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PubMed1999

Regional cerebral blood flow single-photon emission tomography with 99mTc-HMPAO and the acetazolamide test in the evaluation of vascular and Alzheimer's dementia.

The diagnostic potential of technetium-99m hexamethylpropylene amine oxime (HMPAO) following systemic administration of the cerebral vasodilator acetazolamide (acetazolamide test) was evaluated by regional cerebral blood flow (rCBF) single-photon emission tomography (SPET) in patients with Alzheimer's disease (AD) or vascular dementia (VD). An initial, high-resolution SPET study was performed with 99mTc-HMPAO, and after 2 days the patients were re-evaluated with 99mTc-HMPAO following systemic administration of acetazolamide. Reconstructed SPET slices were evaluated visually and semiquantitatively by a semi-automatic rCBF map method. When 99mTc-HMPAO alone was used, bilateral hypoperfusion was found in the temporal and/or parietal regions in 33% (6/18) of the VD patients and in 70% (23/33) of the AD patients. The corresponding data obtained by quantitative evaluation were 41% (7/17) and 71% (15/21), respectively. The vascular reserve capacity, as determined with the acetazolamide test, was preserved visually in 22% (4/18) and quantitatively in 29% (5/17) of the VD patients, but in 73% (24/33) and 76% (16/21) of the AD patients. The differences in the perfusion patterns between the VD and AD patients were statistically significant (P<0.01, Fischer's exact test). Of the VD patients with hypoperfusion (bilateral temporal and/or parietal), 4/6 (67%, visual evaluation) and 4/7 (57%, quantitative evaluation) had a decreased vascular reserve capacity as determined with the acetazolamide test. In the AD group of patients the corresponding results were 3/23 (13%) and 4/15 (27%). It is concluded that the acetazolamide test is promising in rCBF SPET to differentiate VD from AD.

Acetazolamide↗

PubMed1987

A randomized trial of dexamethasone and acetazolamide for acute mountain sickness prophylaxis.

Forty-seven climbers participated in a double-blind, randomized trial comparing acetazolamide 250 mg, dexamethasone 4 mg, and placebo every eight hours as prophylaxis for acute mountain sickness during rapid, active ascent of Mount Rainier (elevation 4,392 m). Forty-two subjects (89.4 percent) achieved the summit in an average of 34.5 hours after leaving sea level. At the summit or high point attained above base camp, the group taking dexamethasone reported less headache, tiredness, dizziness, nausea, clumsiness, and a greater sense of feeling refreshed (p less than or equal to 0.05). In addition, they reported fewer problems of runny nose and feeling cold, symptoms unrelated to acute mountain sickness. The acetazolamide group differed significantly (p less than or equal to 0.05) from other groups at low elevations (1,300 to 1,600 m), in that they experienced more feelings of nausea and tiredness, and they were less refreshed. These drug side effects probably obscured the previously established prophylactic effects of acetazolamide for acute mountain sickness. Separate analysis of an acetazolamide subgroup that did not experience side effects at low elevations revealed a prophylactic effect of acetazolamide similar in magnitude to the dexamethasone effect but lacking the euphoric effects of dexamethasone. This study demonstrates that prophylaxis with dexamethasone can reduce the symptoms associated with acute mountain sickness during active ascent and that acetazolamide can cause side effects that may limit its effectiveness as prophylaxis against the disease.

Acetazolamide↗

PubMed1975

Acetazolamide, metabolic acidosis, and intraocular pressure.

In order to investigate whether or not there is a causal relationship between the metabolic acidosis and the ocular hypotension induced by acetazolamide, we undertook to correlate over a period of time the blood-acidifying and ocular-hypotonizing effects of administering the lowest intravenous effective dose of acetazolamide; to treat the metabolic acidosis induced by acetazolamide by means of the intravenous introduction of bases, and pulmonary hyperventilation (respiratory alkalosis); to evaluate the effects on the intraocular pressure (IOP) by neutralizing the acetazolamide-induced metabolic acidosis by means of a continuous infusion of sodium bicarbonate; to determine the relationship between the metabolic acidosis induced by blood-acidifying agents, which do not inhibit carbonic anhydrase, and the IOP; and to determine the changes in the acid-base status of the aqueous humor induced by acetazolamide and other blood-acidifying drugs. We found that the hypertonic buffering solution of sodium bicarbonate could reduce the IOP by itself through an osmotic mechanism. On the basis of our results, we believe that a causal relationship exists between the metabolic acidosis induced by acetazolamide, and by other drugs that have a blood-acidifying effect as the result of other mechanisms, and ocular hypotension, bothin the animal and in the glaucomatous patient.

Acetazolamide↗

PubMed1984

Local ocular hypotensive effect of topically applied acetazolamide.

Acetazolamide's usefulness in the treatment of the glaucomas is limited by the systemic side effects that often accompany its oral administration, and topical administration was initially thought to have no effect upon the intraocular pressures of human and rabbit eyes. Recent studies, however, have shown the usefulness of water-loading tests for screening drugs with potential antiglaucomatous activity. We found evidence that topical acetazolamide has the ability to lessen the increase in intraocular pressure after water-loading in pigmented rabbits and correlated this observation with low levels (0.0 to 0.7 microgram/ml) of plasma acetazolamide. Further, a separate study showed that 10% topical acetazolamide can enhance the ocular hypotensive effects of systemically administered acetazolamide in normal pigmented rabbits, suggesting that topically applied acetazolamide can have a local effect on intraocular pressure.

Acetazolamide↗

PubMed1988

Enhancement of the ocular hypotensive effect of acetazolamide by diflunisal.

We studied the effect of diflunisal on intraocular pressure in patients with glaucoma who were receiving maximally tolerated therapy. Diflunisal therapy, 500 mg twice daily, was started in 48 patients for one week. No changes were made in their regular antiglaucoma medications. Intraocular pressure was reduced an additional 3.8 +/- 3.1 mm Hg (+/- S.D.) in the acetazolamide-treated patients (P less than .0001) and 1.6 +/- 1.5 mm Hg in methazolamide-treated patients (P less than .02), while no significant reduction in intraocular pressure was found in patients receiving topical medications alone. In 15 acetazolamide-treated patients, total plasma concentrations of acetazolamide after diflunisal therapy were significantly higher than the prediflunisal levels, suggesting a modest decrease in renal excretion. In seven acetazolamide-treated patients, free plasma concentrations of acetazolamide were found to increase 5.6-fold after diflunisal therapy. We concluded that diflunisal potentiated the ocular hypotensive effect of acetazolamide by increasing its free plasma level.

Acetazolamide↗

PubMed1987

Gastric mucosal protection by acetazolamide derivatives: role of carbonic anhydrase and sulfhydryls.

Acetazolamide, a carbonic anhydrase inhibitor, prevents acute gastric hemorrhagic lesions induced by ethanol. We used acetazolamide and other carbonic anhydrase inhibitors to correlate their gastroprotective effects with the degree of inhibition of carbonic anhydrase. Since acetazolamide is a thiadiazole, we also investigated structurally related thiadiazoles that contain sulfhydryls to test the hypothesis that the protection against ethanol-induced gastric erosions is related to the presence of sulfhydryls. Dose-response studies with acetazolamide revealed that the protection did not correlate with the inhibition of carbonic anhydrase in the rat gastric mucosa. The carbonic anhydrase inhibitors sulfanilamide and ethoxzolamide, did not offer protection. Bismuthiol I, a thiadiazole with two sulfhydryls, was twice as protective as 2-amino-5-mercapto-1,3,4-thiadiazole with only one sulfhydryl group. We conclude that the protection by acetazolamide against ethanol-induced lesions is not related to the inhibition of carbonic anhydrase in the gastric mucosa. The gastroprotective effect of acetazolamide and its derivatives may be related to their content of sulfhydryls in an oxidized or reduced state.

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PubMed1992

Effects of intravenous acetazolamide on retinal pH in the cat.

Double-barreled H(+)-selective microelectrodes were used to study the effect on intravenous acetazolamide on intraretinal pH in the cat. Acetazolamide (11.4-27.8 mg kg-1 intravenously) caused a rapid acidification of the subretinal space. This change in pH originated in the most distal portion of the subretinal space and could not be attributed to a change in pH or PCO2 of the arterial blood. Slow light-evoked alkalinizations in distal retina, attributable to a decrease in rod photoreceptor energy metabolism, were relatively unaltered by acetazolamide. This result indicated that acetazolamide had not crossed the blood-retinal barrier in sufficient amounts to change this response. In time, following intravenous perfusion of acetazolamide, continuous depth profiles of intraretinal pH showed an acidification of the entire retina and the vitreous also became more acidic. These results indicate that the rapid or primary effect of acetazolamide is an acidification of the distal portion of the subretinal space, which is thought to originate in a change in the transport of H+ or HCO3- by the retinal pigment epithelium. This is followed by an acidification of the entire retina and vitreous, presumably due to diffusion of acid from the distal retina, although there could be additional causes.

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PubMed1995

Correlation of cerebral blood flow and MCA flow velocity measured in healthy volunteers during acetazolamide and CO2 stimulation.

The assessment of the cerebrovascular reserve capacity (RC) has become a widely used tool in the management of cerebrovascular disease. Discrepancies become obvious, however, if results obtained with different methods are compared. Aim of the present study, therefore, was to compare blood velocity and cerebral perfusion data in the same group of healthy test persons. In 32 volunteers regional cerebral blood flow (rCBF) was measured with the 133Xe-inhalation method. F1 as grey matter flow and the initial slope index (ISI) were computed. Simultaneously flow velocity in the middle cerebral artery (VMCA) was assessed by transcranial Doppler sonography (TCD). Measurements were performed in the resting state, during inhalation of 7% CO2 and after 1 g acetazolamide. Baseline VMCA was 62.38 +/- 16.1 cm/s, 90.84 +/- 23.85 cm/s during hypercapnia and 84.91 +/- 24.54 cm/s after acetazolamide. There was no significant change of baseline or stimulated values with age. F1 rose from baseline 76.25 +/- 12.48 ml/100 g/min to 103.90 +/- 14.6 ml/100 g/min in hypercapnia and to 98.4 +/- 14.9 ml/100 g/min after acetazolamide. The baseline F1 values and the response to CO2 decreased with age (p = 0.01) whereas for the acetazolamide reaction an age dependency could not be proven. ISI baseline values (41.5 +/- 6.1 ml/100 g/min) as well as those found after CO2 or acetazolamide decreased significantly with age. In hypercapnia changes of F1 and ISI were not too well related with changes of VMCA (F1: r = 0.599; ISI: r = 0.473), but better during acetazolamide exposure (F1: r4 = 0.715; ISI: r = 0.522). The age dependency of resting and stimulated values has to be considered when assessing the reserve capacity. There is a correlation between changes of the perfusion and flow parameters in healthy individuals which, however, may be worse in cerebrovascular disease.

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PubMed1994

The effects of acetazolamide in albino rabbits, pigmented rabbits, and humans.

In three separate experiments albino rabbits, pigmented rabbits, and humans were tested following administration of acetazolamide and without acetazolamide. In all three experiments, we recorded electroretinograms (ERGs) under dark adapted and light adapted conditions and measured the b-wave amplitudes. Dark adapted ERG b-wave amplitudes were increased following administration of acetazolamide as compared to control conditions, in albino rabbits, pigmented rabbits and humans. Light adapted b-wave amplitudes showed no statistically significant changes as a function of acetazolamide administration although in all three experiments there was a trend toward light adapted b-wave amplitude reduction following administration of acetazolamide. In the human experiments, ERG a-wave amplitudes were also measured. Light adapted a-wave amplitudes were reduced following administration of acetazolamide. In the human experiments, several behavioral tests were performed, including L'Anthony desaturated D-15, Farnsworth-Munsell 100 hue, Cogan-Gunkel chromatograph, Nagel anomaloscope, Goldmann-Weekers dark adaptometry. There were no consistent changes in the human dark adaptation thresholds or color discrimination, although several measures approached significance.

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PubMed2005

The use of acetazolamide in idiopathic intracranial hypertension during pregnancy.

PURPOSE: To describe the pregnancy outcomes after the use of acetazolamide in pregnant patients with idiopathic intracranial hypertension (IIH). DESIGN: Observational case series. METHODS: setting: Two tertiary care academic neuro-ophthalmology units. patient population: Patients with IIH treated with acetazolamide. observation procedure: Documentation of pregnancy outcome. main outcome measures: Normal pregnancy, fetal loss, or congenital malformation. RESULTS: Twelve patients were treated with acetazolamide for IIH during pregnancy, and there were no adverse pregnancy outcomes. A critical review of the English language literature on the subject failed to demonstrate any convincing evidence for any adverse effect on pregnancy for acetazolamide. CONCLUSIONS: Acetazolamide at high doses may produce birth defects in animals, but there is little clinical or experimental evidence to support any adverse effect of the drug on pregnancy outcomes in humans. If the clinical situation warrants the use of acetazolamide in IIH, then the drug probably can be offered after appropriate informed consent.

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PubMed2004

The cerebrovascular dilatation effects of olprinone, a phosphodiesterase III inhibitor, in comparison with acetazolamide--a pilot study.

To examine the effects of olprinone, a phosphodiesterase III inhibitor, on cerebral blood flow (CBF), we compared the effects of olprinone on CBF to that of acetazolamide. Using technetium-99m-ethyl cysteinate dimer (99mTc-ECD) brain SPECT, we measured regional CBF (rCBF) at 33 sites, including 16 right and left pairs of non-infarct cerebral cortexes, in seven stroke patients (66.0+/-3.2 years) in a resting state and 15 min after the administration of acetazolamide. Within 1 week, rCBF at each site was measured 15 min after the initiation of olprinone infusion. Resting rCBF showed a significant negative correlation with the change in rCBF (DeltaCBF) during olprinone infusion (r = -0.43, P=0.013), but no significant correlation was seen following acetazolamide administration. The difference in rCBF between the right and left cortex increased more following acetazolamide administration (14.1+/-10.9 ml/(min 100 g)) than during olprinone infusion (5.4+/-4.8 ml/(min 100 g), P=0.013). The rCBF at four regions of interest (ROI) with low-resting CBF (< 49 ml/(min 100 g)) further decreased following the administration of acetazolamide. The vasodilatory effects of olprinone are dependent on resting CBF instead of on the intracerebral steal phenomenon that occurs with acetazolamide.

Acetazolamide↗

PubMed2000

Acetazolamide reduces hypoxic pulmonary vasoconstriction in isolated perfused rabbit lungs.

Carbonic anhydrase (CA) may modulate regional blood flow by mediating changes in extra- and intracellular pH. We hypothesized that CA inhibition with acetazolamide would inhibit the kinetics and magnitude of hypoxic pulmonary vasoconstriction (HPV). Isolated rabbit lungs were ventilated and perfused in situ at constant flow, with buffer containing red blood cells. Preparations were sequentially challenged with hypoxic (FI(O(2)) 0.05) and/or hypercapnic (FI(CO(2)) 0.10) gas mixtures for 5 or 10 min. In the experimental groups, acetazolamide (33 microM) was added to the perfusate after establishing baseline responses, and gas challenges were repeated; control groups were studied without acetazolamide. Acetazolamide reduced the increase in pulmonary artery pressure (DeltaPAP) and the rate of pressure rise by approximately 30-50% during hypoxia and combined hypoxia/hypercapnia. The reduction in DeltaPAP occurred for both 5 and 10 min challenges. Acetazolamide did not affect expired nitric oxide concentrations. We conclude that acetazolamide reduces both the magnitude and kinetics of HPV by a mechanism that does not involve nitric oxide.

Acetazolamide↗

PubMedDate not supplied

Exacerbation of acetazolamide teratogenesis by amiloride and its analogs active against Na+/H+ exchangers and Na+ channels.

Postaxial forelimb ectrodactyly induced by acetazolamide given on Day 9.5 of murine gestation is thought to be mediated by reduced intracellular pH (pHi) within the limb bud. Coadministration of amiloride increases the incidence and severity of acetazolamide-induced forelimb malformations and further reduces limb bud pHi. These findings were hypothesized to be attributable to the action of amiloride as an inhibitor of Na+/H+ exchangers (NHEs), plasma membrane-localized proteins involved in the maintenance of cellular pH homeostasis. Here, we explored this hypothesis further by coadministering with acetazolamide, amiloride, or analogs known to preferentially inhibit NHEs 5-(N-methyl-N-isobutyl)-amiloride, 5-(N, N-hexamethylene)-amiloride, 5-(N, N-dimethyl)-amiloride, and 5-(N-ethyl-N-isopropyl)-amiloride or amiloride-sensitive Na+ channels (benzamil). The coadministration of either amiloride, benzamil, 5-(N, N-dimethyl)-amiloride, 5-(N-ethyl-N-isopropyl)-amiloride, or 5-(N-methyl-N-isobutyl)-amiloride all dose responsively increased the frequency and severity of forelimb malformations compared to acetazolamide alone. None of the analogs given alone induced forelimb ectrodactyly. The data are consistent with the original hypothesis that the exacerbation of acetazolamide teratogenesis is due to NHE inhibition. Surprisingly, benzamil was the most potent potentiator of acetazolamide teratogenesis. This result strongly suggests that amiloride-sensitive Na+ channels are also present within the murine embryo and are likely to play a role in pHi homeostasis.

Abnormalities, Drug-Induced↗

PubMed2003

Evaluation of the effect of acetazolamide on cystoid macular oedema in patients with Behcet's disease.

AIM: To study the effect of acetazolamide on cystoid macular oedema (CMO) in patients with Behcet's disease. PATIENTS AND METHODS: A total of 67 eyes of 35 Behcet's patients with chronic, but well-controlled uveitis, and CMO were randomised into a double-masked, crossover trial comparing the effect of acetazolamide vs placebo. The patients received an initial 4-week course of either 250 mg acetazolamide twice daily (b.i.d.) or placebo, followed by a 4-week washout period. They then received a 4-week course of the reverse study medication. An improvement in visual acuity and fundus fluorescein angiographic findings was assessed. RESULTS: In total, 29 patients (55 eyes) completed the trial and were available for analysis. Of the 29, 16 men and 13 were women. The age range was 13-50 years (mean 33.6 years). Patients on acetazolamide showed a slightly better improvement of angiographic signs (at least by one grade improvement) over that of placebo (12 vs five eyes). They also had less deterioration of angiographic signs over that of placebo (three vs seven eyes). However, these findings were not statistically significant (P=0.99). Acetazolamide had no statistically significant effect (P=0.53) on the improvement of visual acuity of patients over that of placebo (13 vs eight eyes), nor on the deterioration of visual acuity (three vs 11 eyes). CONCLUSION: Despite seemingly favourable results, the 4-week course of acetazolamide (250 mg b.i.d.) has no statistically significant effect on the improvement of the visual acuity and the fluorescein angiographic findings in Behcet's patients with CMO.

Acetazolamide↗

PubMed1991

Feedback-mediated reduction in glomerular filtration during acetazolamide infusion in insulin-dependent diabetic patients.

1. A sustained high glomerular filtration rate in diabetes mellitus is associated with increased proximal reabsorption, suggesting alterations in the tubuloglomerular feedback system. To test this hypothesis, renal function was studied in eight control subjects and 14 recent-onset euglycaemic insulin-dependent diabetic patients before and after infusion of the carbonic anhydrase inhibitor, acetazolamide (5 mg/kg body weight). 2. Acetazolamide induced a dramatic fall in glomerular filtration rate in both diabetic patients and control subjects (from 138 +/- 5 to 114 +/- 4 and from 127 +/- 3 to 113 +/- 2 ml min-1 1.73 m-2, respectively, P less than 0.0001). This fall in glomerular filtration rate was strongly correlated with the acetazolamide-induced decrease in absolute proximal reabsorption calculated by using lithium clearance. 3. To further assess the potential role of angiotensin II in the acetazolamide-induced tubulo-glomerular feedback response, 11 additional diabetic patients were investigated before and after the administration of acetazolamide plus the angiotensin-converting enzyme inhibitor, enalaprilat (1.25 mg intravenously). Despite the effective blockade of angiotensin II formation and a slight decrease in renal vascular resistance, the glomerular filtration rate fell significantly and by a similar magnitude as seen with acetazolamide alone. 4. These results indirectly suggest that there is an altered basal tubulo-glomerular feedback system in diabetic patients but a normal response to the increase in distal delivery. No convincing role for an angiotensin II-mediated effect on the afferent limb of the tubuloglomerular feedback response could be demonstrated.

Acetazolamide↗

PubMed2004

Effect of acetazolamide on the optic disc oxygenation in miniature pigs.

BACKGROUND: The purpose of our study was to evaluate the variations of the optic disc PO (2) during normoxia and hyperoxia (100 % O (2)), before and after intravenous administration of acetazolamide. MATERIAL AND METHODS: PO (2) measurements were obtained at intervascular areas of the optic disc in 11 anaesthetized miniature pigs using oxygen-sensitive microelectrodes introduced through the vitreous cavity by a micromanipulator. PO (2) was measured continuously during 10 minutes under systemic normoxia and systemic hyperoxia. Oxygen measurements were repeated under these conditions after intravenous injection of acetazolamide (bolus of 500 mg) in 8 animals. RESULTS: In systemic hyperoxia, the optic disc PO (2) increased moderately (DeltaPO (2) = 4.7 +/- 2.5 mmHg; p < 0.001; n = 11) in parallel with systemic PaO (2). Acetazolamide led to a slow and progressive increase in the optic disc PO (2) (DeltaPO (2) = 2.1 +/- 1.7 mmHg; p > 0.1; n = 8 after 10 min, while DeltaPO (2) = 4.3 +/- 3.2 mmHg; p < 0.05; n = 8 after 30 min), in parallel with a slow and progressive increase in systemic PaCO (2). The optic disc PO (2) increased much more significantly after injection of acetazolamide under systemic hyperoxia (DeltaPO (2) = 13.3 +/- 3.1 mmHg; p < 0.001; n = 8). CONCLUSIONS: Systemic hyperoxia alone is not sufficient to increase substantially the optic disc PO (2) in miniature pigs due to a vasoconstrictor effect. Intravenous injection of acetazolamide can increase the optic disc PO (2) progressively, due to a vasodilatory effect of elevated systemic PaCO (2). The association of acetazolamide injection with systemic hyperoxia can further improve the oxygenation of the optic disc.

Acetazolamide↗

PubMed1997

Comparison of vasodilatory effect of carbon dioxide inhalation and intravenous acetazolamide on brain vasculature using positron emission tomography.

Carbon dioxide (CO2) and acetazolamide are increasingly being used as vasodilators to detect cerebrovascular reserve capacity in patients of chronic cerebrovascular disease. The functional cerebrovascular reserve or ability of cerebral vessels to lower their resistance in response to decrease in cerebral perfusion pressure is expressed as change in cerebral blood flow from baseline under a vasodilatory stimuli. Theoretically a vasodilator causing maximum vasodilation, and thereby expressing complete reserve capacity would be more suitable for such a purpose. We quantitatively compared the vasodilating effect of 5% CO2 inhalation and 1 g of intravenous acetazolamide by positron emission tomography. Cerebrovascular reserve was quantified in six patients with chronic cerebrovascular disease in the same sitting, using oxygen-15 labeled water (H2(15)O) positron emission tomography at rest, during 5% CO2 inhalation and after 1 g intravenous acetazolamide. A significant linear correlation in both nonlesion hemisphere (r = 0.701, p < 0.001) and in lesion hemisphere (r = 0.626, p < 0.005) was found between CO2 and acetazolamide for cerebrovascular reserve capacity. This correlation improved by considering cerebrovascular reserve per unit change in arterial carbon dioxide (r = 0.744, p < 0.001 in nonlesion hemisphere and r = 0.721, p < 0.001 in lesion hemisphere). The quantitative value of global reserve capacity was different by CO2 stimuli (5.2%) and acetazolamide (49.7%). Though a similar vasodilatory response is elicited by both vasodilators, acetazolamide seems to be more potent and therefore should be preferred to detect patients with exhausted cerebrovascular reserve capacity.

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PubMed1986

Dissociation of renal and respiratory effects of acetazolamide in the critically ill.

The effects of acetazolamide on renal and erythrocyte carbonic anhydrase were studied in 12 critically ill patients. In the first part of the investigation (n = 6) we examined the renal effects of increasing doses of acetazolamide. The maximal renal excretion of water and bicarbonate was achieved with acetazolamide 2.5-5 mg kg-1 i.v. In the second part (n = 6), the associated respiratory effects of the effective renal dose of acetazolamide 5 mg kg-1 were evaluated. We found a statistically significant 4% decrease in pulmonary carbon dioxide excretion in the 10-min sampling period immediately following the administration of acetazolamide, but thereafter carbon dioxide elimination proceeded at a normal rate. The observed carbon dioxide retention is clinically unimportant, and we recommend acetazolamide as an effective means of eliminating surplus water and bicarbonate in the critically ill.

Acetazolamide↗