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PubMed1984

Pathogenesis of gastric ulceration produced by acetazolamide in rats.

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.

Acetazolamide↗
PubMed1989

SPECT study of cerebral blood flow reactivity after acetazolamide in patients with transient ischemic attacks.

We investigated 15 patients with one or more transient ischemic attacks (TIAs) in the internal carotid artery territory within the month following the most recent TIA. Cerebral blood flow (CBF) was measured by single-photon emission computed tomography, using intravenous xenon-133 before and after injection of 1 g acetazolamide. Six patients had severe carotid stenosis or occlusion; the other nine patients had no significant carotid lesions. Twenty age-matched volunteers free of neurologic symptoms or history were used as controls. Mean CBF in the sylvian region was not significantly different between patients and controls. Seven patients exhibited a focal hypoperfusion at rest in the symptomatic hemisphere, and their hypoperfused areas were hyporeactive after administration of acetazolamide. Seven other patients exhibited hyporeactive areas after acetazolamide administration while their CBF tomograms at rest were normal. Thus, CBF abnormalities were detected in 14 of the 15 patients. Our findings suggest that CBF measured early after acetazolamide administration could be useful to confirm the clinical diagnosis of TIA. In the nine patients with no significant lesion of the internal carotid artery, the areas of hypoperfusion were small and were probably related to the focal ischemic event. In the six patients with severe lesions of the internal carotid artery, abnormalities were of variable size and intensity but were often large and pronounced. The discrepancy between these two subgroups of patients could be ascribed to the hemodynamic influence of the internal carotid artery lesions. Moreover, our findings may provide some insight into the pathophysiology of TIAs.

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PubMed1999

Influence of acetazolamide and CO2 on extracranial flow volume and intracranial blood flow velocity.

BACKGROUND AND PURPOSE: The vasomotor response can be tested by means of transcranial Doppler sonography. If a constant vessel diameter is assumed, the flow velocity changes will reflect blood flow volume changes. This hypothesis is difficult to verify. Simultaneous assessment of intracranial flow velocity and extracranial flow volume changes may solve this problem. METHODS: We tested vasomotor response in 32 volunteers (age, 42+/-18 years) with 5% CO2. Acetazolamide (1 g) was tested in 15 volunteers (age, 28+/-8 years). To evaluate drug-dependent flow changes in the external carotid artery territory, acetazolamide was administered in 7 patients with unilateral occlusion of the internal carotid artery without evidence of collateralization through the ophthalmic artery (age, 67+/-12 years). Simultaneous recording included measurements of flow volume in the common carotid arteries (M-mode color duplex system) and flow velocity in the middle cerebral arteries. RESULTS: With CO2 and acetazolamide, intracranial flow velocity increased by 31% and 39%, respectively, with a simultaneous increase of common carotid artery flow volume of 47% and 50%, respectively. No change in extracranial flow volume was observed in patients with an occluded internal carotid artery. CONCLUSIONS: These data show not only the expected increase of flow velocity in the middle cerebral artery but also suggest an increase in cross-sectional vessel diameter of 6% and 4% with CO2 and acetazolamide, respectively. It remains unresolved whether this observation is due to a direct effect of the drug on the vessel walls or is simply pressure dependent.

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PubMed1999

Acetazolamide and breathing. Does a clinical dose alter peripheral and central CO(2) sensitivity?

Improvement of blood gases with the carbonic anhydrase inhibitor acetazolamide in some patients with chronic obstructive pulmonary disease (COPD) is believed to result from an effect on the ventilatory control system. Carbonic anhydrase is ubiquitously present within the body, particularly in tissues involved in the control of breathing. Because low inhibitor concentrations are sufficient to block the enzyme in many tissues, it is of interest to document the effect of clinical doses of acetazolamide on the CO(2) sensitivities of the peripheral and central chemoreflex loops. In this study we measured the effect of chronic acetazolamide (250 mg by way of mouth, every 8 h during 3 days) on the dynamic ventilatory response to step changes in end-tidal PCO(2) in nine healthy volunteers. Data were analyzed using a two-compartment model comprising a fast peripheral and slow central compartment, enabling us to separate drug effects on the peripheral and central chemoreflex loops, respectively. Compared with placebo, acetazolamide did not change the CO(2) sensitivities and time constants of both chemoreflex loops. However, mean (+/- SD) resting ventilation increased from 12.22 +/- 2.41 to 14.01 +/- 1.85 L. min(-1), resulting in a decrease in end-tidal PCO(2) from 40.0 +/- 4.7 to 33.3 +/- 3.5 mm Hg. Base excess decreased from -0.08 +/- 1.20 to -7.48 +/- 2.07 mmol. L(-1), indicating metabolic acidosis and explaining a leftward shift of the CO(2) response curve by 7.3 mm Hg. Possible clinical implications of these results are discussed.

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PubMed1992

Acetazolamide and furosemide attenuate asthma induced by hyperventilation of cold, dry air.

We investigated the assumption that the efficacy of inhaled diuretics in asthma is dependent upon inhibition of the Na+/K+/2Cl- cotransporter. We compared the protective effect of acetazolamide, a diuretic without significant effect on the loop cotransporter, with the protection provided by inhaled furosemide in a cold, dry air hyperventilation model of asthma. Seven asthmatic subjects underwent a baseline bronchial challenge and then received a nebulized dose of 80 mg of furosemide or 500 mg of acetazolamide or saline placebo in a randomized, double-blind, placebo-controlled crossover design. Repeat challenges were performed immediately and at 2 and 4 h postnebulization. Acetazolamide caused a 47.2% increase in the amount of cold, dry air required to reduce the FEV1, by 20% (expressed in terms of respiratory heat loss as PD20RHL), from 0.79 multiplied or divided by (x/divided by) 1.13 kcal/min (geometric mean x/divided by geometric SEM) at baseline to 1.17 x/divided by 1.09 kcal/min postnebulization (p < 0.025). Furosemide increased the geometric mean PD20RHL by 53.9%, from 0.86 x/divided by 1.12 kcal/min to 1.33 x/divided by 1.12 kcal/min (p < 0.001). There was no significant change after placebo inhalation (0.81 x/divided by 1.15 kcal/min versus 0.87 x/divided by 1.10 kcal/min, NS). Airway responsiveness had returned to baseline by 2 h postnebulization on all 3 days. Furosemide also caused bronchodilatation, producing a 14.1% rise in the mean FEV1 (p < 0.005 versus prenebulization), whereas neither acetazolamide nor placebo altered airway tone significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed2001

Acetazolamide treatment for infantile central sleep apnea.

Central sleep apnea is a common respiratory pattern in healthy neonates. Nevertheless, frequent central sleep apnea associated with drops in oxygen saturation may contribute to infantile morbidity. Recently, low-dose acetazolamide was shown to reduce symptomatic central sleep apnea in adults. We treated 12 infants, median conceptional age 42 weeks (range, 40-44 weeks), with central sleep apnea. In all cases, the central apnea index was >40/h total sleeping time (apnea > or = 3 sec). The cumulative duration of drops in oxygen saturation below 90% was more than 3 min/h total sleeping time. All individuals received acetazolamide 7 mg/kg/day (orally, divided in three doses) for 11 weeks. Polysomnography was begun 10 hours before the first dose and continued for 10 hours after the third dose. Polysomnography was repeated after 6 weeks of treatment and 1 week after acetazolamide therapy was discontinued. Comparison of the respiratory patterns before and after treatment (10-hour recording after the third dose) showed a decrease in the median central apnea index from 74/h (range, 42-152/h) to 13/h (range, 6-49/h). The median of the cumulative duration of drops in oxygen saturation below 90% decreased from 3.6 min/h (range, 3.1-9.2 min/h) to 0.07 min/h (range, 0-0.5 min/h). Basal oxygen saturation increased from 95 (92-97%) to 98% (96-99%). This improvement was maintained in the final polysomnography (12 weeks after therapy was begun and 1 week after completion of the 11-week course). No adverse effects were noted. We conclude that low-dose acetazolamide treatment may be useful for the treatment of central infantile sleep apnea associated with hypoxemia.

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PubMed1998

Effect of low-dose acetazolamide on the ventilatory CO2 response during hypoxia in the anaesthetized cat.

Acetazolamide, a carbonic anhydrase inhibitor, is used in patients with chronic obstructive pulmonary diseases and central sleep apnoea syndrome and in the prevention and treatment of the symptoms of acute mountain sickness. In these patients, the drug increases minute ventilation (V'E), resulting in an improvement in arterial oxygen saturation. However, the mechanism by which it stimulates ventilation is still under debate. Since hypoxaemia is a frequently observed phenomenon in these patients, the effect of 4 mg x kg(-1) acetazolamide (i.v.) on the ventilatory response to hypercapnia during hypoxaemia (arterial oxygen tension (Pa,O2)=6.8+/-0.8 kPa, mean+/-SD) was investigated in seven anaesthetized cats. The dynamic end-tidal forcing (DEF) technique was used, enabling the relative contributions of the peripheral and central chemoreflex loops to the ventilatory response to a step change in end-tidal carbon dioxide tension, (PET,CO2) to be separated. Acetazolamide reduced the CO2 sensitivities of the peripheral (Sp) and central (Sc) chemoreflex loops from 0.22+/-0.08 to 0.11+/-0.03 L x min(-1) x kPa(-1) (mean+/-SD) (p<0.01) and from 0.74+/-0.32 to 0.40+/-0.10 L x min(-1) x kPa(-1) (p<0.01), respectively. The apnoeic threshold B (x-intercept of the ventilatory CO2 response curve) decreased from 2.88+/-0.97 to 0.95+/-0.92 kPa (p<0.01). The net result was a stimulation of ventilation at PET,CO2 <5 kPa. The effect of acetazolamide is possibly due to a direct effect on the peripheral chemoreceptors as well as to an effect on the cerebral blood flow regulation. Possible clinical implications of these results are discussed.

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PubMed1981

Hypokalemic periodic paralysis exacerbated by acetazolamide.

Although acetazolamide usually prevents paralytic attacks in hypokalemic periodic paralysis, not all patients benefit from this treatment. We studied a father and two sons in whom attack frequency and severity increased on acetazolamide. Administration of triamterene virtually abolished attacks in three separate single-blind trials totaling more than 12 months. Spontaneous and glucose-insulin provoked occurred with only slight hypokalemia. Acetazolamide produced slight hypokalemia and provoked attacks of weakness whereas triamterene increased potassium levels significantly. Certain patients with hypokalemic periodic paralysis are worsened by acetazolamide, perhaps because of its kaliopenic effect. Triamterene may be effective in some of these patients.

Acetazolamide↗
PubMed1992

The use of acetazolamide-enhanced regional cerebral blood flow measurement to predict risk to arteriovenous malformation patients.

Regional hemodynamic disturbances may complicate the treatment of certain cerebral arteriovenous malformations (AVM) and occasionally produce life-threatening situations. Acetazolamide-enhanced quantitative regional cerebral blood flow studies were performed preoperatively in 35 patients to determine if patterns of vasoreactivity could be identified that might be markers for postoperative morbidity. Ipsilateral and contralateral regions of hypoperfusion were identified on resting studies, and a steal index was calculated by dividing the regional cerebral blood flow in the steal region by the flow in a normal cerebellar region. Flow in these regions of interest was again quantitated after the administration of acetazolamide, a known cerebral vasodilator. A delta value was calculated by subtracting the resting index values from the acetazolamide indices. Abnormally enhanced vasoreactivity (vasodilation) to acetazolamide stimulation was noted in these threatened territories in AVM that had perforating vessel feeding and angiographic steal phenomena, that developed hyperemic disturbances, and that resulted in poor outcomes. These findings call into question traditional theories of AVM-related hemodynamic decompensation and suggest unique smooth muscle derangements in cerebral vasculature in some AVM patients.

Acetazolamide↗
PubMed1998

Urinary excretion of acetazolamide in healthy volunteers after short- and long-term exposure to high altitude.

Acetazolamide is recommended for the prophylaxis of acute mountain sickness symptoms which sets in on climbing to high altitudes (H) above 2,500 m. It is primarily excreted unchanged in urine. In a previous study, we reported on the changes in urinary excretion of meperidine and its metabolite normeperidine on exposure to high altitude. In this study, we investigated the effect on urinary excretion of acetazolamide. The study was carried out in three groups of 12 healthy male volunteers each: at sea level (group L), these same volunteers the day after arrival at high altitude of 4,360 m (group HA), and subjects residing for approximately 10 months at high altitude (group HC). Urine was collected for the periods of 0-2, 2-4, 4-8, 8-12, 12-24 and 24-36 h after peroral administration of a single 250 mg dose. Urinary pH was measured and the concentrations of acetazolamide were determined. There were no significant changes observed in the amount of acetazolamide excreted in urine over 36 h. The urinary pH ranged from 4.5 to 7.8 for L, from 4.2 to 6.9 for HA and from 3.1 to 6.7 for HC. The Fel (fraction eliminated unchanged in urine) was calculated from the amount excreted in 36 h in urine and dose, assuming a bioavailability of 1 based on literature data. No significant changes in Fel were seen.

Acetazolamide↗
PubMed1988

Delayed ventilatory response to CO2 after carbonic anhydrase inhibition with acetazolamide administration in the anesthetized rat.

In order to estimate to what extent the stimulatory action of CO2 on ventilation is mediated by the formation of H+, we studied effects on the temporal profile of ventilatory response to CO2 of carbonic anhydrase (CA) inhibition with acetazolamide in the halothane anesthetized spontaneously breathing rat. Since hydration reaction of CO2 yielding H+ is delayed by CA inhibition, the time courses of changes in tidal volume (VT), respiratory frequency (f), and minute ventilation (VE) in response to a stepwise increase in end-tidal PCO2 (delta PETCO2 15 mmHg) were compared before (control state) and after i.v. injection of acetazolamide (50 mg/kg) in the hyperoxic condition. In the control state, an increase in VT was significantly slower than that in f, and the mean response half-times (T1/2) for the increase in VT, f, and VE were 50.6, 18.1, and 31.0 s, respectively. After acetazolamide administration, responses to CO2, especially f-response and consequently VE-response became much slower, and the T1/2 for VT, f, and VE were 67.9, 55.0, and 63.0 s, respectively. The delay in VT-response was not statistically significant. The magnitude of increase in VE in the steady state hypercapnic stimulation was almost the same before and after acetazolamide administration. The results suggest that a rapid increase in f during CO2 inhalation occurs predominantly through an increase in H+ produced by hydration of CO2 with CA, whereas VT-response may occur without involvement of this process. The different time courses of VT- and f-responses and possible effects of molecular CO2 and/or H+ on the regulatory mechanisms for ventilatory pattern were discussed.

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PubMed2006

Stevens-Johnson syndrome associated with intravenous acetazolamide administration for evaluation of cerebrovascular reactivity. Case report.

A 62-year-old man with left middle cerebral artery stenosis manifesting as transient ischemic attack underwent evaluation of regional cerebrovascular reactivity to acetazolamide using single photon emission computed tomography. Three days after intravenous administration of acetazolamide, erythematous eruptions of various sizes appeared on his back and spread over almost his entire body. Subsequently, painful ulcerations developed on his lips, and oral and nasal mucosa, and the conjunctiva became hyperemic, indicating Stevens-Johnson syndrome. The results of the lymphocyte transformation test were positive to only acetazolamide. Stevens-Johnson syndrome, also known as erythema multiforme major, can be life-threatening, and may be induced by intravenous administration of acetazolamide.

Acetazolamide↗
PubMed1991

The effect of acetazolamide on the endolymphatic sac DC potential.

The effect of acetazolamide known as a potent carbonic anhydrase inhibitor of the endolymphatic sac DC potential (ESP) was examined in the guinea pig. Intravenous administration of acetazolamide produced a dose-dependent decrease in ESP amplitude at doses of less than 10 mg/kg. The effect of acetazolamide on ESP was saturated at doses exceeding 10 mg/kg. The maximum reduction of ESP induced by acetazolamide was approximately 50% of the original ESP amplitude. The results suggest that carbonic anhydrase is involved in the generation of ESP.

Acetazolamide↗
PubMed1976

Effect of acetazolamide on glomerular balance and renal metabolic rate.

Glomerulotubular balance, defined as proportionality between filtered and reabsorbed sodium during inhibition of sodium reabsorption in the thick ascending limb of Henle's loop (diluting segment), was examined in anaesthetized dogs by gradual reduction of renal arterial pressure. In control experiments, glomerulotubular balance applied over the whole rante of glomerular filtration rate (GFR) examined but was absent after acetazolamide administration (30 mg/kg/body wt) at GFR above 50% of control. Hence, the inhibitory effect of acetazolamide varied with GFR. At control GFR, acetazolamide reduced tubular sodium reabsorption by 32 +/- 2% chloride reabsorption by 34 +/- 3%, and bicarbonate reabsorption by 52 +/- 2%; no significant effect was observed at GFR below 50% of control. For each bicarbonate ion, three sodium ions and two chloride ions were inhibited. Measurements of renal oxygen consumption and heat accumulation rates showed that acetazolamide did not reduce renal metabolic rate significantly. It is proposed that energy-requiring hydrogen ion secretion occurs at unchanges rate during variations in GFR but that back leakage of hydrogen ions varies with bicarbonate concentration in tubular fluid. Net secretion of hydrogen ions is associated with bicarbonate transport into the intercellular space and is linked with sodium reabsorption. The concentration difference of bicarbonate salts over the tight junction (zonula occludens), which is much less permeable to bicarbonate than to sodium chloride, provides the osmotic force for reabsorption of water and sodium chloride from the tubular lumen into the intercellular space. Glomerulotubular balance is mediated by variations in filtered amounts of bicarbonate.

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PubMed1993

Abnormal cerebral vasodilation in aneurysmal subarachnoid hemorrhage: use of serial 133Xe cerebral blood flow measurement plus acetazolamide to assess cerebral vasospasm.

A patient with cerebral vasospasm following subarachnoid hemorrhage (SAH) was investigated by serial measurement of cerebral blood flow (CBF) using the xenon-133 emission tomography method. The CBF was measured before and after acetazolamide injection. On Day 2 after SAH, there was early local hyperperfusion in the middle cerebral artery (MCA) territory, ipsilateral to the left posterior communicating artery aneurysm. The regional CBF of this arterial territory decreased slightly after acetazolamide injection, probably because of vasoplegia and the "steal" phenomenon, and thus surgery was delayed. A right hemiplegia with aphasia and disturbed consciousness occurred 4 days later (on Day 6 after SAH) due to arterial vasospasm, despite treatment with a calcium-channel blocker. The initial hyperemia of the left MCA territory was followed by ischemia. The vasodilation induced by acetazolamide administration was significantly subnormal until Day 13, at which time CBF and vasoreactivity amplitude returned to normal and the patient's clinical condition improved. Surgery on Day 14 and outcome were without complication. It is concluded that serial CBF measurements plus acetazolamide injection are useful for monitoring the development of cerebral vasospasm to determine the most appropriate time for aneurysm surgery.

Acetazolamide↗
PubMed1977

Acetazolamide-induced weakness in paramyotonia congenita.

Acetazolamide has been shown to be effective prophylaxis for both hypokalemic and hyperkalemic paralysis. A patient with paramyotonia congenita, a related disorder with myotonia and episodic weakness, was studied during treatment with acetazolamide. Athough the patient's myotonia was virtually abolished, severe quadriparesis was produced during each trial of acetazolamide. This response distinguished this patient's condition from other forms of familial periodic paralysis and suggests that acetazolamide may be deleterious to some patients with periodic paralysis.

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PubMed1999

[Salicylism and glaucoma: reciprocal augmentation of the toxicity of acetazolamide and acetylsalicylic acid].

We report a case of salicylism caused by association of acetylsalicylic acid (ASA) and acetazolamide. A 50-year-old woman without chronic renal insufficiency, was admitted for confusion, cerebellar ataxia associated with hyperchloremic acidosis. She was treated with acetazolamide for simple glaucoma and since 14 days with ASA for acute pericarditis. Clinical features evoked salicylism despite low serum salicylate level: 178 mg/l. The carbonic anhydrase inhibitor explained the biochemical pattern. Acetazolamide-induced acidosis enhances the non ionized form of salicylate which crosses the biological membrane more rapidly and better than the ionized form. The tissular tropism of non ionized salicylate increases and cerebral toxicity may occur with low serum level of ASA. ASA also enhances the free form of acetazolamide.

Acetazolamide↗
PubMed1999

[A clinical trial of acetazolamide for SCA6].

Spinocerebellar ataxia type 6 (SCA 6) is an allelic disorder of episodic ataxia type 2 (EA 2) and is caused by a small CAG repeat expansion in the gene encoding the alpha 1A-voltage-dependent-Ca channel subunit (CACNA 1 A) on chromosome 19p13.1. The disorder starts at adulthood with progressive cerebellar ataxia, and the symptoms often fluctuate at early stage. These clinical features overlap with those of EA 2, which has been known as acetazolamide-responsive ataxia. On this background, we studied the clinical effectiveness of acetazolamide for SCA 6 in 9 consecutive patients. Their clinical severity was serially evaluated by ARS (ataxia rating scale) and gravimetric test, over 32 weeks of oral administration of acetazolamide (250-500 mg/day). Consequently, a significant improvement was observed in ARS and postural sway. Our results indicate that acetazolamide is temporally effective for ameliorating the symptoms of SCA 6. However, its effects for the disease progression need to be examined in more large scales in number and duration.

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