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PubMed2001

Correlation of cerebrovascular reserve as measured by acetazolamide-challenged SPECT with angiographic flow patterns and intra- or extracranial arterial stenosis.

BACKGROUND AND PURPOSE: The ability to identify patients at increased risk for stroke from cerebral hemodynamic ischemia may help guide treatment planning. We tested the correlation between regional cerebrovascular reserve (rCVR) on acetazolamide-challenged single-photon emission CT (SPECT) brain scans and intracranial collateral pathways as well as extra- or intracranial (EC-IC) arterial stenosis on cerebral angiography. METHODS: A retrospective analysis of 27 patients who underwent cerebral angiography and acetazolamide-challenged SPECT brain imaging was performed. With cerebral angiography, the anterior, middle, and posterior cerebral artery (ACA, MCA, PCA) territories were evaluated for patterns of flow, including the ipsilateral carotid or basilar arteries, the circle of Willis collaterals, the EC-IC collaterals, and the leptomeningeal collaterals. With acetazolamide-challenged SPECT, the ACA, MCA, and PCA territories were classified as either showing or not showing evidence of decreased rCVR. Statistical significance was determined by the chi(2) test. RESULTS: Patients with decreased rCVR had significantly greater dependence on either the EC-IC or leptomeningeal collaterals (42%) than did patients without decreased rCVR (7%). Similarly, the cerebral hemispheres with decreased rCVR showed a higher prevalence of 70% or greater stenosis or occlusion of the ipsilateral EC-IC arteries in the anterior circulation (74%) than did hemispheres with no evidence of decreased rCVR (16%), and this difference was also statistically significant. CONCLUSION: Acetazolamide-challenged SPECT brain scanning provides additional information regarding rCVR that is not reliably provided by cerebral angiography.

Acetazolamide↗
PubMed2003

[Differential protein analysis in rat renal proximal tubule epithelial cells in response to acetazolamide and its relation with the inhibition of AQP1].

AIM: To study the endogenous mechanism for the inhibition of aquaporin-1 expression in rat renal proximal tubule epithelial cells in response to acetazolamide. METHODS: Primary cultured rat renal proximal tubule epithelia cells were divided into two groups: one was subjected to 1 x 10(-5) mol.L-1 acetazolamide, the other served as normal control. When grown to sub-confluency, the cells were disintegrated to perform isoelectrofocusing electrophoresis in order to find the differential proteins induced by the acetazolamide treatment. The differential proteins were defined by peptide mass fingerprinting technology. RESULTS: Two differential proteins were found in the cell disintegrant. The pI 3.8 protein was reduced after treatment, which showed 21.4% similarity with the brush border membrane myosin from rat brain and testis, and 27% with glycogen phosphorylase; The pI 5.5 protein was increased on the contrary, with 20% similarity to phosphatidylinositol transfer protein alpha isoform. CONCLUSION: Acetazolamide inhibited AQP1 expression probably by affecting the expression of pI 3.8 and pI 5.5 proteins.

Acetazolamide↗
PubMed1992

[The value of acetazolamide provocation combined with blood flow tests in the diagnosis of ischemic cerebrovascular diseases].

In 28 (3 normal, 11 TIA, 14 completed stroke) patients 99mTc-HMPAO rCBF SPECT studies were performed at rest and after acetazolamide administration. For the investigations, a one-day protocol (the stress study directly followed the rest investigation) was used. The reconstructed and normalized slices were evaluated visually and semiquantitatively with a side difference analysis method. In the group of TIA patients, the abnormal results of the rCBF investigations increased from 55% to 82% after acetazolamide provocation. The corresponding results in the completed stroke group were 80% and 87%. After acetazolamide stimulation, hypoperfusion appeared or become more pronounced in the majority of the TIA group patients in contrast with the completed stroke patients with an unchanged or decreased perfusion abnormality. The semiquantitative evaluation method was mostly effective in the TIA group, where predominantly a one-sided cerebrovascular disorder was suspected. It was concluded that the 99mTc-HMPAO studies allow demonstration of the acetazolamide-induced cerebral perfusion alterations, and this method can be useful in the diagnosis and management of cerebrovascular disorders.

Acetazolamide↗
PubMedDate not supplied

The effect of inhaled furosemide and acetazolamide on bronchoconstriction induced by deep inspiration in asthma.

In some asthmatics deep inspiration causes a sustained bronchoconstration, which is dependent on Ca2+ uptake. Inhaled diuretics protect against bronchoconstriction induced by a variety of indirect stimuli, by inhibiting the ionic fluxes involving Ca2+ uptake across the cell membrane of airway epithelium. The aim of this study was therefore to investigate the protective effect of inhaled furosemide on the bronchoconstriction induced by deep inspiration in asthma and to compare it with the effect of acetazolamide, an inhibitor of carbonic anhydrase devoid of effect on ion cotransport but possessing inhibitory effects on chloride ion influx and Na+/K+ exchange. The study was carried out on three different study days according to a randomized, double-blind, placebo-controlled, crossover design. Nine non smoking asthmatic subjects first performed a series of 9 controlled deep inspirations to TLC followed by forced expirations to RV within 20 min, which caused a decrease of FEV1 > 20% from baseline. Two hours later, the subjects inhaled either furosemide (40 mg), or acetazolamide (500 mg), or saline (placebo) in random order, and then two more deep-inspiration challenges were performed after 30 and 140 mins. The progressive percent decrement of FEV1 caused by deep-inspiration challenge was taken as an index of bronchoconstriction. Bronchoconstriction was significantly blunted at 30 mins, but not 140 mins, after inhaling furosemide (p < 0.01) or acetazolamide (p < 0.05) compared to control. We interpret these results as due to a modulation of ionic fluxes across the smooth muscle cell membrane afforded by inhaled furosemide and acetazolamide.

Acetazolamide↗
PubMed2003

Hypoxia and pulmonary acclimatisation at 4578 m altitude: the role of acetazolamide and dexamethasone.

OBJECTIVES: To quantify the changes in ventilatory response and arterial blood gases in healthy male volunteers on acute ascent to 4578 meters altitude along with evaluating the role of acetazolamide and dexamethasone prophylaxis in acclimatisation. METHODS: Forty four lowlander male subjects participated as two groups in the study. Twenty four lowlander healthy male adults (age mean +/- SE 27.8 +/- 1.24 years) comprised the non-acclimatised group. They were sub grouped in a double blind fashion into four. Each subgroup (n=6) received placebo (multivitamin) or acetazolamide (250 mg) or dexamethasone (4 mg) or combined regimen of the two drugs twice daily for 5 days commencing 24 hours before ascent. The volunteers reached the altitude of 4578 meters within a span of one day. The second group (acclimatised) comprised of age and height matched twenty volunteers who had arrived 4 and 8 weeks earlier at the same altitude. Arterial PO2, PCO2, SO2 and minute respiratory rate pH were measured. The pulmonary functions (FVC, %FEV1 PEF, FEF(25-75%) and MVV) were recorded by Compact Spirometer (Vitalograph). Pre and post ascent measurements were carried out in non-acclimatised group whereas one measurement of the same parameters were made in acclimatised group. RESULTS: The study revealed a significant increase in respiratory rate min-1 after 24 hours of ascent along with reduction in PaO2 and SaO2. The gradual increase in PaO2 and SaO2 and reduction in PaCO2 was observed after 4 weeks at the same altitude. The reduction in FVC, %FEV1, PEF, FEF(25-75%) and MW were recorded in our subjects after 24 hours of acute ascent. Nevertheless, all pulmonary parameters in volunteers having 8 weeks of stay at 4578 m altitude, were found equivalent to the non-acclimatised group. The greater increase in minute respiratory rate, PaO2, SaO2 and pulmonary functions was found in volunteers taking acetazolamide. CONCLUSION: It is concluded that hyperventilation and increase in lung volumes are the adaptive pulmonary responses which help in improving levels of PaO2 and SaO2. The acetazolamide-dexamethasone prophylaxis appears beneficial in promoting pulmonary acclimatisation during hypobaric hypoxia.

Acclimatization↗
PubMed1991

Effect of acetazolamide on calcium accumulation by the developing chicken embryo.

The injection of 10 mg of acetazolamide into fertile chicken eggs on the 16th or 17th day of incubation resulted in a decreased accumulation of calcium by the developing embryo. A dose of 1 mg of acetazolamide did not affect embryonic calcium content. Although the eggshell serves as the primary source of calcium for the embryo, acetazolamide did not influence eggshell mobilization as measured by the release of 45Ca from labeled eggshells. Acetazolamide did decrease bone formation resulting in a statistically significant reduction in tibia dry weight and calcium content.

Acetazolamide↗
PubMed1991

[Changes in CSF pressure induced by acetazolamide administration test--as an indicator of shunt operation for so-called normal pressure hydrocephalus].

Lumber subarachnoid pressure was monitored via intrathecally introduced catheter in 9 patients, who showed ventricular dilatation on brain CT and were suspected of normal pressure hydrocephalus. During the pressure measurement, 500 mg of acetazolamide was rapidly injected intravenously and changes of CSF pressure were recorded. The results of the study were compared to clinical signs, brain CT findings and results of continuous pressure monitoring. The types of response of CSF pressure induced by acetazolamide administration were classified into 2 groups. In 5 cases (Group A), more than 50 percent increase of CSF pressure compared to the resting value was noted. On the contrary, in the remaining 4 cases (Group B), CSF pressure showed only slight increase (less than 25 percent or none). VP shunt was performed in 4 cases in Group A. Definite improvement of clinical symptoms was observed in all of these surgically treated cases. Correlation was found between the response to Acetazolamide administration and the appearance of B wave in the continuous spinal pressure monitoring. This study suggests that Acetazolamide test may be useful diagnostic test to select the patients for shunt operation.

Acetazolamide↗
PubMed1990

Use of acetazolamide-challenge xenon CT in the assessment of cerebral blood flow dynamics in patients with arteriovenous malformations.

Arteriovenous malformations (AVMs) may cause symptoms related to a reduction of cerebral blood flow (CBF) to surrounding brain parenchyma. To evaluate this compromise of hemodynamic reserve (commonly referred to as steal phenomenon), we used acetazolamide challenge and stable-xenon CT (Xe/CT). Baseline Xe/CT studies in 13 patients with AVMs were followed by an acetazolamide challenge to the vascular reserve. Blood flow maps were quantitated by using region-of-interest (ROI) software. ROI findings were categorized into four groups on the basis of the presence or absence of normal baseline CBF and presence or absence of normal augmentation of CBF. ROIs were designated as near site (within the vascular territory supplying the AVM) or far site (outside the vascular territory supplying the AVM). One patient had a normal baseline and normal augmentation of CBF (group 1). The other patients had a combination of one or more of the other three categories. Ten patients had parenchymal areas that exhibited either a normal or low baseline CBF with decreased augmentation; both conditions were interpreted as decreased vascular reserve (groups 2 and 3). Eleven patients had parenchymal areas that showed a low baseline CBF and normal augmentation with acetazolamide (group 4), interpreted as having a decreased demand for CBF but having a normal vascular reserve. Decreased vascular reserve was found in 27% of the nearsite areas and 17% of the far-site areas. No patients had only far-site abnormal vascular reserve. We believe that compromised vascular reserve can best be evaluated with a challenge study, such as this acetazolamide-challenge Xe/CT study.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1990

Successful treatment of intractable gastric ulcers with acetazolamide.

An open-controlled trial performed in gastric ulcer cases resistant to previous cimetidine, antacids, vitamin A and polyvinylbutylether therapy applied for at least 4 weeks. A group of 21 patients treated with acetazolamide was compared with 16 patients treated with cimetidine (controls). The period of management was 3 weeks. The number of healed patients (P = 0.009), the surfaces of ulcers after treatment (P = 0.0166) and the duration of complaints (P = 0.0003) differed favourably and significantly in the acetazolamide group as compared to the cimetidine group. In the acetazolamide group, however, several side effects (in 11 cases metabolic acidosis, in 9 cases tingling of extremities) were registered. Side effects were not seen in the control group. It is supposed that in the treatment of gastric ulcers a compound with less carbonic anhydrase inhibition but with the same or more cytoprotective effect would have wider clinical perspectives than acetazolamide alone.

Acetazolamide↗
PubMed1990

[Brain perfusion SPECT imaging before and during the acetazolamide test using 99mTc-HMPAO].

A new method using brain perfusion 99mTc-HMPAO SPECT imaging was developed for evaluating cerebral perfusion reserve by the acetazolamide test with a short period. The first SPECT study was carried out for 13.5 min to obtain SPECT images at the resting state after 3 min postinjection of 555 MBq (15 mCi) of 99mTc-HMPAO. At the same time as the start of the first SPECT study, 1 g of acetazolamide was intravenously injected. Immediately after the stop of the 1st SPECT study, 925 MBq (25 mCi) of 99mTc-HMPAO from the same vial as in the first study was additionally injected. Three minutes later the second SPECT study was carried out for 10 min. After reconstruction the tomographic images in the first study were subtracted from the images in the second study to obtain those during the acetazolamide test after correction of the time differences in data acquisition between the two studies. This subtraction technique gives independent brain perfusion SPECT images before and during the acetazolamide test. Besides, the regional flow changes during the test were quantitatively analyzed. In conclusion this method seems to be practically useful for evaluating regional brain perfusion before and during drug treatments as a consecutive study with a short period of approximately 30 min.

Acetazolamide↗
PubMed1989

Long-term effect of acetazolamide and chlorthalidone on the hearing loss of Menière's disease.

A retrospective computerized analysis of the records of patients with Meniere's disease was made to evaluate the effect of acetazolamide and chlorthalidone on the rate of hearing loss. Three groups were compared as follows: (1) 79 patients treated with chlorthalidone for 5 to 13.4 years; (2) 42 patients medicated with acetazolamide between 5 and 7.8 years; and (3) a control group of 71 patients who received only intermittent symptomatic treatment for vertigo, followed for 5 to 24.1 years. In the short term, after 2 to 6 weeks of treatment, a statistically significant decrease of the average hearing loss was observed with both chlorthalidone and acetazolamide. In the long term, more than 5 years, no preventive effect on the deterioration of the hearing loss could be detected. Both acetazolamide and chlorthalidone can be useful for diagnostic purposes by causing a fluctuation of hearing, as well as for the management of the vertigo attacks, but it is not useful for the long-term prevention of the hearing deterioration in Meniere's disease.

Acetazolamide↗
PubMed1989

[Effect of acetazolamide on aqueous flare in normal human eyes].

A newly developed instrument for the quantitative measurement of aqueous flare, the laser flare-cell meter, is now being introduced clinically. The present experiment was designed to assess the effect of a commonly administered drug, acetazolamide, on measurements obtained in normal, healthy subjects. Control measurements were taken over a 24 hr period, from 0900 hrs to 0900 hrs of the next day in 12 drug-free, normal, healthy subjects. A second, similar time-course measurement was conducted in the same subjects on another day after oral administration of 500 mg acetazolamide. Results revealed that acetazolamide increased aqueous flare from 2 hrs to 10 hrs post-administration. The peak effect was observed approximately 6 hrs after acetazolamide administration, reaching a level 41% greater than that on the control day. Anterior chamber volume and serum protein concentration were not affected by the drug treatment. The use of the laser flare-cell meter in the clinic and possible mechanisms contributing to the effect of the drug are discussed.

Acetazolamide↗
PubMed1988

Prolonged aqueous humor levels of subconjunctival antibiotics after treatment with acetazolamide and/or timolol.

Many ophthalmologists routinely administer subconjunctival antibiotics at the end of cataract surgery for prophylaxis against bacterial endophthalmitis. Additionally they use acetazolamide and/or timolol to control intraocular pressure in the first 24-hour postoperative period. An animal study was undertaken to learn whether treatment with the aqueous humor suppressants, acetazolamide, and timolol prolongs the concentrations of antibiotics in the aqueous humor after subconjunctival administration of the antibiotic. Treatment with acetazolamide significantly increased concentrations of piperacillin; it had less consistent effects on tobramycin levels. Timolol treatment did not produce increased piperacillin concentrations at six hours; however, concentrations at 12 and 24 hours were significantly higher than in the controls. Timolol treatment increased tobramycin concentrations only at six hours. The combined use of timolol and acetazolamide produced significantly higher concentrations of piperacillin, but not of tobramycin.

Acetazolamide↗
PubMed1985

Significant metabolic acidosis induced by acetazolamide. Not a rare complication.

Blood gas and serum electrolyte levels were measured in 27 elderly patients (mean age +/- SD, 63.3 +/- 13.5 years) who were receiving acetazolamide (250 to 1,000 mg/day) for glaucoma. Eleven glaucomatous patients (mean age, 69.1 +/- 7.4 years) who were not receiving acetazolamide served as a control group. In the acetazolamide-treated group, four patients (14.8%) had mild acidosis (7.29 greater than pH less than or equal to 7.31), ten (37%) had moderate acidosis (7.20 greater than pH less than or equal to 7.29), and one patient (3.7%) had severe acidosis (pH, 7.15). None of the patients in the control group had acidosis. It is concluded that moderate metabolic acidosis of potential clinical significance is common among glaucomatous elderly patients who receive acetazolamide. The exact clinical significance of our observations is yet to be determined.

Acetazolamide↗
PubMed1980

Different mechanisms of action of acetazolamide and parathyroid hormone on proximal tubular absorption of fluid and 5,5-dimethyl-2,4-oxazolidinedione.

The effects of acetazolamide (Diamox), parathyroid hormone (PTH) and dibutyrylcyclic-adenosine 3':5'-monophosphate (db-cAMP) on fluid and 5,5-dimethyl-2,4-oxazolidinedione (DMO) absorption in the rat proximal convoluted tubule were studied by using microperfusion methods. The rate of tubular absorption of DMO was used to estimate the rate of hydrogen ion secretion. When the tubular and the peritubular capillaries were perfused simultaneously with bicarbonate-free Ringer's solution containing DMO, the rate of DMO absorption (JDMO) was 140 +/- 15.7 pmol/min . mm, a value comparable to the rate of absorption of bicarbonate and glycodiazine, and net fluid absorption (JV) was 2.20 +/- 0.19 nl/min . mm. Administration of PTH (10(-6) M) to the capillary perfusate caused a decrease of JDMO by 23% and a decrease of JV by 28%. Similar results were observed when db-cAMP (10(-4) M) was administered to the luminal perfusate. Addition of acetazolamide (10(-4) M) to the luminal perfusate caused a decrease of JDMO by 66% and a decrease of JV by 45%. The effect of either PTH or db-cAMP was additive to the maximal effect of acetazolamide. However, the effect of PTH was not additive to the effect of db-cAMP. Thus, the results suggest that PTH and acetazolamide have different mechanisms of action on fluid and DMO absorption by proximal tubule and that cAMP mediates the effect of PTH.

Absorption↗
PubMed1984

Cognitive impairment of acute mountain sickness and acetazolamide.

In a trial to assess the cognitive impairment attributable to benign acute mountain sickness (AMS) and to acetazolamide, six women and five men, 20-35 years old, ascended from sea-level to 3600 m in 36 h and were assessed for deterioration in performance on psychological tests. Of five sex-matched pairs with a mean age difference of 3.4 years (S.D. +/- 4.4 years), one member took slow-release acetazolamide 500 mg daily and one placebo on a double-blind basis during the ascent and again for an identical course at low altitude 32-38 d later. The unmatched woman took placebo during ascent. Before, during, and after each drug course each subject performed an Environmental Symptom Questionnaire (ESQ) and a psychological test battery consisting of trail-making, paced auditory serial addition test (PASAT), letter-digit code, dual-task cancellation and subtraction, and memory subtests. On ascent, ESQ score deteriorated by an average of 62 points in placebo subjects compared with 32 in acetazolamide subjects (p = 0.055). Deterioration in the psychological test battery was only significant in the PASAT (p less than 0.05) and memory (p less than 0.01) subtests of subjects taking placebo. For those taking acetazolamide, no test showed significant impairment, suggesting it had no detectable cognitive impairment at this dose.

Acetazolamide↗
PubMed1983

Pharmacodynamics of the diuretic effects of aminophylline and acetazolamide alone and combined with furosemide in normal subjects.

The current study was performed in normal subjects to assess the mechanism of the natriuretic effects of aminophylline, to confirm the effect of acetazolamide on the proximal tubule and to assess the pharmacodynamics of the combination of aminophylline and of acetazolamide with furosemide. None of these agents or their combination affected renal hemodynamics. Aminophylline inhibited solute reabsorption at the diluting segment manifested by a 15% decrease in free water clearance relative to solute delivery (P less than .001). In addition, it decreased solute reabsorption in the proximal nephron. Acetazolamide affected only the proximal tubule. The combination of either aminophylline or of acetazolamide with furosemide was little different from furosemide alone. Analysis of dose-response curves to furosemide revealed a minor additive, i.e., parallel upward shift, of the dose-response curves with both combinations.

Acetazolamide↗
PubMedDate not supplied

Effect of acetazolamide on insulin sensitivity in dogs with alloxan diabetes.

The effect of acetazolamide on the sensitivity to exogenous insulin in the alloxanised diabetic dogs was studied. The administration of acetazolamide caused acidosis and insulin resistance. The liver insulinase activity of diabetic dogs after acetazolamide administration was also studied to evaluate the role of this enzyme for the destruction of exogenous insulin. It was observed that insulinase did not play role for the development of insulin resistance after acetazolamide administration.

Acetazolamide↗