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At least 19 recordsLinked to original sources
PubMed1996

Cerebral blood flow alteration by acetazolamide during carotid balloon occlusion: parameters reflecting cerebral perfusion pressure in the acetazolamide test.

BACKGROUND AND PURPOSE: We attempted to clarify the role of the acetazolamide-reactive mechanism in cerebral hemodynamic autoregulation and to establish a useful method of estimation using the acetazolamide test. METHODS: We examined 18 patients whose cerebral hemodynamics were considered to be normal and whose cerebral blood flow (CBF) was maintained during the balloon occlusion test (BOT) of the internal carotid artery. We measured the mean stump pressure (MSTP) and the mean CBF in the middle cerebral arterial territory using a xenon-enhanced CT system during BOT with and without acetazolamide activation. We obtained the asymmetry ratio (AR=occluded CBF/contralateral CBF) and the increased CBF parameters caused by acetazolamide activation expressed as an absolute value (delta CBF) and a percentage (%delta CBF) for the occluded side. RESULTS: AR during BOT with and without acetazolamide activation differed significantly (P<.001, paired t test) despite the lack of significant MSTP changes. Furthermore, although there was no significant correlation between MSTP and AR without acetazolamide activation, a positive significant correlation was detected with acetazolamide activation (r=.634, P=.005, linear regression analysis). There were significant correlations between delta CBF and MSTP (r=.574, P=.013) and %delta CBF and MSTP (r=.640, P=.004). CONCLUSIONS: We consider that the acetazolamide-reactive mechanism functions as autoregulation at the lower end of the autoregulatory range. The acetazolamide test, using %delta CBF or delta CBF as parameters (which both directly reflect MSTP), is useful for estimating the cerebral perfusion pressure decrease and presence of hemodynamic compromise.

Acetazolamide↗
PubMed1998

Acetazolamide plus low-dose dexamethasone is better than acetazolamide alone to ameliorate symptoms of acute mountain sickness.

METHODS: In a double-blind study, we compared the efficacy of a combination of sustained-release acetazolamide and low-dose dexamethasone and acetazolamide alone for prophylaxis against acute mountain sickness (AMS) caused by rapid ascent to high altitude. Before ascent, 13 subjects were randomly assigned to receive a combination of one sustained-release acetazolamide capsule (500 mg) in the afternoon and 4 mg dexamethasone every 12 h, or a combination of the same dose of acetazolamide once daily and a placebo every 12 h. Days 1 and 2 were spent at 3698 m (La Paz, Bolivia), while days 3 and 4 were spent at 5334 m (Mount Chaclataya, Bolivia). Ascent was by 2 h motor vehicle ride. Heart rates, peripheral oxygen saturations and a modified score derived from the Environmental Symptom Questionnaire (modified-ESQ) were measured on each day. In addition, weighted averages of the cerebral (AMS-C) and respiratory (AMS-R) symptoms were calculated for days 3 and 4. RESULTS: Heart rate and modified-ESQ scores increased on days 3 and 4 compared with the other days in the acetazolamide/placebo group only (p < 0.05). Oxygen saturations decreased in both groups on days 3 and 4 (p < 0.05), but the decrease was greater in the acetazolamide/placebo group (p < 0.05). AMS-C and AMS-R scores rose above the suggested thresholds for indication of AMS on days 3 and 4 in the acetazolamide/placebo group only (p < 0.05). CONCLUSION: We conclude that this combination of sustained-release acetazolamide once daily and low-dose dexamethasone twice daily is more effective in ameliorating the symptoms of AMS than azetazolamide alone at the ascent that was studied.

Acetazolamide↗
PubMed1984

Dissociation of glucose and potassium arterial-venous differences across the forearm by acetazolamide. A possible relationship to acetazolamide's beneficial effect in hypokalemic periodic paralysis.

We studied the effect of acetazolamide on arterial-venous (A-V) glucose and potassium differences across the forearm following oral glucose loading in eight normal subjects. Administration of acetazolamide for 72 hours prior to glucose loading resulted in increased A-V glucose differences and decreased A-V potassium differences. Acetazolamide may, therefore, increase glucose uptake across muscle while decreasing potassium uptake following glucose ingestion. This glucose-potassium dissociation observed in normal subjects may relate to acetazolamide's beneficial effect in hypokalemic periodic paralysis.

Acetazolamide↗
PubMed1982

Effect of exogenous adenosine 3':5'-cyclic monophosphate, parathyroid hormone and acetazolamide on electrolyte hormone and acetazolamide on electrolyte excretion by the isolated perfused rat kidney.

The effects of exogenous adenosine 3':5'-cyclic monophosphate (cyclic AMP), parathyroid hormone (PTH) and acetazolamide (Az) on renal calcium and phosphate excretion of the isolated perfused rat kidney were compared. Both PTH and Az evoked an early increase in urinary cyclic AMP excretion followed by a later more prolonged increase in phosphate excretion. All of the increased urinary cyclic AMP was derived from renal cells. Calcium excretion decreased with PTH but was unchanged with Az. Sodium and potassium excretion increased with Az but not PTH. Transitory urinary cyclic AMP excretion rates following bolus additions of exogenous cyclic AMP to perfusate were up to twentyfold greater than those evoked by PTH or Az but unassociated with changes in calcium, phosphate, sodium or potassium excretion. Sustained perfusate levels (above 0.5 microM) and excretion rates of cyclic AMP induced phosphaturia proportional to the perfusate cyclic AMP concentrations achieved up to 2.0 microM. Clearances of exogenous cyclic AMP exceeded inulin clearance at perfusate concentrations greater than 1.0 microM. Aminophylline evoked a small phosphaturia which increased further on addition of cyclic AMP to 5 microM. Glomerular filtration was not affected by any of the agents except Az. Since increased phosphate excretion could be evoked only at perfusate concentrations exceeding either plasma or intracellular concentrations observed in vivo, it is concluded that circulating cyclic AMP at levels in vivo is unlikely to mediate a significant fraction of the renal effects of PTH.

Acetazolamide↗
PubMed1996

Growth suppression in children receiving acetazolamide with antiepileptic drugs.

To clarify the effect of the clinical dosage of acetazolamide on growth in children with epilepsy or febrile convulsion, the standard scores of height and weight in 17 subjects receiving acetazolamide as an adjunct to unchanged monotherapy of antiepileptic drug were compared longitudinally through four phases: before antiepileptic drug administration, with monotherapy of antiepileptic drug, with acetazolamide in addition to monotherapy, and after acetazolamide discontinuation. The standard scores of both height and weight in the subjects were significantly reduced during the phase of acetazolamide administration. During this period, serum concentrations of potassium and total CO2 decreased while that of chloride increased, suggesting the existence of metabolic acidosis in the subjects. For both height and weight, there was no correlation between the degree of standard score reduction during acetazolamide administration and age at the time of acetazolamide initiation, duration of acetazolamide administration, dosages of acetazolamide, and variety of antiepileptic drugs concomitantly administered with acetazolamide. We speculate that metabolic acidosis induced by acetazolamide suppressed the growth of the subjects and that there were large individual differences in the susceptibility to acetazolamide for growth suppression among patients receiving acetazolamide.

Acetazolamide↗
PubMed1987

Role of carbonic anhydrase in bone resorption: effect of acetazolamide on basal and parathyroid hormone-induced bone metabolism.

The effects of the carbonic anhydrase inhibitor acetazolamide on basal and parathyroid hormone (PTH)-induced bone metabolism were studied to evaluate the manner in which acetazolamide inhibits bone resorption. Half-calvaria from 5 to 6-day-old mice were cultured using the following treatments: control; acetazolamide (10, 33, or 100 microM); PTH (16.7 nM bovine PTH 1-34); acetazolamide + PTH. The effects of acetazolamide on PTH-induced cAMP accumulation and protein synthesis were determined. Media from bones cultured for 48 hours were analyzed for calcium to assess bone resorption, glucose to assess calvarial glucose utilization, and lactic acid to assess calvarial lactic acid release. Media were also assayed for beta-glucuronidase activity as an indicator of lysosomal enzyme release and for lactate dehydrogenase activity as an indicator of cytosolic enzyme release and cytotoxicity. Acetazolamide at 100 microM completely inhibited PTH-induced bone resorption. This inhibition did not appear to be due to cell death, as acetazolamide did not increase lactate dehydrogenase release. Acetazolamide had no effect on PTH-enhanced cAMP levels, indicating that receptor binding and adenylate cyclase activation were unaffected. Acetazolamide alone did not alter calvarial protein synthesis, but did significantly inhibit protein synthesis in the presence of PTH. PTH significantly enhanced calvarial glucose utilization, lactic acid release, and beta-glucuronidase release. Acetazolamide inhibited all of these PTH-induced parameters in a manner that roughly paralleled its inhibition of bone resorption; acetazolamide alone had no effect on the basal values. Our results indicate that acetazolamide inhibition of bone resorption in vitro may involve general alterations in hormonally stimulated bone cell metabolism secondary to carbonic anhydrase inhibition.

Acetazolamide↗
PubMed1986

Toxic interaction between acetazolamide and salicylate: case reports and a pharmacokinetic explanation.

Two elderly patients, who were chronically receiving aspirin, developed lethargy, incontinence, and confusion after dosing with acetazolamide. Unbound plasma acetazolamide concentrations were elevated and plasma protein binding was reduced, suggesting an interaction with aspirin. In vitro studies demonstrated a concentration-dependent effect of salicylate on acetazolamide binding to serum proteins. At a therapeutic serum acetazolamide level of 8.0 micrograms/ml, the unbound percentage of acetazolamide in serum was 3.3% and increased to 11.0% and 30.0%, with serum salicylate levels of 200 and 386 micrograms/ml, respectively. Furthermore, the apparent association constant of acetazolamide for binding to serum proteins was decreased by 58% and 86% of its control value at these respective salicylate concentrations. The maximal binding capacity of serum for acetazolamide was not affected by salicylate. Pharmacokinetic studies in four volunteers showed that the plasma protein binding and renal clearance of acetazolamide were significantly reduced during chronic salicylate dosing. Salicylate appears to competitively inhibit the plasma protein binding of acetazolamide and simultaneously to inhibit acetazolamide renal tubular secretion. Caution is advised when acetazolamide and salicylate are used concurrently.

Acetazolamide↗
PubMed2002

Tolerability and efficacy of dorzolamide versus acetazolamide added to timolol.

PURPOSE: Evaluate the safety and efficacy of dorzolamide versus acetazolamide when added to once daily 0.5% timolol maleate ophthalmic gel forming solution (timolol gel). METHODS: This was a randomized, double-masked, multicenter, active-controlled, parallel group study of 215 patients with open-angle glaucoma or ocular hypertension. Following a two-week treatment period with timolol gel, patients with IOP > or = 22 mm Hg and who tolerated one week of acetazolamide 250-mg q.i.d. either were randomized to acetazolamide or dorzolamide 2% three times daily for 12 weeks. RESULTS: In 155 randomized patients (dorzolamide, N = 80, acetazolamide, N = 75), compared to the dorzolamide, acetazolamide had a statistically greater number of systemic adverse events (dorzolamide 50%, acetazolamide 75%, p = 0.001), adverse events associated with carbonic anhydrase inhibitor (CAI) therapy (dorzolamide 26%, acetazolamide 53%, p < 0.001) and discontinuations due to CAI adverse experiences (dorzolamide 8%, acetazolamide 24%, p = 0.007). Intent to treat analysis found that changes from baseline in IOP were similar at both troughs (dorzolamide 1.4 +/- 0.46 mm Hg, acetazolamide 0.8 +/- 0.47 mm Hg, p = 0.386). However, per-protocol analysis found statistically improved pressure control with acetazolamide (0.1 +/- 0.42 mm Hg) compared to dorzolamide (1.9 +/- 0.43 mm Hg) (p = 0.009). CONCLUSIONS: This study found a greater incidence of systemic and CAI adverse experiences and discontinuations due to acetazolamide compared to dorzolamide.

Acetazolamide↗
PubMed1995

Time dependency of the acetazolamide effect on cerebral hemodynamics in patients with chronic occlusive cerebral arteries. Early steal phenomenon demonstrated by [15O]H2O positron emission tomography.

BACKGROUND AND PURPOSE: The acetazolamide effect is thought to reach a maximum at 10 to 20 minutes after administration. However, we sometimes encountered patients who showed a transient deterioration of ischemic symptoms several minutes after acetazolamide administration. We therefore considered that a steal phenomenon may occur before the acetazolamide effect reaches a maximum. We evaluated the time dependency of the acetazolamide effect on cerebral hemodynamics in patients with severe stenosis or occlusion of the unilateral internal carotid artery. METHODS: The subjects consisted of 13 patients with severe stenosis or occlusion of the unilateral internal carotid artery. Regional cerebral blood flow was measured at the resting state and at 5 and 20 minutes after the intravenous administration of 1 g acetazolamide by the use of the [15O]H2O bolus-injection method and positron emission tomography. The steal phenomenon was interpreted as positive when the regional cerebral blood flow values decreased by more than 10% after the administration of acetazolamide in more than one region of interest. RESULTS: A steal phenomenon was observed in 5 of 13 patients at 5 minutes after acetazolamide administration on the occlusive side, whereas it was observed in only 1 patient at 20 minutes. Thus, this phenomenon was observed more frequently in the early phase of the acetazolamide test. It was also observed more frequently in patients with poorly developed collateral circulation. CONCLUSIONS: Our acetazolamide [15O]H2O positron emission tomography study revealed an early steal phenomenon at 5 minutes after intravenous administration of acetazolamide, which may be a cause of the transient deterioration of ischemic symptoms during the acetazolamide test.

Acetazolamide↗
PubMed1989

Effects of acetazolamide on Na+-HCO-3 cotransport in basolateral membrane vesicles isolated from rabbit renal cortex.

We evaluated the effects of acetazolamide on Na+-HCO3- cotransport in basolateral membrane vesicles isolated from the rabbit renal cortex. Na+ uptake stimulated by an imposed inward HCO3- gradient was not significantly reduced by 1.2 mM acetazolamide, indicating that acetazolamide does not directly inhibit Na+-HCO3- cotransport. 4,4'-Diisothiocyanostilbene-2,2'-disulfonate (DIDS)-sensitive Na+-base cotransport was found to be absolutely CO2/HCO3--dependent. We therefore tested whether acetazolamide-sensitive availability of HCO3- at the basolateral membrane could be rate-limiting for Na+-base cotransport under some conditions. In the presence of a CO2/HCO3- buffer system but absence of an initial HCO3- gradient, Na+ influx was stimulated fivefold by an outward NH4+ gradient. This stimulation of Na+ influx by an outward NH4+ gradient was inhibited greater than 75% by 0.6 mM acetazolamide, suggesting that acetazolamide blocked the ability of the NH4+ gradient to generate an inward HCO3- gradient. In the presence of an inward HCO3- gradient, Na+ influx was inhibited greater than 70% by an inward NH4+ gradient. This inhibition of Na+ influx was reduced to only 35% by 0.6 mM acetazolamide, suggesting that acetazolamide blocked the ability of NH4+ to collapse the inward HCO3- gradient. Similarly, Na+ influx in the presence of an inward HCO3- gradient was inhibited greater than 80% by an outward acetate gradient, and this inhibition was reduced to only 50% by acetazolamide. Thus, acetazolamide caused either inhibition or stimulation of Na+ uptake depending on the conditions with respect to pH and HCO3- gradients. The indirect interaction of acetazolamide with the basolateral membrane Na+-HCO3- cotransport system may be an important mechanism underlying inhibition of proximal tubule acid secretion by this agent.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2003

Comparison of acetazolamide and medroxyprogesterone as respiratory stimulants in hypercapnic patients with COPD.

BACKGROUND: Acetazolamide and medroxyprogesterone acetate (MPA) are two respiratory stimulants that can be used in patients with stable hypercapnic COPD. DESIGN AND METHODS: The effects of acetazolamide, 250 mg bid, and MPA, 30 mg bid, on daytime and nighttime blood gas values and the influences on the hypercapnic and hypoxic ventilatory and mouth occlusion pressure (P(0.1)) at 100 ms response were studied in a crossover design in 12 hypercapnic patients with stable COPD (FEV(1), 33 +/- 4% predicted [mean +/- SEM]). RESULTS: Daytime PaCO(2) decreased from 47.3 +/- 0.8 mm Hg (placebo) to 42.0 +/- 1.5 mm Hg during acetazolamide treatment (p < 0.05) and to 42.8 +/- 1.5 mm Hg during MPA treatment (p < 0.05). Daytime PaO(2) improved with acetazolamide from 65.2 +/- 2.3 to 75.0 +/- 3.0 mm Hg (p < 0.05), whereas no significant changes were seen with MPA. Mean nocturnal end-tidal carbon dioxide tension decreased with both treatments, from 42.0 +/- 2.3 to 35.3 +/- 2.3 mm Hg with acetazolamide (p < 0.05) and to 34.5 +/- 0.8 mm Hg with MPA (p < 0.05). The percentage of time that the nocturnal arterial oxygen saturation was < 90% was reduced significantly with acetazolamide, from 34.9 +/- 10.7% to 16.3 +/- 7.5% (p < 0.05). Mean nocturnal saturation did not change with MPA. Resting minute ventilation increased significantly only with MPA from 9.6 +/- 0.7 to 10.8 +/- 0.8 L/min (p < 0.05). The slope of the hypercapnic ventilatory response did not change during acetazolamide and MPA therapy. The hypoxic ventilatory response increased from - 0.2 +/- 0.05 to - 0.4 +/- 0.1 L/min/% during acetazolamide (p < 0.05) and to - 0.3 +/- 0.1 L/min/% during MPA (p < 0.05). The hypoxic P(0.1) response improved with acetazolamide treatment from - 0.05 +/- 0.008 to - 0.15 +/- 0.02 mm Hg/% (p < 0.05). CONCLUSIONS: This study shows that acetazolamide and MPA both have favorable effects on daytime and nighttime blood gas parameters in ventilatory-limited patients with stable COPD. However, the use of acetazolamide is preferred because of its extra effect on nocturnal saturation.

Acetazolamide↗
PubMed1987

Management of acid-base balance with red blood cell carbonic anhydrase (RCA). II. Control of acid-base balance with acetazolamide.

Acetazolamide, a carbonic anhydrase (CA) inhibitor, was used to normalize metabolic alkalemia. A dosage of acetazolamide for normalizing metabolic alkalemia has not yet been experimentally determined. The dosage of acetazolamide for this purpose is experimentally calculated in this paper. The correlation between various concentration of acetazolamide mixed with blood and the base excess (BE) levels in blood at the start of normalizing metabolic alkalosis was studied in vitro. The change rate of the BE level was calculated from BE levels noted before and after tonometry of the blood with and without acetazolamide. A dosage of acetazolamide which can cause the change rate of the BE level to decrease is considered to be an effective dosage. Metabolic alkalosis in vitro was produced by adding bicarbonate into the blood. An effective dosage of acetazolamide for metabolic alkalemia of which the BE range was from 0 to + 30 mEq/liter was calculated. CA activities in the kidney and the blood of dogs administered acetazolamide were examined. The effective dosage of acetazolamide obtained from in vitro experiments inhibited the CA activities not only in the blood but also in the kidneys. An effective dosage of acetazolamide to normalize a BE of + 10 mEq/liter in vitro was converted into about 7-12 mg/kg in vivo. This dosage inhibited the red blood cell carbonic anhydrase (RCA) activity to 20-40%, whereas the normal physiological variation range is 25%. An effective dosage of acetazolamide in the blood did not proportionally increase with an increase of HCO3- during severe alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed2001

Preretinal neovascularization associated with acetazolamide-induced systemic acidosis in the neonatal rat.

PURPOSE: NH4Cl gavage in the neonatal rat produces a metabolic acidosis-induced retinopathy which serves as a model for retinopathy of prematurity (ROP). Acetazolamide induces a metabolic acidosis via an alternative biochemical mechanism (bicarbonate loss versus hydrogen ion load). In the present study, the following hypothesis was tested: acetazolamide-induced acidosis is associated with preretinal neovascularization in the neonatal rat. METHODS: All studies used newborn Sprague-Dawley rats raised in expanded litters of 25. Arterial blood pH was measured to determine the level of acidosis induced by intraperitoneal (IP) acetazolamide (50 or 200 mg/kg) or saline. In a separate retinopathy study, newborn rats (n = 75) were randomized to either IP acetazolamide, 50 mg/kg (low-dose), or IP saline twice daily from days 2 to 7. After 5 days of recovery, retinal vasculature was assessed using ADPase staining and light microscopy. The presence and severity (clock hours) of neovascularization were assessed by three masked observers. In an additional retinopathy study, newborn rats (n = 100) were randomized to either IP acetazolamide, 200 mg/kg (high-dose), or IP saline twice daily from days 2 to 7. After 5 days of recovery, the retinas were similarly analyzed. RESULTS: Neovascularization occurred in 59% of rats receiving high-dose acetazolamide (200 mg/kg). High-dose acetazolamide produced a severe acidosis (pH 7.13 +/- 0.06) during drug delivery. Low-dose acetazolamide (50 mg/kg) produced a pH (7.22 +/- 0.07) that was intermediate between high-dose (200 mg/kg) acetazolamide (P < 0.001) and saline controls (7.42 +/- 0.06, P < 0.001); however, neither low-dose acetazolamide nor saline induced preretinal neovascularization. CONCLUSIONS: Acidosis induced by high-dose acetazolamide, independent of hyperoxemia or hypoxemia, is associated with preretinal neovascularization in the neonatal rat. Induction of neovascularization appears to depend on a critical threshold of acidosis severity. This study further supports a proposed independent role for acidosis in the pathogenesis of ROP.

Acetazolamide↗
PubMed1992

Determination of acetazolamide in human serum by enzymatic assay.

Carbonic anhydrase (CA) inhibitors, such as acetazolamide (AZ), formerly used as diuretics, still play a role in the treatment of glaucoma, epilepsy, and altitude sickness. There is now hard evidence from both in vitro and in vivo studies in animals that carbonic anhydrase plays a vital function in bone loss. Acetazolamide blocks bone resorption in these experimental models. We have postulated that acetazolamide has potential for the treatment of human conditions associated with bone loss. In preparation for a clinical trial of acetazolamide's effectiveness in this regard, we developed an enzymatic method for determining the total concentration of acetazolamide in human serum. Acetazolamide is stripped from binding to serum proteins by adding 10(-6) M salicylic acid and adjusting the pH to 2.5, followed by ultrafiltration through a membrane (10 kD cutoff). The latter permits the free acetazolamide to enter the filtrate but retains any carbonic anhydrase (31 kD) which may contaminate the serum from hemolysis. The carbonic anhydrase inhibitory activity in the filtrate, representing the acetazolamide, is determined in a carbonic anhydrase assay using acetazolamide as the standard. Recoveries of acetazolamide added to human serum ranged from 83% to 94% depending on the concentration. Precision, as judged by the coefficient of variation, was 10.5%.

Acetazolamide↗
PubMed1996

Dissociation of vasoreactivity to acetazolamide and hypercapnia. Comparative study in patients with chronic occlusive major cerebral artery disease.

BACKGROUND AND PURPOSE: The aim of this study was to compare the effect of vasodilative stimuli for the measurement of cerebrovascular reactivity obtained by acetazolamide and hypercapnia in patients with chronic occlusive major cerebral artery disease. METHODS: We examined 24 patients with unilateral occlusive lesions of a major cerebral artery using the 133Xe inhalation technique and single-photon emission CT. Regional cerebral blood flow (CBF) was measured during a resting state, during inhalation of 5% CO2, and 15 minutes after the administration of acetazolamide consecutively in the same patients. Normative values of resting CBF and acetazolamide reactivity were obtained in 21 normal subjects. RESULTS: All patients with the exception of 1 showed an increase in CBF during hypercapnia ipsilateral to the occlusive lesion. Ipsilateral acetazolamide reactivity was preserved in 13 patients. Conversely, 11 patients showed an absent response or paradoxical CBF reduction. Ipsilateral CO2 reactivity did not correlate with acetazolamide reactivity when all 24 patients were considered. However, there was a significant correlation between acetazolamide and CO2 in the 13 patients who showed preserved acetazolamide reactivity (r = .60, P < .05). No significant correlation was present in the remaining 11 patients with reduced acetazolamide reactivity. Although significant blood pressure augmentation was observed in hypercapnia, we could not find a correlation between change of blood pressure and CO2 reactivity. CONCLUSIONS: Acetazolamide identified patients with reduced vasomotor reactivity who appeared to have preserved CO2 reactivity. Acetazolamide testing may be useful in the assessment of cerebral hemodynamics. However, further investigations are necessary to assess the clinical utility of these tests.

Acetazolamide↗