological symptoms by means of 99mTc-HMPAO SPET with acetazolamide.

The detection of subclinical abnormalities in cerebral blood flow could be of great value in identifying diabetic patients at risk of stroke. The aim of this study was to assess the contribution of semiquantified post-acetazolamide technetium-99m hexamethylpropylene amine oxime single-photon emission tomography (99mTc-HMPAO SPET) in 15 diabetic patients with no clinical history of central neurological disease. After baseline 99mTc-HMPAO SPET, a second SPET scan was acquired after activation of the cerebrovascular reserve (CVR) with an injection of 1 g of acetazolamide (post-ACZ SPET). Semiquantitative analysis was made in 16 regions of interest (ROIs) drawn for each of the three supratentorial slices selected, and in two ROIs in the infratentorial slice. The CVR was calculated in each ROI by subtracting the decay-corrected baseline images from those obtained in the post-ACZ SPET and expressed as the percent increase in the average counts between the two scans. Baseline perfusion and CVR values in the study group were compared with the corresponding values in a control group. Of 750 cortical ROIs studied, 332 showed a decreased CVR (44.3%). The baseline perfusion SPET study showed hypoperfusion in 65 ROIs (8.6%) and hyperperfusion in 56 (7.4%). Of the 65 hypoperfused regions, 66.2% had a normal CVR and 33.8% had a decreased CVR, whereas of the 56 hyperperfused regions, 51.8% had a CVR within normal limits and 48.2% showed a decreased CVR. In conclusion, in comparison with baseline 99mTc-HMPAO SPET, the ACZ activation test provided additional information in the study of cerebrovascular impairment, and allowed characterisation of the subclinical abnormalities in the population studied. The technique may therefore prove useful in evaluating future preventive strategies for stroke in diabetic patients.

Acetazolamide↗
PubMed2001

Lack of gender difference in acetazolamide-induced cerebral vasomotor reactivity in patients suffering from type-1 diabetes mellitus.

The aim of the present work was to investigate the impact of gender on resting cerebral blood flow velocity and cerebrovascular reserve capacity among diabetic patients. Middle cerebral artery mean blood flow velocity (MCAV) was measured in 72 patients suffering from type 1 diabetes mellitus at rest and 5, 10, 15 and 20 min after intravenous administration of 1 g acetazolamide. Cerebrovascular reserve was calculated as the maximal percent increase in MCAV after acetazolamide. Resting MCAV and cerebrovascular reserve capacity were compared between males and females. Resting cerebral blood flow velocity was higher in diabetic females than in males (men, 55.0+/-17.0 cm/s; women, 64.4+/-12.6 cm/s, p=0.0094). Cerebrovascular reserve capacity was similar in diabetic women and men (men, 44.0%+/-18.6%; women, 52.6%+/-32.9%, p=0.17). Comparing MCAV and cerebrovascular reserve capacity among the diabetic subgroups with disease duration < or = 10 years and >10 years, we did not detect any differences between women and men. Duration of diabetes was an important factor in determining cerebrovascular reserve capacity in both sexes: long-term diabetic women and men showed lower CRC values than diabetics with < or = 10 years disease duration. Cerebrovascular reserve capacity is similar in diabetic women and men. Taking into consideration that cerebrovascular reserve is normally higher among women, our finding indicates a relatively more serious worsening of cerebral vasodilatory responses in women suffering from type 1 diabetes.

Acetazolamide↗
PubMed1985

Failure of acetazolamide to decrease intraocular pressure in patients with carbonic anhydrase II deficiency.

The effect of the carbonic anhydrase inhibitor acetazolamide on intraocular pressure was studied in two patients with carbonic anhydrase II deficiency and in six control subjects. The deficient patients had the autosomal recessive syndrome of osteopetrosis with renal tubular acidosis and cerebral calcification. A dose of 125 mg of intravenous acetazolamide caused a significant (P less than .01) decrease in intraocular pressure from baseline (15.0 +/- 1.5 mm Hg) in the control subjects one hour (11.3 +/- 1.5 mm Hg) and four hours (13.8 +/- 1.2 mm Hg) after drug administration. In contrast, the patients with carbonic anhydrase deficiency showed no such decrease in intraocular pressure; baseline intraocular pressure (19.2 +/- 0.2 mm Hg) was significantly unchanged (P greater than .5) at one hour (20.0 +/- 0.1 mm Hg) and four hours (19.2 +/- 0.2 mm Hg).

Acetazolamide↗
PubMedDate not supplied

[3H]acetazolamide binding to carbonic anhydrase in normal and transformed cells.

The binding of [3H]acetazolamide (AZ), a carbonic anhydrase (CA) inhibitor, to soluble and particulate forms of CA was investigated. Sources for the assays were purified CA II, adult rat cortical, oligodendrocyte and neuronal enriched preparations; cultured murine glial cells, rat C-6 glioma, rat hepatoma and human glioblastoma cells. CA enzyme activity in the same preparations was also assayed by following change in pH during incubation. A gel permeation chromatographic method was developed to assess [3H]AZ binding to soluble CA, while glass fiber filter vacuum filtration was used for particulate CA binding. Saturable specific binding of [3H]AZ to rat cortical soluble and particulate CA preparations was demonstrated. Computer-assisted data analysis estimated the binding parameters of [3H]AZ to soluble rat cortical CA to be Bmax = 0.38 +/- 0.13 pmol/mg protein and Kd = 34.7 +/- 17.5 nM. The rat cortical particulate fraction Bmax was 2.05 +/- 0.28 pmol/mg protein with a Kd of 107.1 +/- 24.2 nM. Purified bovine CA-II bound 1.15 +/- 0.19 pmol [3H]AZ/mg protein with a Kd of 54.0 +/- 3.4 nM. The pH optima for [3H]AZ binding to soluble and particulate CA was between 6.5 and 7.5. Binding was linear with respect to protein up to 1.0 mg/mL. The particulate fraction bound 3-4 times more [3H]ligand per unit protein than the soluble fraction. Interestingly, no detectable CA enzyme activity or [3H]AZ binding was observed in the soluble or particulate fractions of human glioblastoma, rat C-6 glioma or rat hepatoma cells. Binding of [3H]AZ to other soluble enzymes or proteins was negligible. In competition binding experiments, a rank order of inhibition of [3H]AZ binding to rat cortical CA by established CA inhibitors was: dichlorphenamide greater than acetazolamide greater than or equal to benzolamide greater than methazolamide greater than hydrochlorothiazide greater than or equal to sulfanilamide. [3H]AZ binding was not affected by other classes of pharmacologic characterizing agents. The binding of [3H]AZ to the CA enzyme molecule is highly specific and sensitive and may prove useful in vitro or in situ as a probe for this enzyme.

Acetazolamide↗
PubMed1984

Effects of acetazolamide and electrical stimulation on cerebral oxidative metabolism as indicated by the cytochrome oxidase redox state.

The intravenous administration of acetazolamide to rats caused a prompt oxidation of cytochrome a,a3 that was associated with an increase in the rate at which this cytochrome underwent additional oxidation and reductive recovery after electrical stimulation of the cerebral cortex. These effects were not observed in animals made hypercapnic after ventilation with 5% CO2. The speed with which these and other metabolic and physiological events occur, after administering the drug, suggests that acetazolamide exerts its effects by complex mechanisms and that the site of action may be in the region of the blood-brain barrier, an area rich in carbonic anhydrase, and noradrenergic innervation.

Acetazolamide↗
PubMed1993

Acetazolamide specifically inhibits lingual trigeminal nerve responses to carbon dioxide.

The goal of this study was to examine the role of the enzyme, carbonic anhydrase, in oral trigeminal chemoreception with particular regard to the reception of CO2. Using both single and multiunit recordings of trigeminal neurons in the lingual nerve of rat, we measured responses to cool (24 degrees C), noxiously hot (55 degrees C) and cold (8 degrees C) H2O, NH4Cl and supersaturated solutions of CO2 (24 degrees C and 33 degrees C). The importance of peripheral carbonic anhydrase was tested by inhibiting enzyme activity with acetazolamide (15 mg/kg b.w.). Single unit responses to CO2 and HCl suggest that neural sensitivity to CO2 is not simply a function of extraepithelial pH. Responses to CO2 were significantly inhibited by acetazolamide while the responses to thermal stimuli and NH4Cl were not. The results support a role for carbonic anhydrase in trigeminal responses to CO2. Furthermore, the results suggest that intraepithelial acidification mediated by carbonic anhydrase may be the basis for sensitivity to CO2.

Acetazolamide↗
PubMed1994

Microdialysis analysis of effects of loop diuretics and acetazolamide on chloride transport from blood to CSF.

With the hypothesis that the NaCl cotransporter in mammalian choroid plexus (CP) has a role in CSF formation, we postulated that loop diuretic agents would curtail transport of Cl from blood to CSF. Microdialysis in the cisterna magna of Sprague-Dawley rats was used to assess the ability of furosemide and ethacrynic acid (i.e. loop agents that interfere directly with cotransport) to inhibit 36Cl transport from blood to CSF over a 3-h period. Cl uptake by CSF was quantified as % volume of distribution (Vd) of 36Cl, i.e. 100 x cpm/g CSF divided by cpm/ml plasma. Uptake curves of Vd vs. time were constructed for the various treatments; then, to compare drug effects, the curves were analyzed for: (i) the early slope of uptake (Kin), (ii) the steady-state value for Vd, and (iii) the area-under-curve (AUC). Assessment of the curve parameters collectively revealed that at 5 mg/kg, both furosemide (FUR) and ethacrynic acid (EA) reduced Cl penetration into CSF by one quarter; at 50 mg/kg, these loop agents decreased Cl uptake by about a third. On the other hand, 50 mg/kg of the carbonic anhydrase inhibitor, acetazolamide, reduced Cl uptake into CSF by 55-60%. Thus, NaCl cotransport inhibitors maximally reduced Cl transport in the rat by about 35%; this inhibition was less extensive than that brought about by acetazolamide, which interferes with CSF secretion by a different mechanism.

Acetazolamide↗
PubMed1984

Combined effect of forskolin and acetazolamide on intraocular pressure and aqueous flow in rabbit eyes.

Forskolin, a diterpene, a potent and direct stimulator of the catalytic unit of adenylate cyclase, can reduce intraocular pressure when administered topically to rabbit eyes in a 1% suspension. Using an intravitreal plant of fluorescein-dextran, aqueous flow was measured by a modification of the method of Maurice. Forskolin reduces net aqueous flow by 51% compared to the controls. Acetazolamide (25 mg kg-1) administered intravenously reduces net aqueous flow by 45%. Forskolin and acetazolamide together reduce net aqueous flow by 72%, an important additive effect undoubtedly produced by different pathways.

Acetazolamide↗
PubMed1995

Prophylactic efficacy of phenytoin, acetazolamide and hydrochlorothiazide in horses with hyperkalaemic periodic paralysis.

Horses with hyperkalaemic periodic paralysis were challenged with an oral dose of potassium chloride, and the prophylactic efficacy of phenytoin, acetazolamide and hydrochlorothiazide was evaluated, with at least three weeks separating the trials of each drug. After the administration of potassium chloride without prophylactic medication the horses' clinical signs ranged from generalised fine muscle fasciculations to gross tremors, and weakness with occassional prolapse of the nictitating membrane; plasma potassium concentration increased significantly (P < 0.01) from 4.0 +/- 0.2 to 6.0 +/- 1.01 mmol litre-1. After treatment with acetazolamide the administration of potassium chloride resulted in a significant (P < 0.02) increase in plasma potassium from 3.7 +/- 0.3 to 4.5 +/- 0.4 mmol litre-1 and two of five horses showed clinical signs unless the dosage was increased from 2.2 to 4.4 mg kg-1 twice daily. Three of the four horses treated with hydrochlorothiazide showed clinical signs but their plasma potassium did not rise significantly (3.6 +/- 0.3 to 4.6 +/- 1.0 mmol litre-1). None of the five horses treated with phenytoin showed clinical signs despite a significant increase in plasma potassium from 3.8 +/- 0.6 to 5.3 +/- 1.1 mmol litre-1 (P < 0.05). In general the clinical signs were not correlated consistently with the plasma levels of potassium, and phenytoin appeared to prevent the clinical signs in spite of the hyperkalaemia.

Acetazolamide↗
PubMed1975

The effect of acetazolamide on myocardial carbon dioxide space.

Carbon dioxide, water and vascular space were measured in the heart muscle of the dog before and after the administration of acetazolamide. In contrast to the skeletal muscle whose CO2 space was markedly reduced by acetazolamide, cardiac muscle CO2 space was only minimally reduced. This suggests that cardiac muscle does not have extravascular carbonic anhydrase. Its presence in skeletal muscle and absence in cardiac muscle probably relates to the differences in cell size between the two types of muscle and their differing degree of vascularity.

Acetazolamide↗