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PubMed1986

Correction of metabolic alkalosis by HCl and acetazolamide: effects on extracellular and intracellular acid-base status in rats in vivo.

Extracellular plasma pH (pHe) of nephrectomized male or female Sprague-Dawley rats was changed by infusion of either sodium bicarbonate or HCl to predetermined values in the pH range of 7.53-7.14, and then held constant for 2 h. Intracellular pH (pHi) of the liver, heart, brain, and two skeletal muscle groups as calculated from the distribution of 14C-labelled DMO (5.5-dimethyl-2,4-oxazolidinedione) was compared to corresponding tissues of a control group and rats treated with the carbonic anhydrase inhibitor acetazolamide (Diamox). When compared to control, changes of the extracellular pH in male or female rats were followed by similar effects on pHi in the investigated tissues. At the same extracellular pH there were no statistical differences between pHi values of HCl or acetazolamide treated rats, though the arterial PCO2 following acetazolamide administration was significantly increased when compared to control or the corresponding HCl group. This study shows that administration of acetazolamide or HCl results in a dose-dependent decrease of plasma and tissue pH, and that both agents may be used as a logical and safe therapy during severe metabolic alkalosis in rats.

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PubMed1989

Inhibitory effect of ouabain and acetazolamide on secretin-stimulated pancreatic exocrine secretion in anaesthetized dog.

1. The effects of ouabain and acetazolamide on the secretion of pancreatic juice stimulated by secretin in anaesthetized dogs were investigated. 2. Intra-arterial injection of ouabain (1-10 micrograms) and acetazolamide (1-10 mg) caused dose-dependent decreases in the volume of pancreatic juice. When both drugs were added together, the inhibitory effects were significantly higher than for each drug alone. 3. The bicarbonate concentration in the pancreatic juice was decreased and the chloride concentration was increased by ouabain and acetazolamide, but sodium and protein concentrations were not modified. 4. The results suggest that the Na+,K+-ATPase and carbonic anhydrase activities play important roles in water and electrolyte secretion, and that ouabain and acetazolamide inhibit secretin-stimulated pancreatic secretion by acting on different systems in the exocrine cells in dogs.

Acetazolamide↗
PubMedDate not supplied

Induction of new carbonic anhydrase II following treatment with acetazolamide in DBA and C57 mice.

The mechanism by which animals develop tolerance to the antiepileptic effects of the carbonic anhydrase (CA) inhibitor, acetazolamide, was explored using a quantitative immunocytochemical method. Cerebral cortex sections of DBA/2J mice susceptible to audiogenic seizures and of C57BL/6J nonsusceptible mice were stained with antibody to mouse CA II in controls and following treatment with acetazolamide (40 and 200 mg/kg) for 1, 3, and 5 days. The percentage increases in CA II fluorescent intensity of cells from C57 mice treated with 40 and 200 mg/kg acetazolamide over those of untreated mice were 22 and 36%, respectively, after 1 day, 32 and 40%, respectively, after 3 days, and 17 and 40%, respectively, after 5 days of treatment. The corresponding percentage increases in fluorescent intensity of cells from DBA mice over controls were 13 and 32%, respectively, after 1 day, 17 and 41%, respectively, after 3 days, and 26 and 58%, respectively, after 5 days of treatment. The fluorescent intensity of cells from untreated DBA mice was 35% greater than those of untreated C57 mice. In C57 mice the maximum amount of CA II per cell at each dose occurred 24 h after acetazolamide treatment, whereas the amount in DBA mice continued to increase with time and dose up to 5 days. The differences between the two strains can be explained by changes in distribution of CA II to subcellular locations or by defects in phosphorylation of the molecule.

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PubMed1992

Obstructive sleep apnea in Arnold-Chiari malformation treated with acetazolamide.

We studied respiratory patterns and transcutaneous gas pressures in two infants with Arnold-Chiari type II malformation referred to us due to repeated episodes of stridor and cyanosis. During both active and quiet sleep, respiration was irregular and absent or inverse thoracic breathing movements and frequent decreases in oxygen saturation to below 80% were observed. When breathing air with 2% CO2 or when given acetazolamide 10 mg/kg, chest wall movements normalized and oxygenation increased to near normal levels. After three months of treatment with acetazolamide 20 mg/kg/24 h no further episodes of hypoventilation or hypoxemia were observed and further treatment could be discontinued. We conclude that stimulation of respiration by CO2 or by acetazolamide appears to recruit chest wall muscles and promote upper airway patency in Arnold-Chiari malformation. A treatment trial with acetazolamide seems justifiable in these infants when respiratory problems are present.

Acetazolamide↗
PubMed1983

Acute effects of acetazolamide on cerebral blood flow in man.

We have followed the time course of the effect of the carbonic anhydrase inhibitor acetazolamide injected i.v. in unanesthetized healthy human beings. The dose administered was 500 mg as a bolus. Cerebral blood flow (CBF) was measured continuously before, during and after the injection, using a pulsed ultrasound doppler system, which measured the instantaneous mean velocity across the lumen of the internal carotid artery, just below its entrance into the skull. Ventilation, heart-rate, end-expiratory PCO2, arterial PCO2, pH and systemic blood pressure was also measured. We found that acetazolamide caused a rise in CBF which could be detected as early as 2 min after the injection. A maximal average response of 75% increase in CBF was seen after 25 min. The half-time of the declining phase of the response was 95 min. There were no systematic differences in the CO2 reactivities, given as delta CBF/delta PACO2 in % of CBF at normocapnia, before and after acetazolamide injection, regardless of the absolute PACO2 level. The present dose of the drug caused no change in ventilation, alveolar and arterial PCO2 or in arterial blood pH indicating that the carbonic anhydrase was not fully inhibited. Our observations show that acetazolamide nevertheless caused a rapid vasodilation in the brain and over a wide range of PCO2's. We suggest that this agent has a local vasodilator effect on the cerebral arterioles, unrelated to its specific effects as a carbonic anhydrase inhibitor.

Acetazolamide↗
PubMed1982

Monitoring acetazolamide treatment.

Electron capture gas chromatography was used to determine plasma concentrations after various doses of acetazolamide. In 40 patients steady state plasma concentrations were determined for daily doses of 187.5, 375, 750, and 1000 mg. Mean plasma concentrations increased with increasing dosages but there were marked interindividual variations. Part of the interindividual variation was explained by a positive correlation between age and plasma concentration. In 10 patients with previously untreated glaucoma intraocular pressure (IOP) responses and plasma concentrations were determined for increasing doses of acetazolamide. Increasing IOP reductions were obtained up to a dose of 750 mg while a daily dose of 1000 mg acetazolamide had no further effect on IOP. The relationship between IOP reduction and plasma concentration showed great interindividual variations, from a pressure reduction of 11 mmHg at 6 micrograms/ml acetazolamide to a pressure reduction of 0 mmHg at 11 micrograms/ml. As a rule, the maximal effect on IOP was obtained at a plasma concentration between 5 and 10 micrograms/ml. In most patients a daily dose of 1000 mg resulted in plasma concentrations above 10 micrograms/ml.

Acetazolamide↗
PubMed1994

Ocular and cerebral blood flow measurements in healthy subjects. A comparison of blood flow velocity and dynamic tonometry measurements before and after acetazolamide.

The ocular and cerebral blood flow was studied in 15 healthy subjects using transcranial Doppler ultrasonography (2 MHz). The blood flow velocity in the precerebral carotid arteries, in the ophthalmic artery and in the middle cerebral artery was measured under baseline conditions and after i.v. administration of 1 g acetazolamide. To measure the intraocular pressure and the corneal indentation pulse amplitude, a dynamic tonometer was used. Pulsatile ocular blood volume was calculated from these values. After one single dose of acetazolamide a significant decrease in ophthalmic artery flow velocity, and a significant increase both in internal carotid and in middle cerebral artery velocity was found. A significant decrease in intraocular pressure and in pulsatile ocular volume after acetazolamide was also demonstrated. These findings suggest that the acute effect of acetazolamide may be associated with a reduced ocular blood flow, explaining some of the reduction in IOP.

Acetazolamide↗
PubMed1996

Time course of acetazolamide effect in normal persons.

The intravenous injection of the carbonic anhydrase inhibitor acetazolamide causes a sustained increase of blood flow velocity in the middle cerebral artery. This effect is used in the acetazolamide test of the so-called cerebrovascular reserve capacity. The acetazolamide test is performed routinely as a two-point measurement of the blood flow velocity by transcranial Doppler before and 15 to 20 minutes after drug injection. Based on the assumption that evaluation of the time course will more sensitively detect an impaired cerebrovascular reserve capacity, suitable parameters for description of the time course were developed and normal values were established from 18 healthy persons (31 hemispheres). The mean value for the maximal increase of the mean flow velocity (MFV) was 29.7 +/- 8.3 cm/sec (as percentage of increase, 62.0 +/- 17.3%) and the time of the maximal increase was 15.35 +/- 8.46 seconds. Also calculated were the velocity of the MFV rise to the maximal value (3.0 +/- 3.2 cm/sec/min), the mean of the changes of the continuously measured MFV to the baseline value (21.0 +/- 7.4 cm/sec), and the integral of MFV represented by the plane under the MFV curve (967.8 +/- 350.0 cm). The best parameter for the description of the time dependency of the acetazolamide effect is the integral of MFV.

Acetazolamide↗
PubMed1989

Acetazolamide and transient responses of basolateral membrane potential of rabbit kidney proximal tubules perfused in vitro.

1. A study was made of the partial recovery of basolateral membrane potential that follows some depolarizing manoeuvres in cells of isolated perfused segments of rabbit proximal convoluted tubules. 2. Peritubular application of 10(-4) M-acetazolamide (a known inhibitor of the basolateral sodium-bicarbonate co-transporter) caused a hyperpolarization of both the basolateral membrane potential (Vbl) and the transepithelial potential (Vte). 3. Activation of electrogenic apical sodium co-transport caused a depolarization of the basolateral membrane followed by partial recovery of potential, and a sustained transepithelial hyperpolarization. The partial recovery of basolateral membrane potential was significantly smaller in the presence of 10(-4) M-acetazolamide applied to the peritubular fluid, although the magnitude of the initial depolarization was not significantly altered. 4. Addition to the bath of 0.5 mM-barium, a potassium conductance blocker, caused a transepithelial and basolateral membrane depolarization followed by partial recovery of potential. The partial recovery of basolateral membrane potential was significantly smaller in the presence of 10(-4) M-acetazolamide applied to the peritubular fluid, although the magnitude of the initial depolarization was again not significantly altered. 5. Increases in bath potassium concentration from 5 to 20 mM led to transepithelial and basolateral membrane depolarization followed by partial recovery of potentials. In paired experiments the partial recovery of basolateral potential was significantly reduced when 10(-4) M-acetazolamide was present in the bath. 6. These observations are consistent with the hypothesis that the basolateral sodium-bicarbonate co-transporter plays a role in the recovery of Vbl following these depolarizing manoeuvres.

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PubMed1999

Biochemical and ultrastructural changes in rabbit sclera after treatment with 7-methylxanthine, theobromine, acetazolamide, or L-ornithine.

AIMS: To examine a possible effect of 7-methylxanthine, theobromine, acetazolamide, or L-ornithine on the ultrastructure and biochemical composition of rabbit sclera. METHODS: Groups of pigmented rabbits, six in each group, were dosed during 10 weeks with one of the substances under investigation, and one untreated group was the control. Samples of anterior and posterior sclera were taken for determination of hydroxyproline, hydroxylysine, proline, proteoglycans, uronic acids and dermatan sulphate, chondroitin sulphate, and hyaluronic acid. Sections were examined with electron microscopy, and the diameter of the individual collagen fibrils was measured. RESULTS: Treatment with theobromine produced a significant increase in the contents of hydroxylysine, hydroxyproline, and proline in both anterior and posterior sclera, while 7-methylxanthine increased the contents of hydroxyproline and proline selectively in posterior sclera. Acetazolamide, on the other hand, significantly decreased the contents of hydroxyproline and proline in samples from anterior sclera. Uronic acids in both anterior and posterior sclera were significantly reduced by treatment with 7-methylxanthine, and L-ornithine significantly reduced uronic acids in posterior sclera. An inverse correlation between contents of hydroxyproline and uronic acids was found. The mean diameter of collagen fibrils was significantly higher in the posterior sclera from rabbits treated with 7-methylxanthine or theobromine, and significantly lower in rabbits treated with acetazolamide or L-ornithine compared with controls. In the anterior sclera, fibril diameter was significantly reduced in all treatment groups compared with controls. A positive, significant correlation between fibril diameter and content of hydroxyproline and proline was found in posterior sclera. CONCLUSION: 7-Methylxanthine, a metabolite of caffeine, increases collagen concentration and the diameter of collagen fibrils in the posterior sclera, and may be useful for treatment or prevention of conditions associated with low level and/or inferior quality of scleral collagen, such as axial myopia, chronic open angle glaucoma, and possibly neovascular age related macular degeneration. The apparent loss of collagen induced by chronic treatment with acetazolamide should be taken into consideration as a potentially harmful side effect. These results may indicate that scleral biochemistry and ultrastructure are influenced by the retinal pigment epithelium. One possible explanation is that the scleral fibroblasts which produce the collagen are sensitive to changes in the physiological electric field created by the retinal pigment epithelium.

Acetazolamide↗
PubMed1997

Changes in cerebral blood flow and vasoreactivity in response to acetazolamide in patients with transient global amnesia.

OBJECTIVE: Previous reports about changes in cerebral blood flow (CBF) in transient global amnesia disclosed decreased flow in some parts of the brain. However, CBF analyses in most reports were qualitative but not quantitative. The purpose of this study was to determine changes in CBF in transient global amnesia. METHODS: The CBF was measured and the vasoreactive response to acetazolamide was evaluated in six patients with transient global amnesia using technetium-99m hexamethylpropylene amine oxime single-photon emission computed tomography (SPECT). The CBF was measured during an attack in two patients and soon after an attack in the other four. About one month later, CBF was re-evaluated in each patient. RESULTS: Two patients examined during an attack and one patient examined five hours after an attack had increased blood flow in the occipital cortex and cerebellum. Three patients examined at six to 10 hours after an attack had decreased blood flow in the thalamus, cerebellum, or putamen. These abnormalities of blood flow almost disappeared in all patients one month after onset. The vasodilatory response to acetazolamide, which was evaluated initially using SPECT, was poor in areas of increased blood flow. By the second evaluation of CBF with acetazolamide, the vasodilatory response had returned to normal. CONCLUSIONS: In a patient with transient global amnesia, CBF increased in the vertebrobasilar territory during the attack and decreased afterwards. The vasodilatory response to acetazolamide may be impaired in the parts of the brain with increased blood flow. It is suggested that transient global amnesia is distinct from migraine but may share the same underlying mechanism.

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PubMed1987

Effect of acetazolamide on blood gases and 2,3 DPG during ascent and acclimatization to high altitude.

Blood gases and red cell 2,3 DPG concentrations were measured during ascent and a stay for 6 days at 4846 m in 20 subjects. Acetazolamide improved Pa,O2 and reduced pH and Pa,CO2. 2,3 DPG concentrations were lower in the acetazolamide group during ascent and at high altitude. However, 2,3 DPG concentrations were significantly greater at high altitude in both the acetazolamide and placebo groups compared with low altitude. The acetazolamide group remained different from the placebo group during the stay at high altitude with higher Pa,O2, lower PaCO2, lower pH and lower 2,3 DPG concentrations.

2,3-Diphosphoglycerate↗
PubMed1987

Effects of acetazolamide on cerebral blood flow and brain tissue oxygenation.

Oral administration of 1 g of acetazolamide to 8 normal subjects studied at sea level and in normoxia caused an acute increase in cerebral blood flow (CBF). During the subsequent prolonged oral treatment with 1 g of acetazolamide daily, CBF returned to normal within 2 days. The alveolar CO2 tension decreased gradually to 70% of the control value, indicating hyperventilation. At sea level hyperventilation will not increase brain oxygenation significantly in normal man, as the arterial oxygen content only increases minimally, while CBF is unchanged. At high altitude the beneficial effects of acetazolamide on the symptoms of acute mountain sickness may well be due to an improved oxygen supply to the brain, as hyperventilation will, at the low ambient PO2, cause a significant increase of the arterial oxygen content, while CBF presumably is unaffected by the drug. During hypoxia at high altitude the overall effect of prolonged acetazolamide treatment may thus be equivalent to a descent by several hundred metres.

Acetazolamide↗
PubMed1988

Effects of acetazolamide in patients with the sleep apnoea syndrome.

There is as yet no convincing evidence that acetazolamide, a carbonic anhydrase inhibitor, is effective in obstructive sleep apnoea. A study was therefore designed to examine the effect of acetazolamide (250 mg/day) on sleep events and ventilatory control during wakefulness in nine patients with the sleep apnoea syndrome. In eight of the nine patients the apnoea index and the total duration of apnoea were reduced by acetazolamide, and the mean (SEM) apnoea index of all patients changed from 25.0 (6.7) to 18.1 (5.8) episodes an hour. Furthermore, the total time of arterial oxygen desaturation (SaO2)--more than 4% depression in SaO2 from the baseline sleeping level--divided by total sleep time was also significantly decreased and its mean (SEM) value improved from 24.1 (7.9) to 13.6 (4.8)% of total sleep time. Five of the seven patients with varying degrees of daytime hypersomnolence had their symptoms obviously improved. There was no patient whose predominant type of apnoea was converted from the obstructive to the central type, or vice versa. In the studies of wakefulness, metabolic acidosis, an increase of arterial oxygen tension (PaO2) and a decrease of arterial carbon dioxide tension (PaCO2) were observed. The slopes of the occlusion pressure response and the ventilatory response to carbon dioxide increased, and the carbon dioxide ventilatory response line shifted to the left. It is suggested that acetazolamide cannot remove apnoea completely but has a beneficial effect in mild cases of obstructive sleep apnoea through an augmentation of central (CO2, H+) drive and a stabilising effect on ventilatory control.

Acetazolamide↗
PubMed1994

Effect of acetazolamide and amiloride against sodium metabisulphite-induced bronchoconstriction in mild asthma.

BACKGROUND: Inhaled frusemide but not bumetanide, another loop diuretic, reduces bronchial responsiveness to sodium metabisulphite (MBS). To investigate whether the effect of frusemide could be mediated through mechanisms other than Na+/K+/Cl- cotransporter inhibition, the effects of amiloride--an inhibitor of sodium channels in the airway epithelium--and of acetazolamide--a specific inhibitor of carbonic anhydrase--against MBS challenge were studied. METHODS: In two separate randomised double blind placebo controlled studies, 10 subjects with mild asthma attended on four separate occasions to inhale 7.5 mg amiloride or matched placebo, and 500 mg acetazolamide or placebo, immediately before MBS challenge. The concentration of MBS required to cause a 20% fall in baseline FEV1 (PC20) was measured. RESULTS: Amiloride and acetazolamide had no effect on baseline FEV1. Amiloride had no effect against MBS challenge, but acetazolamide increased -log PC20 from a mean (SE) of 0.75 (0.09) to 0.98 (0.06) representing a 0.77 (0.24) doubling dose increase. CONCLUSIONS: These results suggest that carbonic anhydrase activity in the airways, but not sodium flux, modulates bronchial responsiveness to MBS challenge. The action of frusemide is not likely to involve inhibition of carbonic anhydrase activity.

Acetazolamide↗
PubMed2001

Model of ionic transport for bovine ciliary epithelium: effects of acetazolamide and HCO.

The possible existence of transepithelial bicarbonate transport across the isolated bovine ciliary body was investigated by employing a chamber that allows for the measurement of unidirectional, radiolabeled fluxes of CO2 + HCO. No net flux of HCO was detected. However, acetazolamide (0.1 mM) reduced the simultaneously measured short-circuit current (I(sc)). In other experiments in which (36)Cl- was used, a net Cl- flux of 1.12 microeq. h(-1). cm(-2) (30 microA/cm(2)) in the blood-to-aqueous direction was detected. Acetazolamide, as well as removal of HCO from the aqueous bathing solution, inhibited the net Cl- flux and I(sc). Because such removal should increase HCO diffusion toward the aqueous compartment and increase the I(sc), this paradoxical effect could result from cell acidification and partial closure of Cl- channels. The acetazolamide effect on Cl- fluxes can be explained by a reduction of cellular H+ and HCO (generated from metabolic CO2 production), which exchange with Na+ and Cl- via Na+/H+ and Cl-/HCO exchangers, contributing to the net Cl- transport. The fact that the net Cl- flux is about three times larger than the I(sc) is explained with a vectorial model in which there is a secretion of Na+ and K+ into the aqueous humor that partially subtracts from the net Cl- flux. These transport characteristics of the bovine ciliary epithelium suggest how acetazolamide reduces intraocular pressure in the absence of HCO transport as a driving force for fluid secretion.

Acetazolamide↗
PubMed1990

Acetazolamide and insulin alter choroid plexus epithelial cell [Na+], pH, and volume.

Agents that inhibit or stimulate Na+ transport were tested for their effects on the ionic composition and volume of the in vivo choroid plexus (CP) epithelium. Ketamine-anesthetized adult Sprague-Dawley rats treated 1 h with acetazolamide or insulin were analyzed for choroid cell [Na+]i, [HCO3-]i, and pHi (dimethadione method); for transmembrane Na+ and H+ gradients; and for the kinetics of penetration of 22Na from plasma to plexus epithelium to CSF. Acetazolamide (25 mg/kg) reduced [Na+]i by 5-10 mmol/l and substantially elevated [HCO3-]i and pHi; the concurrent 22Na uptake by the in vivo choroid plexus and CSF, as quantified by the transfer coefficient, Kin (ml.g-1.h-1), was curtailed by 55-60%. Such effects on Na+ transport and distribution are likely secondary to the alkalinization of pHi induced by carbonic anhydrase inhibition. Conversely, insulin (3 U/kg ip) stimulated Na+ transport, i.e., manifested as enhanced uptake of 22Na from plasma to choroid cell and increased [Na+]i. For various treatments altering the basolateral membrane H+ gradient, the regression analysis of the 22Na Kin vs. log [H+]i/[H+]ISF (where ISF is interstitial fluid) was significant at P less than 0.01. This is consistent with effects mediated by Na(+)-H+ exchange. K+ and Cl- redistribution phenomena were coincident with altered Na+ transport, as choroidal cells retained K+, Cl-, and H2O after acetazolamide but lost K+, Cl-, and H2O with insulin treatment. A model is presented relating alterations in CP Na+ transport, KCl content, and cell volume. Overall, the findings encourage the postulate for effects of these drugs on Na+ transport basolaterally, either indirectly by attenuating [H+]i/[H+]ISF (acetazolamide) or directly by accelerating Na+ transport (insulin).

Acetazolamide↗
PubMed1979

Effects of acetazolamide and changes of acid-base balance on the content of cyclic nucleotides in the rat kidney.

Changes in tissue levels of cyclic adenosine 3':5'-monophosphate (cAMP) and cyclic guanosine 3':5'-monophosphate (cGMP) in the rat kidney in response to acid-base changes and administration of acetazolamide were measured. cAMP was determined according to the method described by Gilman and cGMP by radioimmunoassay. 1 mg/kg acetazolamide increased bicarbonate excretion 100-fold over the control values to 2.52 +/- 0.5 mEq/min (mean +/- SEM; n = 6), but did not influence cGMP and cAMP tissue content. 10 and 100 mg/kg acetazolamide increased cGMP tissue levels to 0.277 +/- 0.048 and 0.482 +/- 0.07 pmol/mg dry weight in comparison to 0.192 +/- 0.04 in the controls, whereas no changes in cAMP levels occurred. Chronic as well as acute metabolic alkalosis induced an increase of cGMP levels (0.26 +/- 0.03 and 0.29 +/- 0.06 pmol/mg), whereas chronic metabolic and acute respiratory acidosis lowered cGMP levels to 0.14 +/- 0.02 and 0.13 +/- 0.02 pmol/mg. cAMP tissue levels were not affected by changes in acid-base balance. The data could suggest that cGMP participates in the regulation of acid-base balance and renal effects of acetazolamide.

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