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PubMed1962

Enhancement of cesium-137 excretion by rats treated with acetazolamide.

Acetazolamide (10 mg/kg, intraperitoneally) increases the urinary excretion of cesium-137 in the rat. Meralluride (6.8 mg of Hg per kilogram, subcutaneously) blocks the effect of acetazolamide on the cesium-137 excretion without any influence on the urine volume and pH of the urine. This indicates that acetazolamide increases the urinary excretion of cesium-137 by increasing its secretion through the renal tubule in the same manner as it increases the excretion of potassium and rubidium-86.

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PubMed1994

Reduction of macular oedema by acetazolamide in patients with chronic iridocyclitis: a randomised prospective crossover study.

Thirty patients with cystoid macular oedema secondary to chronic iridocyclitis were enrolled in a two period, prospective, randomised, double masked, crossover study that compared sustained release acetazolamide (500 mg twice a day) with a placebo to measure the effects on the reduction of cystoid macular oedema and improvement of visual acuity. All patients were treated for 1 month with either acetazolamide or placebo, received no treatment for 1 month, and were then treated for 1 month with the other medication. Statistically significant improvement in visual acuity was seen at 14 and 28 days in the treated patients. No improvement was seen when patients received placebo. Improved visual acuity was not associated with race or sex. However, younger patients (under age 55 years) were more likely to benefit from treatment. Results of vitreous fluorophotometry, obtained at baseline and 4 weeks, demonstrated an improvement in posterior vitreous penetration ratios and mid vitreous penetration ratios after treatment with acetazolamide but not with placebo.

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PubMed1987

The effect of acetazolamide on breath holding at high altitude.

The effect of altitude and acetazolamide on breath holding was studied in 20 individuals. Breath holding time was reduced progressively during ascent. There was an additional reduction in the acetazolamide group at low but not at high altitude. The initial difference between the two groups may have been related to a lower CSF pH when on acetazolamide. At high altitude the finding of similar breath holding times in the two groups may have been due to acclimatization in the placebo group.

Acetazolamide↗
PubMed1982

Effect of acetazolamide and furosemide on the production and composition of cerebrospinal fluid from the cat choroid plexus.

The effect of acetazolamide and furosemide on choroid plexus (CP) production and electrolyte composition of cerebrospinal fluid (CSF) from the cat CP in situ was investigated. Both drugs decreased CSF production by the CP by 50--90% from a control rate of 0.53 microL . min-1 . mg-1 CP within 1.5--2.5 h after the start of drug treatment. The results were similar whether the drug was administered intravenously or applied directly to the CSF side of the CP. A number of experiments in which the effect of administering drugs via the chamber were studied were continued with the drugs removed by washing the preparation with drug-free artificial CSF and the responses measured. The results demonstrated that the effects of acetazolamide and furosemide were reversed during the 1st h following the washout. Both drugs decreased K concentration of nascent CSF when administered intravenously and furosemide also did so when administered on the CSF side of the CP. It is concluded from these and previous data that acetazolamide and furosemide markedly inhibit the transport mechanism(s) in the cat CP that are responsible for CP secretion which represents about 40--60% of the total CSF production and that K transport is also affected.

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PubMed1996

Cerebrovascular reserve capacity in patients with occlusive cerebrovascular disease: assessment with dynamic susceptibility contrast-enhanced MR imaging and the acetazolamide stimulation test.

PURPOSE: To quantitatively assess cerebrovascular reserve capacity in patients with occlusive cerebrovascular disease. MATERIALS AND METHODS: In 21 symptomatic patients with occlusive cerebrovascular disease, magnetic resonance (MR) imaging was performed with a 1.5-T system. Before, during, and after a brief bolus injection of gadopentetate dimeglumine into the antecubital vain, a series of 32 rapid T2*-weighted gradient-echo images of two different sections were acquired simultaneously to measure the concentration-time-curves in the brain tissue and in the brain-feeding arteries. Principles of indicator dilution analysis were applied to compute regional cerebral blood flow (rCBF) and volume. Each patient underwent two examinations, the first before and the second after acetazolamide stimulation. RESULTS: In the asymptomatic hemisphere, a mean increase in rCBF value of 47.1% was observed after acetazolamide stimulation. In the affected areas of the symptomatic hemisphere, a statistically significantly reduced response to acetazolamide stimulation was found, indicating a severely compromised cerebrovascular reserve capacity. CONCLUSION: MR imaging with the described techniques provides quantitative information about the cerebrovascular reserve capacity in patients with occlusive cerebrovascular disease.

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PubMed1976

Additive inhibition of renal bicarbonate reabsorption by maleate plus acetazolamide.

The effects of two potent inhibitors of renal bicarbonate reabsorption--maleate and acetazolamide--were investigated in the rat using clearance techniques. Acetazolamide given in high dose (50 mg/kg body wt) inhibited fractional bicarbonate reabsorption by ca. 30%, maleate (2.58 nmol/kg body wt) by 25%, and maleate plus acetazolamide by 54-72%. GFR was depressed, and urine volume was increased by both drugs in an additive manner. Maleate was equally effective as inhibitor of HCO3- reabsorption in the presence and absence of carbonic anhydrase activity. It is suggested that the site of action of both drugs is predominantly proximal, but they act on different steps in the transcellular HCO3- transport. A hypothetical mechanism of maleate action is presented, which takes into account the changes in passive HCO3- flux through the basolateral membrane.

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PubMed1978

Acetazolamide and renal ammoniagenesis.

The effect of acetazolamide on ammonia-producing enzyme systems was determined in vitro at concentrations comparable to those which have been shown to abolish ammonium excretion in vivo. No change in the activity of glutaminase or gamma-glutamyl transpeptidase could be observed at concentrations up to 0.2 mM acetazolamide, and concentrations up to 1 mM were without effect on D-glutamyltransferase activity. Therefore, the effect of acetazolamide to abolish ammonium excretion cannot be explained by an action of the drug to inhibit ammoniagenesis.

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PubMed1982

Bicarbonate reabsorption in the papillary collecting duct: effect of acetazolamide.

The present study was designed to characterize bicarbonate (total CO2) reabsorption in the papillary collecting duct of the kidney of the Munich-Wistar rat when total CO2 delivery to this segment was increased by the systemic infusion of a bicarbonate-rich solution. Additional studies examined the effect of the systemic administration of acetazolamide, a carbonic anhydrase inhibitor, on total CO2 reabsorption. Employing free-flow micropuncture techniques, tubular fluid samples were obtained from the base and tip of the exposed papilla and subsequently analyzed for total CO2 and inulin. Total CO2 reabsorption increased in a linear fashion, approximating 34% of that delivered to the base, as total CO2 delivery increased from 3 to 20% of the filtered load. When examined at comparable absolute rates of total CO2 delivery (mumol/min) to the papillary collecting duct, acetazolamide administration resulted in marked inhibition of total CO2 reabsorption. The results of these studies suggest that the papillary collecting duct of the rat kidney possesses a significant capacity for reabsorption of total CO2 and that this reabsorption is diminished by the administration of acetazolamide.

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PubMed1986

Cerebrospinal fluid ions in metabolic acidosis in dogs: effects of acetazolamide.

We hypothesized that, during isosmotic isonatremic HCl acidosis with maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide, by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS), should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood and CSF ions and acid-base variables were measured in two groups of anesthetized and paralyzed dogs with bilateral ligation of renal pedicles during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical ventilation was regulated such that arterial PCO2 dropped and CSF Pco2 remained relatively constant. In group I (control group, n = 6), CSF [Na+] remained unchanged, [HCO3-] and strong ions difference (SID) fell, respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+] remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively, and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic acidosis in CSF, which is more severe than that observed in controls.

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PubMed1995

Acetazolamide slows VA/Q matching after changes in regional blood flow.

Inhibition of carbonic anhydrase (CA) by acetazolamide increases ventilation-perfusion (VA/Q) heterogeneity (E. R. Swenson, H. T. Robertson, and M. P. Hlastala. J. Clin. Invest. 92: 702-709, 1993), possibly because of slowing of CO2/H(+)-dependent mechanisms of VA/Q matching with temporal fluctuations of regional ventilation and perfusion. To study this concept, we imposed abrupt changes in regional perfusion by lobar or left main pulmonary artery occlusions (PAOs) in anesthetized mechanically ventilated dogs before and after CA inhibition (20 mg/kg iv acetazolamide). The rate of ventilation redistribution and change in VA/Q distributions with changes in perfusion were measured by planar gamma imaging of the lungs during continuous inhalation of 81mKr gas ventilation scanning and the multiple inert-gas elimination technique. PAO for 5 min caused regional Kr activity to fall by 30 +/- 5% (SD) with a half time (t1/2) of 75 +/- 10 s. With release of the occlusion, counts returned to baseline with t1/2 of 79 +/- 12 s. Acetazolamide increased these respective t1/2 values (161 +/- 16 and 180 +/- 17 s). Consistent with these kinetics, VA/Q mismatch was greater with lobar PAO at 2 min but not at 10 min with CA inhibition compared with that caused by lobar PAO alone. Cyclical lobar PAO and release (10 cycles of 1-min occlusion and 1-min release) caused more VA/Q heterogeneity during CA inhibition. The arterial-to-alveolar inert-gas area difference rose minimally from 0.18 to 0.23 (P < 0.05) with cyclical PAO and from 0.24 to 0.48 (P < 0.01) after CA inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1989

The possible role of metabolic acidosis in acetazolamide-induced gastric lesion formation in rats.

The effects of acetazolamide on blood acid/base balance and the relationship of the latter to gastric lesion formation were studied in rats. Acetazolamide (200 mg/kg, s.c.) produced haemorrhagic gastric lesions which were accompanied by lowered arterial blood pH and HCO3- levels. High dose (6.2%) of NaHCO3 infusion normalised the arterial blood pH and decreased lesion formation. It also markedly raised the blood HCO3- level. However, a lower dose (3.1%) of the drug only raised the HCO3- to a normal level and slightly reduced the severity of ulceration. These results suggest that metabolic acidosis is the main causative factor while depletion of blood HCO3- may play a minor role in acetazolamide-evoked lesion formation in rat stomachs.

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PubMed1989

Effect of acetazolamide (Diamox) on the endolymphatic sac.

The effect of acetazolamide on the ultrastructures of the murine endolymphatic sac was investigated. The animals were given a single intravenous dose of acetazolamide (100 mg/b.w.) and were sacrificed 0, 15, 30, 60 and 120 min after the injection, respectively. Prominent changes in the fine structure of the epithelial cells could be observed after 30 min. These alterations were even more pronounced after 1 h. After 2 h, the normal cell structure became to be reestablished. The most conspicuous change was a general reduction in the electron density of the dark cells. This was accompanied with a decreased number of cell organelles, especially ribosomes. Some light cells also underwent temporal modifications in their structure in the form of a reduced nuclear stainability associated with a loss of pinocytotic vesicles near the apical plasmalemma. In general, the dark cells seemed to be more influenced by acetazolamide than the light cells. The possibility that the dark cell changes are related to a modification of transepithelial ion and water flow is discussed.

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PubMed1990

Acetazolamide effect on cerebellar blood flow in crossed cerebral-cerebellar diaschisis.

We studied the effect of acetazolamide on cerebellar blood flow in 11 stroke patients with large, unilateral cerebral hemispheric infarcts and no evidence of cerebellar infarction, but with cerebrocerebellar diaschisis of cerebral blood flow. Blood flow was determined with xenon-133 inhalation and dynamic single-photon emission computed tomography at rest and 20 minutes after the intravenous injection of 1.0 g acetazolamide. After acetazolamide, the mean +/- SD increases in blood flow in the affected and contralateral cerebellar hemispheres were 11.1 +/- 3.7 and 12.0 +/- 5.3 ml/100 g/min, respectively; the difference between hemispheres was not significant. The absolute increase in cerebellar flow in these 11 patients was of the same magnitude as that in 12 healthy controls. We conclude that cerebellar vasoreactivity is intact in stroke patients with crossed cerebrocerebellar diaschisis of cerebral blood flow. Our results lend further support to the concept that reduced cerebellar blood flow is secondary to functional deactivation. Our patients were studied 2 weeks to 5 years after their stroke, indicating that this phenomenon may be persistent.

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PubMed1990

A simple test to assess cerebrovascular reserve capacity using transcranial Doppler sonography and acetazolamide.

The goal of this study was the development of a simple bedside test to assess cerebrovascular reserve capacity using transcranial Doppler sonography. We studied 33 normal persons at rest and after stimulation of cerebral blood flow with 1 g acetazolamide. Their mean +/- SD increase in blood flow velocity in 54 middle cerebral arteries 10 minutes after stimulation was 24.4 +/- 9.2 cm/sec. We tried to validate the increase in blood flow velocity as cerebrovascular reserve capacity in 21 patients with obstructive carotid artery disease and symptoms of cerebral ischemia. The patients were studied using transcranial Doppler sonography and xenon-133 dynamic single-photon emission computed tomography after acetazolamide stimulation. Their increases in blood flow velocity (delta FV) and increases in cerebral blood flow (delta CBF) correlated significantly in both hemispheres (asymptomatic: Y = 0.32X + 10.65, r = 0.45, p = 0.04; symptomatic: Y = 0.36X + 2.28, r = 0.59, p = 0.004). There was no significant difference between the slopes of the regression lines. Blood flow velocity and cerebral blood flow at rest were not correlated. The increase in blood flow velocity after acetazolamide stimulation offers a simple and reliable method for assessing cerebrovascular reserve capacity.

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PubMed1992

99mTc-HMPAO-SPECT with acetazolamide challenge to detect hemodynamic compromise in occlusive cerebrovascular disease.

BACKGROUND AND PURPOSE: Insufficiency of collateral supply may lead to low-flow infarcts in severe occlusive cerebrovascular disease. The aim of this study was to evaluate the feasibility of technetium-99m-labeled hexamethylpropyleneamine oxime (99mTc-HMPAO) single-photon emission computed tomography (SPECT) to assess hemodynamic compromise in the anterior circulation. METHODS: Cerebral blood flow before and after 1 g acetazolamide was analyzed by 99mTc-HMPAO-SPECT in 21 symptomatic patients with documented extracranial obstructions. SPECT findings were correlated with the results of angiography, transcranial Doppler sonography, and computed tomographic scan. RESULTS: The acetazolamide-induced increase of cerebral blood flow could be reliably monitored by increase of cerebral 99mTc-HMPAO uptake, which varied between 11.4% and 47.6% in the less-affected hemisphere. Increment of hemispheric side-to-side asymmetry of tracer uptake after drug challenge revealed significant restriction of regional vasoreactivity in 11 patients. Agreement in assessing hemodynamic compromise was reached in 81% of patients with ophthalmic artery collaterals on angiography (p < 0.001), in 76% with low-flow infarcts on computed tomographic scan (p < 0.01), and in 91% with markedly reduced flow velocities on transcranial Doppler (p < 0.0001). One patient developed a low-flow infarct in the area predicted by SPECT during follow up. CONCLUSIONS: We conclude that 99mTc-HMPAO-SPECT with acetazolamide challenge is a useful method for assessment of the adequacy of hemispheric collateral pathways in patients with severe occlusive cerebrovascular disease.

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PubMed2001

Long-term prognosis of medically treated patients with internal carotid or middle cerebral artery occlusion: can acetazolamide test predict it?

BACKGROUND AND PURPOSE: The importance of hemodynamic parameters for predicting outcome in patients with occlusive carotid disease remains controversial. The present study was aimed at testing the hypothesis that regional cerebrovascular reactivity (rCVR) to acetazolamide can be a reliable predictor of subsequent ischemic stroke in medically treated patients with internal carotid artery or middle cerebral artery occlusion. METHODS: Seventy-seven symptomatic patients were enrolled in this prospective, longitudinal cohort study. All patients met inclusion criteria of cerebral angiography, no or localized cerebral infarction on MRI or CT, and no or minimal neurological deficit. Regional cerebral blood flow (rCBF) and rCVR to acetazolamide were quantitatively determined by (133)Xe SEPCT. All patients were categorized into 4 types on the basis of SPECT studies. RESULTS: During an average follow-up period of 42.7 months, 16 total and 7 ipsilateral ischemic strokes occurred. The annual risks of total and ipsilateral stroke in patients with decreased rCBF and rCVR were 35.6% and 23.7%, respectively, risks that are higher than those in other types of patients. When strokes were categorized into patients with and without decreased rCBF and rCVR, Kaplan-Meier analysis revealed that the risks of total and ipsilateral stroke in patients with decreased rCBF and rCVR were significantly higher than in those without (P<0.0001 and P=0.0001, respectively, log-rank test). Relative risk conferred by decreased rCBF and rCVR was 8.0 (95% CI, 1.9 to 34.4) for ipsilateral stroke and 3.6 (95% CI, 1.4 to 9.3) for total stroke. CONCLUSIONS: Decreased rCBF and rCVR to acetazolamide may identify a subgroup of patients who have a higher risk of subsequent ischemic stroke when treated medically.

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PubMed2001

Low-dose acetazolamide does affect respiratory muscle function in spontaneously breathing anesthetized rabbits.

Patients with chronic obstructive pulmonary diseases (COPD) and/or central sleep apnea are sometimes treated with the carbonic anhydrase inhibitor acteazolamide to improve blood gas values. Studies have shown that this agent may have a complicated effect on lung ventilation, because carbonic anhydrase has a widespread distribution within the body, particularly in tissues involved in the control of breathing. To investigate whether acetazolamide may have (neuro)muscular effects on respiration, we measured the responses of ventilation, phrenic nerve activity, and transpulmonary pressure to changes in arterial PCO2 before and after intravenous administration of a low-dose (4.6 +/- 0.2 mg x kg(-1), mean +/- SEM) of this inhibitor in anesthetized spontaneously breathing rabbits. The agent decreased the mean resting end-tidal PCO2 by 1 kPa and increased ventilation from 258 +/- 15 to 292 +/- 14 ml x min(-1) x kg(-1) (p < or = 0.05). The ventilatory and tidal volume responses to CO2 were reduced, and the response curves were shifted to lower PCO2 values. At the level of phrenic activity, however, the response was shifted leftward without altering CO2 sensitivity. With an unchanged lung compliance, the slopes of the relationships between tidal volume and phrenic activity and that between the tidal change in transpulmonary pressure and phrenic amplitude were both reduced by about 40%, indicating an action of acetazolamide on (neuro)muscular level. The results raise the suggestion that treatment of some hypercapnic COPD patients with acetazolamide may have undesired clinical implications, particularly in those with already weakened respiratory muscles.

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PubMed1978

The effect of acetazolamide on cerebral blood flow and oxygen utilization in the rhesus monkey.

The brain is critically dependent for its moment to moment function and survival on an adequate supply of oxygen. The enzyme carbonic anhydrase (EC 4.2.1.1) may play an important role in oxygen delivery to brain tissue by facilitating the hydration of metabolically produced carbon dioxide in erythrocytes in brain capillaries, thus permitting the Bohr effect to occur. We examined the effect of 30 mg/kg i.v. acetazolamide, a potent inhibitor of carbonic anhydrase, upon cerebral blood flow and oxygen consumption in lightly anesthetized, passively ventilated rhesus monkeys. Cerebral blood flow and oxygen consumption were measured with oxygen-15-labeled water and oxygen-15-labeled oxyhemoglobin, respectively, injected into the internal carotid artery and monitored externally. Acetazolamide produced an immediate and significant increase in cerebral blood flow (from a mean of 64.7 to 83.8 ml/100 g per min), an increase in arterial carbon dioxide tension (from a mean of 40.7 to 47.5 torr), and a decrease in cerebral oxygen consumption (from a mean of 4.16 to 2.82 ml/100 g per min). Because the change in cerebral oxygen consumption occurred within minutes of the administration of acetazolamide, we believe that this effect probably was not due to a direct action on brain cells but was achieved by an interference with oxygen unloading in brain capillaries. A resultant tissue hypoxia might well explain part of the observed increase in cerebral blood flow.

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