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 415 records · Page 23Linked to original sources
PubMed2000

New alternative agents in essential tremor therapy: double-blind placebo-controlled study of alprazolam and acetazolamide.

Propranolol and primidone are widely used, effective agents in essential tremor although they are not tolerated by all patients. In the present study, the effectiveness of alprazolam, a triazole analog of benzodiazapine class, and acetazolamide, a carbonic anhydrase inhibitor, were investigated as symptomatic treatments for essential tremor. We studied 22 patients with essential tremor in a double-blind, cross-over, placebo-controlled design. The patients received in random order alprazolam, acetazolamide, primidone and placebo for four weeks, each separated by a two-week washout period. The study demonstrated that alprazolam was superior to placebo and equipotent to primidone, whereas there was no statistically significant difference between acetazolamide and placebo. The mean effective daily dose of alprazolam was 0.75 mg and there was not any troublesome side effect reported by the patients on alprazolam. Alprazolam can be used as an alternative agent in elderly essential tremor patients who can not tolerate primidone or propranolol.

Acetazolamide↗
PubMed1982

The effects of timolol maleate and acetazolamide on the rate of aqueous formation in normal human subjects.

We used a double-masked, randomized, placebo-controlled study of the effect of acetazolamide alone and timolol maleate alone and of the two in combination on the rate of aqueous humor flow in 21 normal subjects. The rate of aqueous flow was measured by fluorophotometry over an eight-hour period. Timolol decreased the flow by 33%, acetazolamide by 27%, and the drug combination by 44%, compared to the placebo treated eye (P less than .01). Timolol produced a 26% decrease in intraocular pressure. Timolol decreased the intraocular pressure in the fellow eye by 16%, acetazolamide by 21%, and the two drugs together by 35% (P less than .01). Neither drug significantly affected the anterior chamber volume, the endothelium's permeability, or the estimated endothelial pump rate.

Acetazolamide↗
PubMed1983

The effects of carbonic anhydrase inhibitors formate, bicarbonate, acetazolamide, and imidazole on photosystem II in maize chloroplasts.

Inhibitors of carbonic anhydrase were tested for their effects on Photosystem II (PS II) activity in chloroplasts. We find that formate inhibition of PS II turnover rates increases as the pH of the reaction medium is lowered. Bicarbonate ions can inhibit PS II turnover rates. The relative potency of the anionic inhibitors N-3, I-, OA-c, and Cl- is the same for both carbonic anhydrase and PS II. The inhibitory effect of acetazolamide on PS II increases as light intensity decreases, indicating a lowering of quantum yields in the presence of the inhibitor. Imidazole inhibition of PS II increases with pH in a manner suggesting that the unprotonated form of the compound is inhibitory. Formate, bicarbonate, acetazolamide, and imidazole all inhibit DCMU-insensitive, silicomolybdate-supported oxygen evolution, indicating that the site(s) of action of the inhibitors is at, or before, the primary stable PS II electron acceptor, Q. This inhibitory effect of low levels of HCO-3 along with the known enhancement by HCO-3 of quinone-mediated electron flow suggests an antagonistic control effect on PS II photochemistry. We conclude that the responses of PS II to anions (formate, bicarbonate), acetazolamide, and imidazole are analogous to the responses shown by carbonic anhydrase. These findings suggest that the enzyme carbonic anhydrase may provide a model system to gain insight into the "bicarbonate-effect" associated with PS II in chloroplasts.

Acetazolamide↗
PubMed1990

Possible association between acetazolamide administration during pregnancy and metabolic disorders in the newborn.

Development of metabolic acidosis, hypocalcemia and hypomagnesemia in a preterm infant whose mother was treated with acetazolamide throughout pregnancy is described. These neonatal metabolic alterations possibly related to acetazolamide administration in pregnancy have not been previously described in the literature. The metabolic acidosis was transient and resolved spontaneously despite breast feeding and continued administration of acetazolamide to the mother. Hypocalcemia and hypomagnesemia resolved quickly with appropriate treatment with calcium gluconate and magnesium sulphate, respectively. At follow-up at ages 1, 3 and 8 months, the baby showed mild hypertonicity of the lower limbs requiring physiotherapy.

Acetazolamide↗
PubMed1987

Effects of PGE1 or PGE2 and/or acetazolamide on expulsion of Nippostrongylus brasiliensis from rats.

PGE1 and PGE2 have been reported to enhance natural expulsion of Nippostrongylus brasiliensis, a nematode parasite, from the intestine of the rat. Mucus production may also be a key element of worm rejection. Our study attempts to determine if 1) PGE1 or PGE2 alter the normal course of infection with N. brasiliensis in rats, 2) a known mucous enhancing drug, acetazolamide, can augment the rate of worm expulsion, and 3) combinations of prostaglandins and acetazolamide affect N. brasiliensis in the rat. Rats were inoculated with approximately 1,000 infective larvae of N. brasiliensis. Animals were administered, intraduodenally, one of the following: 0.2 ml 0.9% NaCl; 0.2 ml 100% ethanol; 250 micrograms PGE1/0.2 ml 100% ethanol; 250 micrograms PGE2/0.2 ml 100% ethanol; 250 micrograms acetazolamide/0.2 ml 100% ethanol; 250 micrograms PGE1 or PGE2 + 250 micrograms acetazolamide/0.2 ml 100% ethanol. These solutions were given in a single bolus on day 6 postinoculation (PI) or twice daily on days 6-9 PI. Following these treatments the number of parasite ova per gram feces per day for days 6-10 PI and numbers of worms present at necropsy on day 10 PI were determined. Treatment with prostaglandins or acetazolamide or both failed to adversely affect egg deposition by adult female worms or the number of worms in the small intestine. These results do not support the involvement of prostaglandins in the expulsion of N. brasiliensis from the host intestine.

Acetazolamide↗
PubMed1988

Effects of urinary crystals induced by acetazolamide, uracil, and diethylene glycol on urinary bladder carcinogenesis in N-butyl-N-(4-hydroxybutyl)nitrosamine-initiated rats.

In order to examine the promoting effect of urinary crystals on urinary bladder carcinogenesis, acetazolamide, uracil, and diethylene glycol, all of which have been reported to cause urinary crystals or calculi, were administered to male F344 rats for 32 weeks after pretreatment with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 4 weeks. A marked increase in urinary crystals was observed in acetazolamide-treated rats and a slight increase in crystals was observed in uracil- and diethylene glycol-treated rats. Histological examination of the urinary bladder revealed that the BBN-acetazolamide treatment resulted in a higher incidence of carcinoma than BBN-control. Uracil and diethylene glycol did not cause any significant difference compared to the control. Promoting effects by urinary crystals were not clearly shown in the present experiment and, therefore, urinary crystals appear to play a very limited role, if any, in urinary bladder carcinogenesis.

Acetazolamide↗
PubMedDate not supplied

The effect of acetazolamide and carbon dioxide on cerebral hemodynamic changes on near-infrared spectroscopy in young rabbits.

The changes of cerebral blood oxyhemoglobin (HbO2), deoxyhemoglobin (HbR), and total hemoglobin (tHb) induced by acetazolamide and CO2 loading on near-infrared spectroscopy (NIRS) were recorded. In anesthetized 2-week-old rabbits, acetazolamide (10 mg/kg i.v.) increased HbO2 and tHb, concomitant with an increase in tissue PCO2, and decreased HbR only at 5 and 10 min. CO2 loading significantly increased HbR and decreased HbO2, and after the termination of CO2 loading, tHb and HbO2 significantly increased and HbR decreased to nearly the baseline value. Thus, NIRS demonstrated cerebral hemodynamic responses as a function of vasomotor reactivity to acetazolamide as well as CO2 loading.

Acetazolamide↗
PubMed1995

A comparative cerebral blood flow study in a baboon model with acetazolamide provocation: 99mTc-HMPAO vs 123I(IMP).

Pharmacological interactions are important when nuclear medical procedures are applied to patients under drug therapy, or drug provocation. This study compares in baboon models (regional) cerebral blood flow [(r)CBF] results from 99mTc-HMPAO and 123I-iodoamphetamine [123I(IMP)] each with and without acetazolamide, the latter a suggested drug for testing cerebrovascular reserve. Expected differences in cerebral uptake were observed between the two radio-tracers without acetazolamide. The increase in tracer uptake resulting from acetazolamide is significantly enhanced for 123I(IMP), which could have diagnostic implications.

Acetazolamide↗
PubMed2004

The protein profile of acetazolamide-treated sera in mice bearing Lewis neoplasm.

The aim of the present research is to analyze the proteome of neoplasm serum before and after treated with acetazolamide (20, 40, 80 mg kg(-1) d(-1) for 3 days p.o.). The Lewis lung carcinoma mice were used and carried out a comprehensive proteomic analysis by using the technologies of high-resolution two-dimensional polyacrylamide gel electrophoresis (2D PAGE) and mass spectrometry (MS). The results showed that the acetazolamide could dramatically reduce the lung metastasis and primary tumor growth. Its most potent inhibition rate on lung metastases was reach to 77.7% at the dose of 80 mg kg(-1) d(-1). The two dimension electrophoresis and software analysis reveal 393 protein spots in control gel, 385 protein spots were detected in treated gel and matched 209 protein spots with control gel, indicating that intensive changes had occurred during the process of treatment. Two obviously different spots were cut off from gel and for the peptide mass fingerprinting. Data base searching showed the two proteins' peptide much more mach with Histone H2B fragment and Ubc-like protein CROC1 fragment. The results suggest that acetazolamide has a strong anti-tumor and anti-metastasis effect on Lewis-lung-carcinoma. The mechanism may be related to its regulation on plenty of proteins, in particular, on upregulation of H2B and CROC-1 expression of postreplicational DNA repair related protein in serum.

Acetazolamide↗
PubMed2004

Acetazolamide-enhanced neuroSPECT scan reveals functional impairment after minimal traumatic brain injury not otherwise discernible.

A patient suffering from aggressive personality changes and cognitive impairment following head trauma, without neurological or anatomical imaging findings, underwent neuroSPECT scans with and without acetazolamide injection, both before treatment and during treatment with valproate. Acetazolamide injection induced increased prefrontal perfusion not evident at baseline. Valproate treatment was associated with increased prefrontal perfusion concomitant with clinical improvement and abolished response to acetazolamide challenge.

Acetazolamide↗
PubMed2002

Effect of acetazolamide on ocular hemodynamics in pseudotumor cerebri associated with inflammatory bowel disease.

PURPOSE: To describe the hemodynamic effect of oral acetazolamide administration on ocular perfusion in a patient with pseudotumor cerebri associated with Crohn disease. DESIGN: Interventional case report. METHODS: A 20-year-old woman with a 5-year history of Crohn disease presented with a 2-week history of headache and blurred vision in both eyes. Ophthalmologic examination was normal. Fluorescein angiography showed a profound delay in retinal and choroidal perfusion. Lumbar puncture showed an opening pressure of 320 mm water. Therapy was initiated with oral acetazolamide 750 mg per day. RESULTS: A subjective improvement of symptoms was noted over 4 days. Repeat fluorescein angiography showed resolution of the ocular perfusion deficit. No recurrent symptoms were noted 19 months after cessation of therapy. CONCLUSIONS: Crohn disease may present with pseudotumor cerebri and severe ocular perfusion deficits that are reversible with oral acetazolamide therapy.

Acetazolamide↗
PubMed1981

Separate and combined effects of timolol maleate and acetazolamide in open-angle glaucoma.

We compared the intraocular pressure-decreasing effect of timolol maleate alone, acetazolamide alone, and combined timolol and acetazolamide therapy in nine patients with bilateral chronic open-angle glaucoma. Timolol decreased intraocular pressure at least as effectively as acetazolamide. The two medications together were more effective than either medication alone, but they did not have a fully additive effect. Episcleral venous pressures and outflow facilities did not vary significantly with any of the three treatment regimens.

Acetazolamide↗
PubMed2003

Effects of acetazolamide and 4-aminoprydine on the responses of deflationary slowly adapting pulmonary stretch receptors to CO2 inhalation in the rat.

The inhibitory effect of CO(2) on deflationary slowly adapting pulmonary stretch receptors (deflationary SARs) was investigated before and after administration of acetazolamide, a carbonic anhydrase (CA) inhibitor, or 4-aminopyridine (4-AP), a K(+) channel blocker, in anesthetized, artificially ventilated rats after unilateral vagotomy. CO(2) inhalation (maximum tracheal CO(2) concentration ranging from 9 to 12%) for approximately 60 s decreased the impulse activity of deflationary SARs but had no significant effect on tracheal pressure (P(T)) as an index of bronchomotor tone. Acetazolamide treatment (20 mg/kg) diminished the inhibitory response of deflationary SARs to CO(2) inhalation. 4-AP (0.7 and 2.0 mg/kg) dose-dependently attenuated the decrease in deflationary SAR activity induced by CO(2) inhalation. When comparing the maximum attenuation due to 4-AP (2.0 mg/kg) and acetazolamide (20 mg/kg) in CO(2)-induced deflationary SAR inhibition, blockade of K(+) channels had a more pronounced effect. These results suggest that inhibition of deflationary SARs by CO(2) inhalation may be largely mediated by the stimulating action of 4-AP-sensitive K(+) currents in the nerve terminals of the receptors.

4-Aminopyridine↗
PubMed1993

Deteriorating renal function with acetazolamide in a renal transplant patient with pseudotumor cerebri.

Treatment with acetazolamide for pseudotumor cerebri (PTC) in a renal transplant patient led to an acute, but reversible deterioration in renal function. Possible pathogenetic mechanisms behind acute renal failure and acetazolamide are detailed. In summary, caution should be exercised in all patients with chronic renal failure who require acetazolamide. It should be avoided if possible, used in reduced doses when necessary, and coupled with a high fluid intake to avoid dehydration and/or intraluminal obstruction.

Acetazolamide↗
PubMed1993

Post-carotid endarterectomy hyperperfusion syndrome: preliminary observations for identifying at risk patients by transcranial Doppler sonography and the acetazolamide test.

Patients at risk of hyperperfusion syndrome after carotid endarterectomy are often severely hypertensive and have a high grade internal carotid artery stenosis with disordered autoregulation due to a loss of reserve capacity (RC). Cerebral RC can be studied by sophisticated and expensive technical devices (SPECT, PET). Recently it has been demonstrated that the transcranial Doppler (TCD) and acetazolamide provocation test can be used to assess RC. From September 1991 to January 1992, 36 patients were studied by the TCD and acetazolamide test prior to carotid endarterectomy to identify patients at high risk of the hyperperfusion syndrome. Preoperatively, the patients were studied by TCD at rest and after vasolidation with acetazolamide 1 g intravenously (i.v.). Mean blood flow velocity on the middle cerebral artery (MCAv) was recorded for the following 20 min at 5 min intervals. MCAv at rest was 49 +/- 17 cm/s. After acetzaolamide infusion in 33 patients (92%), the mean MCAv was 62 +/- 19 cm/s with an increase of 19 +/- 13 cm/s (normal RC). In three patients (8%), the mean MCAv was 43 +/- 22 cm/s with a decrease of -6 +/- 3 cm/s with respect to base values (reduction of RC). (t = 3.30; p = 0.0022). All these patients were hypertensive (BP > 180/100 mmHg) and had a carotid artery stenosis > 90%. Postoperatively, the three patients with reduction of RC complained of homolateral headache. TCD showed a mean MCAv of 67 +/- 17 cm/s, an increase compared to the preoperative rest values of 17 +/- 8 cm/s, the 33 patients with normal RC showed a mean change in MCAv -2 +/- 12 cm/s.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1987

Treatment of paramyotonia congenita with acetazolamide.

Treatment of paramyotonia congenita with acetazolamide has been shown to reduce myotonic symptoms but severe weakness has developed in some patients leading to a recommendation not to use the drug in this disorder. We studied a patient with the characteristic clinical and electrophysiological profile of paramyotonia congenita. Myotonia was effectively treated with a very low dose of acetazolamide and no weakness developed. We conclude that acetazolamide can be a safe and effective medication in paramyotonia congenita.

Acetazolamide↗
PubMed1984

Quantitative evaluation of the effects of acetazolamide in Friedreich's ataxia: a pilot study.

We evaluated the effects of acetazolamide in 4 young patients with Friedreich's ataxia by clinical and quantitative laboratory methods. Dynamic muscle function of the lower extremity was measured during isokinetic knee movements and gait. The acetazolamide trial was terminated at 7 to 11 weeks because of reported side effects or increased ataxia in 3 of the patients. The quantitative evaluations revealed lower dynamic strength values and alterations in the gait movement pattern in all patients. These changes, which were interpreted as deterioration, were partially reversible with cessation of acetazolamide. The advantages of such quantitative evaluations of dynamic muscle function in the evaluation of therapy in Friedreich's ataxia are discussed.

Acetazolamide↗
PubMed1989

Neuronal pH regulation: constant normal intracellular pH is maintained in brain during low extracellular pH induced by acetazolamide--31P NMR study.

The intracellular pH in the brain was studied in six healthy volunteers before and immediately after the administration of 2 g of acetazolamide. Phosphorus-31 nuclear magnetic resonance spectroscopy by a 1.5 tesla whole-body scanner was used. The chemical shift between the inorganic phosphate and the phosphocreatine resonance frequencies was used for indirect assessment of the intracellular pH. The mean baseline intracellular pH was 7.05 +/- 0.04 (SD). The mean pH changes obtained at 15-min intervals within the first hour of acetazolamide administration were -0.03 +/- 0.04 (SD), -0.02 +/- 0.03 (SD), and 0.00 +/- 0.04 (SD), i.e., no statistically significant pH decrease was observed during the period where extracellular pH is known to drop markedly. Although several factors contribute to the lack of change of the intraneuronal pH, we will discuss that this observation in addition might suggest a direct intracerebral effect of acetazolamide.

Acetazolamide↗