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PubMedDate not supplied

Acute and chronic acetazolamide administration in DBA and C57 mice: effects of age.

The clinical utility of the carbonic anhydrase (CA) inhibitor acetazolamide (ACTZ) is limited because of rapid development of tolerance to its effects. Tolerance is thought to develop as a result of glial cell proliferation and/or increased CA synthesis. DBA mice, susceptible to audiogenic seizures (AGSs) in an age-dependent manner, have increased CA activity as compared with C57 (non-audiogenic seizure susceptible) mice at 21 and 110 days of age. The present work utilized ACTZ to help determine the relationship between increased CA activity in brain and AGSs in DBA mice. Also, minimal electroshock seizure threshold (EST) was measured at various ages in DBA and C57 mice to determine age-related changes in CNS excitability. EST was significantly lower in DBA as compared with C57 mice at 18 days and between 40 and 115 days of age, suggesting that DBA mice remain hyperexcitable to electrical stimulation after they develop resistance to AGSs. ACTZ ED50s against maximal electroshock seizures (MES) were significantly higher in DBA as compared with C57 mice at 26,36, and 115 days of age. This finding correlates with higher CA activity in this strain at 110 days of age, noted previously. However, at 21 days of age, when CA activity is also higher in DBA versus C57 mice, there were no significant differences in ACTZ ED50s against MES between the strains. ACTZ ED50s against AGSs in DBA mice were considerably lower than ACTZ ED50s against MES in either strain, suggesting that a particular fraction of CA is intimately involved in the production of AGSs.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMedDate not supplied

Use of acetazolamide as an adjunct to carbamazepine in refractory partial seizures.

Acetazolamide (Diamox) (AZM) was evaluated as an adjunct to carbamazepine (CBZ) monotherapy in 48 refractory partial seizure patients at a tertiary care referral center. Patient ages ranged from 6 to 64 years (average 28 years). Seizure frequencies for the pre-AZM baseline period (CBZ monotherapy) were compared with the seizure frequencies at different daily doses of AZM. Patients with a 50% decrease in seizure frequency were considered responders. Twenty-one patients were responders (44%) and three became completely seizure-free. Effective doses ranged from 3.8 to 22.0 mg/kg/day. Effective plasma concentrations ranged from 1 to 22 micrograms/ml in selected patients. Durations of response time to AZM ranged from 3 to 30 months (average 12.9 months). Three patients lost response, one temporarily. Side effects were seen in 10 patients, requiring discontinuation in three.

Acetazolamide↗
PubMedDate not supplied

Mechanisms of tolerance to the anticonvulsant effects of acetazolamide in mice: relation to the activity and amount of carbonic anhydrase in brain.

The mechanism by which tolerance develops to the anticonvulsant effects of acetazolamide (AZM) was investigated in Swiss-Webster mice. The effects of single and six daily doses of 40 mg or 200 mg/kg AZM on electroshock seizure threshold (EST), maximal electroshock (MES) seizure pattern, and on the activity and total amount of carbonic anhydrase II (CAII) in various subcellular fractions (cytosol, microsomes, and myelin) of cerebral cortex, cerebellum, and brainstem were assessed. The activity of CAII was measured by microassay, and the total amount was measured by immunoassay methods developed in this laboratory. From the activity (units per microgram of protein) and total amount (nanograms per microgram protein) data, the specific activity (units per nanogram CAII) of the enzyme was calculated. With multiple doses, tolerance developed to both elevation of the EST and modification of the MES pattern noted with single doses of AZM. Accompanying the development of tolerance to the anticonvulsant effects of AZM was an increase in both the activity and specific activity of CAII in the various subcellular fractions and areas of the brain. The effects were dose dependent. Tolerance to the EST-elevating effects of AZM correlated with increases in the activity, total amount, and specific activity of CAII in the myelin fraction of the cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1996

Early cerebral blood flow and vascular reactivity to acetazolamide in predicting the outcome after ruptured cerebral aneurysm.

The sequential cerebral blood flow (CBF) and CBF response to acetazolamide (AZ; 1 g i.v.) within 4 days after initial subarachnoid hemorrhage (SAH) were monitored in 50 patients by stable xenon-enhanced computed tomography (xenon CT). The mean global CBF of the subjects declined with the neurological grading (Hunt & Kosnik), and it was impossible to predict the occurrence of vasospasm from the value of the plain CBF at the acute phase of SAH. However, the CBF response to AZ at the acute phase of SAH among patients resulting in a poor outcome was significantly diminished compared to that among patients resulting in a good outcome. The usefulness of the CBF response to AZ in the acute phase of SAH is discussed.

Acetazolamide↗
PubMed1996

Hemodynamics of hypertensive putaminal hemorrhage evaluated by Xenon-enhanced computed tomography and acetazolamide test.

Cerebral blood flow (CBF) is usually decreased in patients with hypertensive putaminal hemorrhage (HPH). However, there are few reports concerning cerebrovascular reserve capacity (CRC) in these cases. This study evaluated cerebral hemodynamics in patients with HPH by measuring CBF and CRC. CBF and CRC were measured by stable xenon enhanced computed tomography (Xe-CT) in 11 patients with HPH (HPH group) and 11 patients with essential hypertension without intracerebral hematoma (non-HPH group). CBFs of the hemisphere and thalamus in the HPH group were lower than those in the non-HPH group. And the CBF of the hemisphere was increased transiently after the surgical evacuation of the hematoma. Thereafter, it fell gradually. The CRCs were also lower in acute stage of the HPH group. The CRC recovered during the chronic stage. Hemodynamics in patients with HPH can be modulated by surgical removal of hematoma. However, some adjunct therapies are necessary to prevent delayed neuronal inactivity, Stable Xe-CT with acetazolamide test is useful to evaluate hemodynamics in the HPH patients.

Acetazolamide↗
PubMed1982

Evidence for feedback mediated reduction of glomerular filtration rate during infusion of acetazolamide.

Systemic administration of acetazolamide (ACZ) causes glomerular filtration rate (GFR) to fall. Clearance and micropuncture experiments were done to define the mechanism of this drug effect. When rats were infused with ACZ intravenously, kidney GFR fell by 30% and single nephron (SN) GFR (measured by collecting distal tubule fluid) fell by 23%. Changes in arterial blood pressure, arterial pH, extracellular fluid volume, and proximal tubule pressure were not sufficient to account for the decrease in GFR. When SNGFR was measured by collecting proximal tubule fluid, with the loop of Henle having been blocked for 2-5 min, SNGFR was higher than the distally measured value and was not different than control. The results are consistent with the fall in GFR being caused by activation of the tubulo-glomerular feedback mechanism.

Acetazolamide↗
PubMed2002

Acetazolamide vasoreactivity in vascular dementia and persistent vegetative state evaluated by transcranial harmonic perfusion imaging and Doppler sonography.

To clarify the pathophysiological differences of the cerebrovascular reserve capacity in relation to cerebral cognitive impairments between vascular dementia (VaD) and persistent vegetative state (PVS), we evaluated acetazolamide (ACZ) vasoreactivity testing by transcranial harmonic perfusion imaging (HPI) and Doppler sonography (TCD). Sixteen patients (age: 29-85 years; mean: 62) were divided into three groups: 7 VaD, 4 PVS, and 5 nondementia patients. Mean velocity (Vm) in the middle and posterior cerebral artery (MCA, PCA) was measured, and time-intensity curves of the HPI were evaluated at three regions of interest-the bilateral temporal lobe (TL), basal ganglia (BG), and thalamus (Th). TCD and HPI were evaluated before (resting state) and after ACZ administration, and vasoreactivity was compared among the three groups in terms of resting values and relative changes (%Delta) of Vm, peak intensity (PI), area under curve (AUC), and mean transit time (MTT). Results of the resting state: Decreased Vm, PI, and AUC of the VaD and PVS groups were more obvious in the right side. Results of vasoreactivity: In the PVS group, %DeltaVm decreased in the left PCA and MCA; %DeltaPI and %DeltaAUC decreased in the left TL and bilateral BG. In the VaD group, %DeltaPI and %DeltaAUC decreased in the right TL; %DeltaMTT tended to increase in the left side. ACZ vasoreactivity tests by transcranial HPI and TCD allowed bedside, noninvasive quantitative evaluation of the pathophysiology of cognitive function impairment in relation to cerebrovascular reserve capacity in VaD and PVS.

Acetazolamide↗
PubMed1975

The immediate response in applanation pressure to intravenous acetazolamide in primary glaucomas and glaucoma suspects.

The decays in the applanation pressures of both eyes, after a reduction of the aqueous secretion by means of intravenous acetazolamide, are studied with respect to shape and steepness by comparison with reference curves calculated from different values of the facility of aqueous outflow. The pressure decays in three out of four eyes with narrow-angle glaucoma exhibited "breaks" possibly resulting from a stepwise reopening of the chamber angle during the decompression. Twenty patients with intraocular hypertension and open angles could be divided into two groups according to the facility of aqueous outflow (in mul mmHg-1 min-1), estimated from approximately matching reference curves: Nine patients with facilities above 0.15 had normal visual fields and nearly indentical pressure curves of the two eyes. Out of 11 patients with facilities below 0.15, seven patients had glaucomatous visual field defects and excavated optic discs. The pressure curves of eye pairs in this low facility group showed asymmetry, and breaks were seen in approximately half of the curves. These might be caused by changes in the outflow facility due to a decompression of collapsed outflow channels. However, the morphological basis for such an interpretation is not as well founded as in the case of narrow-angle glaucoma.

Acetazolamide↗
PubMed2007

Effect of acetazolamide on pulmonary and muscle gas exchange during normoxic and hypoxic exercise.

Acetazolamide (ACZ) is used to prevent acute mountain sickness at altitude. Because it could affect O2 transport in several different and potentially conflicting ways, we examined its effects on pulmonary and muscle gas exchange and acid-base status during cycle exercise at approximately 30, 50 and 90% VO2max in normoxia (F(IO2) = 0.2093) and acute hypoxia (F(IO2) = 0.125). In a double-blind, order-balanced, crossover design, six healthy, trained men (normoxic VO2max= 59 ml kg(-1) min(-1)) exercised at both F(IO2) values after ACZ (3 doses of 250 mg, 8 h apart) and placebo. One week later this protocol was repeated using the other drug (placebo or ACZ). We measured cardiac output (QT), leg blood flow (LBF), and muscle and pulmonary gas exchange, the latter using the multiple inert gas elimination technique. ACZ did not significantly affect VO2, QT, LBF or muscle gas exchange. As expected, ACZ led to lower arterial and venous blood [HCO3-], pH and lactate levels (P < 0.05), and increased ventilation (P < 0.05). In both normoxia and hypoxia, ACZ resulted in higher arterial P(O2) and saturation and a lower alveolar-arterial P(O2) difference (AaD(O2)) due to both less VA/Q mismatch and less diffusion limitation (P < 0.05). In summary, ACZ improved arterial oxygenation during exercise, due to both greater ventilation and more efficient pulmonary gas exchange. However, muscle gas exchange was unaffected.

Acetazolamide↗
PubMed2005

Acetazolamide, a carbonic anhydrase inhibitor, reverses inflammation-induced thermal hyperalgesia in rats.

Inflammatory pain is linked to reduction in tissue pH. Tissue proton generation is mainly mediated by carbonic anhydrases (CAs). We therefore hypothesized that inhibition of CAs with acetazolamide (ACTZ) increases the tissue pH and reverses inflammation-induced pain. CAs are also present in the central nervous system and control anion concentrations. Furthermore, ACTZ has direct effects on ion channels involved in nociception. In the current study, responses to heat and mechanical stimuli (von Frey filaments) of the paw were assessed before and after carrageenan-induced muscle inflammation and after treatment with ACTZ in rats. ACTZ was administered systemically, locally, or intrathecally 24 h after the induction of inflammation. In separate studies, pH was measured in the inflamed and noninflamed muscles and after administration of ACTZ. Carrageenan injection to the gastrocnemius muscle produced heat hyperalgesia and mechanical allodynia of the paw. Systemic ACTZ reversed the heat hyperalgesia but not mechanical allodynia. Similarly, injections of ACTZ into the inflamed muscle or intrathecally reversed the heat hyperalgesia but not mechanical allodynia. Surprisingly, the pH in the inflamed muscle was not reduced compared with noninflamed muscle. Thus, the current data do not support our hypothesis that ACTZ reduces inflammatory hyperalgesia by raising the reduced pH in muscle. Although the possibility of pH changes and the role of CAs in the microenvironment cannot be ruled out, the mechanism of ACTZ-induced antihyperalgesia is not clear from this study. It is possible that the inhibition of ion channels and/or the inhibition of spinally located CAs contribute to the observed antihyperalgesia.

Acetazolamide↗
PubMed1988

Selective medium for Branhamella catarrhalis with acetazolamide as a specific inhibitor of Neisseria spp.

Several semiselective media for Branhamella catarrhalis have been proposed. These media allow growth of all members of the family Neisseriaceae, and further differentiation is necessary. By addition of 10 micrograms of acetazolamide, a carbonic anhydrase inhibitor, per ml and incubation in air, a medium was created which reduced growth of Neisseria spp. When saliva samples from 178 healthy schoolchildren were screened for the presence of B. catarrhalis, the carrier rate for this organism was estimated to be 48.9% with the selective medium compared with 12.4% when a semiselective medium, which contains only 10 micrograms of vancomycin, 5 micrograms of trimethoprim, and 2 micrograms of amphotericin B per ml, was used and 6.2% when a nonselective blood agar plate was used. The number of Neisseria spp. isolated dropped from 297 on the semiselective agar to 55 on the selective agar.

Acetazolamide↗
PubMed2001

Use of acetazolamide to decrease cerebrospinal fluid production in chronically ventilated patients with ventriculopleural shunts.

Acetazolamide (ACTZ), a carbonic anhydrase inhibitor, has been shown to decrease cerebrospinal fluid (CSF) production in both in vivo and in vitro animal models. We report two children with hydrocephalus who experienced multiple shunt failures, and who had externalised ventriculostomy drains (EVD) prior to ventriculopleural shunt placement. The effects of increasing doses of ACTZ on CSF production and subsequent tolerance to ventriculopleural shunts were evaluated. The patients had a 48% and a 39% decrease in their EVD CSF output when compared to baseline with maximum ACTZ dose of 75 mg/kg/day and 50 mg/kg/day, respectively (p < 0.05). This is the first report of change in CSF volume in children after extended treatment with ACTZ. ACTZ treatment in mechanically ventilated paediatric patients with hydrocephalus may improve tolerance of ventriculopleural shunts and minimise respiratory compromise. Potassium and bicarbonate supplements are required to correct metabolic disturbances.

Acetazolamide↗
PubMed1980

Effect of hypercapnea and hyperventilation on human intraocular pressure general anaesthesia following acetazolamide administration.

The changes in intraocular pressure due to blood pH, PCO2, and PO2 alterations induced by hyperventilation and hypercapnea in man undergoing routine general anaesthesia were studied. It was shown that hypercapnea produces elevation of intraocular pressure, while hyperventilation lowers it. Acetazolamide pretreatment did not alter these IOP responses to PCO2, PO2, and blood pH changes.

Acetazolamide↗
PubMed1969

Acetazolamide and sodium bicarbonate in treatment of salicylate poisoning in adults.

Ten adults suffering from salicylate overdosage were treated successfully with a combination of sodium bicarbonate and acetazolamide to exploit the increase in salicylate clearance which is known to occur in very alkaline urine. The advantages of the method include the absence of important complications and the small volume of fluid required.

Acetazolamide↗
PubMed1988

Improvement of muscle strength in familial hypokalaemic periodic paralysis with acetazolamide.

A double blind cross-over study of eight patients with familial hypokalaemic periodic paralysis was made to assess the influence of acetazolamide on muscle strength. All patients had a reduced interictal muscle fibre conduction velocity. Five patients had no attacks at the time of the study. One patient withdrew from the study because of an adverse reaction. The muscle strength of 11 muscle groups was measured with a hand-held dynamometer. The sum of force improved significantly in the seven patients (mean increase: 17%, p less than 0.05; 95% confidence interval: 7.2-26.8%). Endurance tests showed an improvement in the performance of 30 full kneebends. Surface EMG measurement showed no change in the muscle fibre conduction velocity or power spectra during treatment. The integrated EMG showed a (non significant) mean increase of 21%.

Acetazolamide↗
PubMed1995

Hereditary myokymia and paroxysmal ataxia linked to chromosome 12 is responsive to acetazolamide.

A sixth family with autosomal dominantly inherited myokymia and paroxysmal ataxia is described. The syndrome in this family is linked to the recently discovered locus for inherited myokymia and paroxysmal ataxia on the human chromosome 12p, and a missense mutation is shown in the KCNA1 gene. The attacks of ataxia in this family compare well with those of previously described families and similarly are precipitated by kinesigenic stimuli, exertion, and startle. Responsiveness of these attacks to low dose acetazolamide is confirmed, but some loss of efficacy occurs with prolonged treatment, and side effects are notable. Although not all affected family members showed myokymia on clinical examination, electromyography invariably showed myokymic discharges, in one patient only after a short provocation with regional ischaemia. One affected family member also had attacks of paroxysmal kinesigenic choreoathetosis, responsive to carbamazepine.

Acetazolamide↗
PubMed1998

Continuous muscle fibre activity: a case treated with acetazolamide.

A case is reported of the continuous muscle fibre activity syndrome, which includes a group of disorders characterised by sustained motor unit activity due to hyperactivity of peripheral nerve motor axons. In this patient the muscle stiffness and myokymic movements were successfully treated with acetazolamide, which acts as a membrane stabiliser either by blockade of chloride and bicarbonate membrane transport or by producing kaliuresis and raising the transmembrane potential by decreasing extracellular potassium.

Acetazolamide↗
PubMed1998

Spinocerebellar ataxia type 6 with positional vertigo and acetazolamide responsive episodic ataxia.

The SCA6 mutation, a small expansion of a CAG repeat in a calcium channel gene CACNA1A, was identified in three pedigrees. Point mutations in other parts of the gene CACNA1A were excluded and new clinical features of SCA6 reported--namely, central positional nystagmus and episodic ataxia responsive to acetazolamide. The three allelic disorders, episodic ataxia type 2, familial hemiplegic migraine, and SCA6, have overlapping clinical features.

Acetazolamide↗