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 487 records · Page 27Linked to original sources
PubMed1992

Effects of timolol and acetazolamide on intraocular pressure elevation following argon laser iridotomy.

To study the effect of hypotensive agents on intraocular pressure elevation following argon laser iridotomy, 0.5% timolol maleate topically and acetazolamide 125 mg orally were given in 39 eyes, one hour prior to laser iridotomy, with 29 eyes serving as the control. The mean pressure two hours after laser iridotomy was 18.9 +/- 7.2 mmHg in the control group and 12.8 +/- 3.9 mmHg in the pretreated group. Ocular pressure was elevated from the baseline pressure of the prelaser status in two eyes (5%) only in the timolol-acetazolamide treated group and in 16 eyes (55%) in the control group. The pressure elevation two hours after laser iridotomy was significantly less in the timolol-acetazolamide pretreated group.

Acetazolamide↗
PubMed1992

[MR angiography enhanced by sodium acetazolamide].

We tried to use sodium acetazolamide to enhance MR angiography (MRA). Sodium acetazolamide, one of carbonic anhydrase inhibitors, has an effect to increase regional cerebral blood flow. We made a direct comparison between pre and post enhanced MRA (both 3D-TOF and 3D-PC techniques). MRA after administration of sodium acetazolamide could depict more details of cortical branches without enhancement of back-ground. So we recommend this simple method to be used widely in any examination of MR angiography.

Acetazolamide↗
PubMed2004

Correlation of angiographic circulation time and cerebrovascular reserve by acetazolamide-challenged single photon emission CT.

BACKGROUND AND PURPOSE: Although cerebral circulation time (CCT) is one of the main parameters in cerebral blood flow measurements, its clinical significance is controversial. To assess the importance of CCT by using a nondiffusible indicator, we studied the relationship between angiographic CCT and cerebrovascular reserve. METHODS: Twenty-eight patients, each with a unilateral occlusive lesion in the internal carotid artery or middle cerebral artery, were examined. To assess the CCT, the regional arteriocapillary circulation time (rACCT) was measured by angiography and the ratio of the value on the occlusive side to the value on the contralateral side was calculated as the rACCT ratio. To estimate the cerebrovascular reserve, acetazolamide-challenged single photon emission CT was used. Patients with a decreased cerebrovascular reserve were defined as the "poor reserve" group, and those without a decrease were defined as the "normal reserve" group. The ratio of the radioactivity count on the occlusive side to the count on the contralateral side was calculated as the asymmetry index, and the proportion of the acetazolamide-challenged asymmetry index to the baseline asymmetry index was defined as the regional reactivity index. RESULTS: The rACCT ratio in the poor reserve group (n = 19) was significantly (P <.001) larger than that in the normal reserve group (n = 9), and a significant correlation (r = -0.83, P <.01) was found between the rACCT ratio and the regional reactivity index. CONCLUSION: The angiographic CCT and the cerebral vasoreactivity to acetazolamide on single photon emission CT were well correlated, suggesting that measurement of the CCT by using a nondiffusible indicator could be used as an index of cerebrovascular reserve.

Acetazolamide↗
PubMed1992

Acetazolamide enhanced single photon emission computed tomography (SPECT) evaluation of cerebral perfusion before and after carotid endarterectomy.

Twenty-five patients were tested before and after carotid endarterectomy with resting and acetazolamide enhanced single photon emission computed tomography (SPECT) scans with hexamethyl propyleneamine oxine (HMPAO) or iofetamine hydrochloride I123 (123I labeled IMP), both widely available radiopharmaceuticals. Twenty preoperative SPECT studies were asymmetric, revealing focal or diffuse decreased perfusion reserve, and 13 also demonstrated infarcts. Five patients had symmetric (normal) studies. After carotid endarterectomy, 22 cases had changed flow distribution patterns. Usually improvement of reactivity ipsilateral occurred to the area operated on. In four, contralateral improvement was also found. Three of the patients who had preoperative symmetrical scans had increased ipsilateral reactivity after surgery indicating previous global loss of reactivity. Acetazolamide SPECT scans demonstrate a decreased perfusion reserve in 20 patients with carotid artery stenosis, indicating reduced perfusion and poor collateral circulation. Postoperative studies confirm improvement by demonstrating recovery of vascular reactivity in 84% of the patients. Acetazolamide enhanced SPECT scans may be helpful in providing objective evidence for selection of patients for carotid endarterectomy, especially in those who have an 80% carotid artery stenosis, but are asymptomatic.

Acetazolamide↗
PubMed1992

Retinal adhesive force in living rabbit, cat, and monkey eyes. Normative data and enhancement by mannitol and acetazolamide.

Small retinal detachments (blebs) were made in living eyes by injecting balanced salt solution into the subretinal space with a micropipette. A second micropipette, inserted into the same bleb, measured subretinal pressure using a resistance servonulling system. The adhesive force was calculated from the pressure difference across the retina according to Laplace's law. The retinal adhesive force in rabbit, cat, and monkey eyes averaged 1.0, 1.8, and 1.4 x 10(2) dyne/cm, respectively. In rabbit eyes, 2 hr after intravenous administration of 15 mg/kg acetazolamide, the retinal adhesive force was increased to 133%. In monkeys, this dose of acetazolamide increased retinal adhesion to 144% of control values. Mannitol (2 g/kg) increased retinal adhesion in the monkey to 153% of control values 90 min after intravenous injection (compared with an increase of 145% in previous experiments in the rabbit). Because both mannitol and acetazolamide enhance retinal adhesiveness in living primate eyes, it seems likely that they will have a similar effect in humans that they may be clinically useful.

Acetazolamide↗
PubMed1991

Acetazolamide in the treatment of metabolic alkalosis in critically ill patients.

Metabolic alkalosis is a common acid-base disturbance in critically ill patients. In many patients correction of fluid and electrolyte status does not fully correct the metabolic derangement. In this study we examined the effect of 500 mg of intravenous acetazolamide, after correcting for fluid and electrolyte abnormalities, on the acid-base status of 30 ventilated patients. In all patients studied there was a fall of total serum bicarbonate; the mean reduction at 24 hours was 6.4 mmol/L, with a normalization of the base excess and pH. The onset of action was rapid (within 2 hours), and the maximal effect occurred at a mean of 15.5 hours, although there was wide variation. The effect of acetazolamide was still apparent at 48 hours. No adverse effects were noted. We conclude that in patients with metabolic alkalosis, once fluid and electrolyte abnormalities have been corrected, acetazolamide is an effective and safe form of therapy with a quick onset and long duration of action.

Acetazolamide↗
PubMed1977

[Paralysis with hypokalemia by transfer, treated by acetazolamide].

A case of familial paralysis with hypokalemia is presented. Acetazolamide at a dose of 500 mg daily prevents the onset of acute attacks. Under acetazolamide, an oral glucose tolerance test is not followed by hypokalemia. The association of glucose and insulin is unable to trigger off a paralytic attack although without acetazolamide, the same protocol had 5 months previously precipitated tetraplegia with hypokalemia. These results are compared with those in the literature.

Acetazolamide↗
PubMed1991

A direct correlation of the resolution of pseudophakic cystoid macular edema with acetazolamide therapy.

We report the case of a patient with pseudophakic cystoid macular edema whose visual acuity improved promptly with oral administration of 500 mg of acetazolamide extended-release capsules BID for two weeks. However, vision worsened again within two weeks of discontinuation of the treatment. On resumption of acetazolamide therapy for three weeks, and its slow withdrawal during the following three weeks, the macular edema eventually resolved, and vision returned to normal. Our observation provides a direct correlation of the resolution of pseudophakic cystoid macular edema with acetazolamide therapy and shows the importance of tapering the doses of this regimen.

Acetazolamide↗
PubMed1990

Time course of changes in aqueous protein concentration and flow rate after oral acetazolamide.

The coefficient of plasma protein entry into the aqueous humor, kin, was calculated in the human eyes from the aqueous protein concentration measured with a flare-cell meter and from the aqueous flow rate determined with fluorophotometry. The value of kin averaged 3.47 +/- 0.25 x 10(-5) min-1 (mean +/- SEM) in 12 eyes of six normal young volunteers. The time course of changes in aqueous protein concentration after oral administration of 500 mg acetazolamide was measured with a flare-cell meter in 24 eyes of 12 subjects. Aqueous protein concentration significantly increased from 2-10 hr postadministration with a maximum increase of 41 +/- 7% (mean +/- SEM) at 6 hr postadministration. Assuming that kin is not affected by the drug treatment, we calculated the time change of aqueous flow rate from that of aqueous protein concentration using the value of kin above. The calculated flow rate after the administration of acetazolamide decreased between 1.25 and 8 hr, with a maximum reduction of 40 +/- 11% at 1.75 hr postadministration. These measurements obtained with the flare-cell meter corresponded well to those obtained by fluorophotometry in a separate group of volunteers given the same treatment. It was shown that oral acetazolamide increases aqueous protein concentration, and that the time change of its effect on aqueous flow rate can be monitored by measuring aqueous protein concentration.

Acetazolamide↗
PubMed1975

Diuretics, urate excretion and sodium reabsorption: effect of acetazolamide and urinary alkalinization.

The uricosuric properties of acetazolamide were investigated in order to elucidate the relationship between changes in proximal tubular sodium reabsorption and urate excretion in man. Acetazolamide produced a modest uricosuric response which was not suppressible by pyrazinamide. Alkalinization of the urine with sodium bicarbonate elicited an even smaller increment in the urate clearance. If urinary alkalinization does play a role in the uricosuric response to acetazolamide, it probably decreases urate reabsorption within the distal nephron. The present studies, when taken together with previous work, suggest that alterations in proximal tubular sodium and water reabsorption probably do not play an important role in the normal control of urate excretion or in the pathogenesis of hyperuricemic states. Diuretic-induced hyperuricemia occurring during extracellular fluid volume depletion probably results from either diminished tubular secretion of urate, accelerated postsecretory urate reabsorption, or both.

Acetazolamide↗
PubMed1990

[Paroxysmal cerebellar ataxia--an evaluation using the findings from magnetic resonance imaging, positron emission tomography, and acetazolamide treatment].

Paroxysmal cerebellar ataxia (PCA) is a specific disease which exhibits spasmodic cerebellar ataxia but rarely shows abnormal neurological findings in the intermission. Verger first described an isolated case. Subsequent reports of the disease included mostly cases with autosomal dominant inheritance, but the reports have been limited to about 20 families. Although both the lesion and the cause have not been clearly identified, since Vighetto et al. demonstrated the atrophy of the anterosuperior region of the cerebellar vermis using magnetic resonance imaging (MRI), the lesion of PCA captured the attention of researchers. The patient was a 40-year-old male, who exhibited spasmodic inarticulation and dizziness during walking when he was 10 years old. The symptoms gradually became aggravated in both frequency and duration. Abnormal findings were observed by electroencephalography and Hydantol F was given with no successful effect. The results of a CT scan of the head revealed no abnormality, whereas those of MRI revealed the atrophy in the folia of anterosuperior region of the cerebellar vermis by MRI as in the case of Vighetto et al., and PCA was suspected. Findings from positron emission tomography (PET) for the first time disclosed the abnormality in the cerebellar vermis and brainstem, and suggested an organic disorder in the cerebellar vermis and a functional abnormality in the cerebellum and brainstem. Since the report by Griggs et al., it has been known that acetazolamide is effective for PCA although the pharmacological mechanism is not yet clear. In our present case, the attack was improved in both frequency and duration by the administration of acetazolamide, and the effectiveness of acetazolamide in the patient was confirmed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1989

Carbonic anhydrase activity in fetal rat bone resorbing cells: inhibition by acetazolamide infusion.

Skeletal growth during late fetal development is characterized by intense formation and resorption of the cartilage and bone matrix. In this study, we have evaluated the possible role played by carbonic anhydrase during fetal bone resorption in vivo. Pregnant rats were infused continuously from days 14 to 21 of gestation with acetazolamide a specific inhibitor of carbonic anhydrase, using an osmotic minipump. Carbonic anhydrase activity in long bones of 21 days old fetuses was determined by a previously validated histochemical staining method. In vivo infusion of acetazolamide induced a dose-dependent decrease in the number of carbonic anhydrase-positive resorbing cells whereas the total number of resorbing cells was not affected. At the low dose of 8 mg/day per kg, the number of chondroclasts and osteoclasts was decreased by 14.2 and 12.3% respectively (P less than 0.001) whereas serum calcium and phosphate remained unchanged in mothers and fetuses. At the dose of 40 mg/day per kg, acetazolamide reduced further the number of carbonic anhydrase positive-chondroclasts and osteoclasts by 28.8 and 27.5%, respectively (P less than 0.001), and induced a significant fall in serum calcium and phosphorus in fetuses. This study shows that an in vivo 28% inhibition of carbonic anhydrase activity in resorbing cells lowers serum calcium and indicates that the enzyme plays a significant role in bone resorption during normal fetal long bone growth.

Acetazolamide↗
PubMed1987

[Regional cerebral blood flow and its reactivity to acetazolamide in transient ischemic attacks. Study of 20 cases by gamma emission tomography].

We have studied regional cerebral blood flow (= test) and reactivity of acetazolamide injection (= retest) in 20 patients who had presented transient ischemic attacks (TIA). The cerebral blood flow was measured by the atraumatic Xenon 133 inhalation method and single photon emission tomography using a specially dedicated tomograph (TOMOMATIC 64), allowing 3 tomographic levels (OM + 1, + 5, + 9 cm). Measurements were realized in a quiet, dark room. Acetazolamide (500 mg or 1000 mg) was injected intravenously immediately after the test, and the retest was performed 15 minutes after, in the same conditions. Results obtained from paired ROIS were analysed in terms of asymmetric index for the test, of relative reactivity for retest in regard of normal values established in a group of healthy volunteers. All patients had neurological examination, vascular explorations and CT scan. Six of the patients showed a bad reactivity (abolished or strongly decreased) which was evoked a significant hemodynamically stenosis, reflecting the loss of collateral capacity. In the other group results were diversified, and we classified these in 4 groups: "normal" (7), "luxury perfusion" (3), "limited infarction" (1), and "incomplete infarction" (3). When these groups were plotted versus duration of onset and delay between the last attack and the moment of the measurement, "incomplete infarction" clearly appears as a step between brief TIA (less of 1 hour) and "limited infarction". So rCBF and reactivity to acetazolamide are of major interest for the physiopathological classification of TIAs, but also for treatment and prognosis.

Acetazolamide↗
PubMed1988

Acetazolamide and dexamethasone in the prevention of acute mountain sickness.

We randomly assigned 32 healthy backpackers to receive placebo, acetazolamide (250 mg twice a day), dexamethasone acetate (4 mg four times a day), or both drugs in combination to determine the drug efficacy in preventing acute mountain sickness (AMS) at altitudes of 3,650 to 4,050m (12,000 to 13,300 ft). The incidence of AMS was high but symptoms were generally mild. Combined drug therapy was superior to both placebo and single drug therapy in risk reduction. Using acetazolamide alone was moderately beneficial in preventing the occurrence of AMS, although minor side effects were frequent. The use of dexamethasone alone did not significantly reduce the AMS incidence, and discontinuing its use resulted in symptoms suggestive of adrenal insufficiency. For recreational backpackers, routine drug prophylaxis is not recommended, in view of the mild nature of this illness and the adverse effects of medications. The efficacy of combined acetazolamide-dexamethasone therapy warrants further investigation at higher altitudes, where AMS is more severe, and the dexamethasone should be withdrawn gradually to avoid a possible adrenal crisis.

Acetazolamide↗
PubMed1985

The effect of prophylactic acetazolamide on the intraocular pressure rise associated with Healon-aided intraocular lens surgery.

Sixteen consecutive patients undergoing primary posterior chamber lens insertion with Healon were followed closely for any postoperative rise in intraocular pressure. Patients were divided into an experimental group (who received acetazolamide) and a control group (no acetazolamide). Careful attention was given to the same operative technique and the amount of Healon left in the eye. The treated group showed a mean intraocular pressure of 14.7 mm Hg, whereas the pressure in the control group was 22.6 mm Hg on the first postoperative day. These findings support the rationale for the use of prophylactic acetazolamide as an adjunct to Healon-aided cataract surgery.

Acetazolamide↗
PubMed1985

Effects of timolol, epinephrine, and acetazolamide on aqueous flow during sleep.

The effects of timolol, epinephrine, and acetazolamide on the rate of flow of aqueous humor through the anterior chamber of awake and sleeping human subjects was studied. Timolol reduced the rate in awake subjects but not sleeping subjects. Epinephrine increased the rate in sleeping subjects to a greater extent than in awake subjects. Acetazolamide reduced the rate of flow in awake subjects or epinephrine-stimulated subjects. Acetazolamide reduced the rate of flow slightly below the basal rate observed during sleep, but the reduction was small and not statistically significant. The authors propose that the diurnal fluctuation of the rate of aqueous humor flow in humans is driven by changes in the concentration of endogenous epinephrine available to the ciliary epithelia.

Acetazolamide↗
PubMed1984

Differential effects of acetazolamide, benzolamide and systemic acidosis on hydrogen and bicarbonate gradients across the apical and basolateral membranes of the choroid plexus.

The effect after 1 hr of sulfonamide agents and systemic acidosis on pH (dimethyloxazolidinedione method) and [HCO3-] (calculated from pH and estimated cell pCO2) of choroid plexus epithelium was analyzed in adult Sprague-Dawley rats anesthetized with ether. Acetazolamide (20 mg/kg i.p.) caused a striking increase in choroid cell pH (7.0-7.45) and a substantial elevation in [HCO3-]i, and an alkalinization of cerebrospinal fluid (CSF); effects of benzolamide (3 mg/kg i.v.) were less marked. Acetazolamide-induced augmentation of steady-state pH was found in choroid plexus (0.45 pH unit) but not in submaxillary salivary gland, skeletal muscle, erythrocytes and cerebral cortex. Respiratory acidosis (blood pH 6.94) caused choroid cell pH to decrease less extensively than in the other tissues analyzed; metabolic acidosis (blood pH 7.23) did not significantly alter choroid plexus pH. Both sulfonamide agents and systemic acidoses significantly decreased the pH gradient between arterial blood and cisternal CSF. The sulfonamide-induced increase in choroid cell pH is attributed to suppression of buffering of OH- by CO2, leading to elevated [OH]i; and to a build-up in [HCO3-]i. Acetazolamide caused a reversal of the H+ and HCO3- gradients across the basolateral (plasma-facing) membrane of the choroid plexus. It is postulated that carbonic anhydrase inhibitors decrease CSF formation primarily by reducing Na+-H+ exchange at the basolateral membrane of the choroidal epithelium, and secondarily by slowing down HCO3- and Cl- exit across the CSF-facing membrane.

Acetazolamide↗
PubMed1984

Study of the damaging effects of acetazolamide on gastric mucosa in rats.

The present study demonstrated that acetazolamide (100 and 200 mg/kg, s.c.) induced severe gastric hemorrhagic ulceration in rats. The ulceration was aggravated by oral administration of HCl, but was inhibited by NaHCO3. Furthermore, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were accompanied by an increase in serotonin and histamine released from the stomach. Acetazolamide injection also increased the protein level but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increase in serotonin and histamine release also may have been the contributing factors for gastric ulcer formation.

Acetazolamide↗