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PubMed1977

H+ transport from CNS in hypercapnia and regulation of CSF [HCO3-].

CSF HCO3- increases more than plasma HCO3- in hypercapnia, and there are at least two sources for the CSF HCO3- increase--one derived from the simultaneous increase in plasma HCO3-, and the other, HCO3-formed from hydration of CO2 in the choroid plexus and glia and susceptible to inhibition by acetazolamide (J. Appl. Physiol. 38: 504-512, 1975). It was proposed that the H+ formed in the CNS in CO2 hydration is actively exchanged for plasma Na+ utilizing the Na-K ATPase pump. H+ transport from the CNS was therefore studied in four groups of dogs breathing 5% CO2 at constant VA for 4 h with repeated injections of saline, acetazolamide 5 mg/ml, ouabain 0.1 mg/ml, and acetazolamide and ouabain together into lateral cerebral ventricles. Arterial HCO3-increased 2.5 meq/l at 4 h of hypercapnia in all groups. CSF HCO3-increased 5.8 meq/l in the saline-injected animals, but it increased only about 2 meq/l and equaled plasma HCO3- rise in the other three groups. Therefore CNS HCO3- formation in hypercapnia can be blocked by inhibiting the CO2 hydration reaction with acetazolamide or by blocking H+ removal by inhibiting Na-K ATPase with ouabain. The data support the thesis of active H+ removal from the CNS in exchange for plasma Na+ in hypercapnia.

Acetazolamide↗
PubMed1980

Carbonic anhydrase activity of rabbit lungs.

Pulmonary carbonic anhydrase (CA) activity was studied in rabbit lungs perfused with solutions containing no CA. Measurements were made of the amount of 14CO2 appearing in the expired gas following injections of H14CO3(-), 14CO2, or a 20:1 mixture of each into the pulmonary artery. The fraction of the injected label in the expired gas was only 17% greater for 14CO2 than for the mixture, suggesting that equilibration between H14CO3(-) and 14CO2 was nearly complete during the capillary transit time. Inhibition of pulmonary CA decreased excretion of H14CO3(-) and the mixture by 40 and 49% and increased the excretion of 14CO2 by 96%. Addition of CA to the perfusate had no effect. Thus, CO2 exchange is not significantly limited by pulmonary CA if inhibitors are absent. Tissue binding of [3H]acetazolamide injected into the pulmonary artery was diminished by 50% when acetazolamide concentrations reached 0.13 x 10(-6) M. Each liter of extravascular lung water contained 1.25 x 10(-6) mol of receptors for acetazolamide that were accessible to plasma during a single circulation. Binding of [3H]acetazolamide was also observed in lungs of anesthetized rabbits, suggesting that pulmonary CA is accessible to plasma in vivo as well as in situ.

Acetazolamide↗
PubMed1986

Effect of respiratory alkalosis during exercise on blood lactate.

A biofeedback model of hyperventilation during exercise was used to assess the independent effects of pH, arterial CO2 partial pressure (PaCO2), and minute ventilation on blood lactate during exercise. Eight normal subjects were studied with progressive upright bicycle exercise (2-min intervals, 25-W increments) under three experimental conditions in random order. Arterialized venous blood was drawn at each work load for measurement of blood lactate, pH, and PaCO2. Results were compared with those from reproducible control tests. Experimental conditions were 1) biofeedback hyperventilation (to increase pH by 0.08-0.10 at each work load); 2) hyperventilation following acetazolamide (which returned pH to control values despite ventilation and PaCO2 identical to condition 1); and 3) metabolic acidosis induced by acetazolamide (with spontaneous ventilation). The results showed an increase in blood lactate during hyperventilation. Blood lactate was similar to control with hyperventilation after acetazolamide, suggesting that the change was due to pH and not to PaCO2 or total ventilation. Exercise during metabolic acidosis (acetazolamide alone) was associated with blood lactate lower than control values. Respiratory alkalosis during exercise increases blood lactate. This is due to the increase in pH and not to the increase in ventilation or the decrease in PaCO2.

Acetazolamide↗
PubMed1987

Inhibition of mitochondrial carbonic anhydrase and ureagenesis: a discrepancy examined.

The amount of urea synthesized in intact guinea pig hepatocytes in 60 min ([urea]t=60), was determined at 37 degrees C in Krebs-Henseleit buffer plus (in mM) 10 NH4Cl, 5 lactate, and 10 ornithine in 5% CO2-95% O2. The concentrations of sulfonamide carbonic anhydrase (CA) inhibitors required to reduce the rate of urea synthesis by 50% (I50) were (in mM): 0.07 ethoxzolamide, 0.5 methazolamide, 0.7 acetazolamide, and 5.0 p-aminomethylbenzenesulfonamide. At 37 degrees C acetazolamide and ethoxzolamide reduced citrulline synthesis by intact mitochondria in medium containing (in mM) 50 3-(N-morpholino)propanesulfonic acid, 35 KCl, 5 KH2PO4, 2 adenosine triphosphate, 10 ornithine, 10 NH4Cl, 1 [ethylene-bis(oxyethylenenitrile)]tetraacetic acid, 1 MgCl2, 20 pyruvate, and 25 KHCO3 (pH 7.4) in 5% CO2-95% O2; the inhibition by ethoxzolamide was not decreased greater than 50%; 25% inhibition was achieved by 0.65 microM ethoxzolamide. Inhibition constant (Ki) values for CA activity of disrupted mitochondria at 37 degrees C were 0.03 microM ethoxzolamide and 0.16 microM acetazolamide, and for disrupted hepatocytes were 150 microM ethoxzolamide and 50 microM acetazolamide. p-Aminomethylaminosulfonamide-affinity column purification yields one band of 29,000 mol wt for CA V purified from disrupted mitochondria; homogenized whole-liver supernatant yields an additional band of 20,000 mol wt (at greater than 100 times the concentration of CA V), which has some glutathione S-transferase activity. It is concluded that this 20,000-mol wt protein modifies the potency of ethoxzolamide in the liver cytosol.

Acetazolamide↗
PubMed1990

Regional cerebral blood flow and distribution of [99mTc]ethyl cysteinate dimer in nonhuman primates.

Increases in regional cerebral blood flow have been described in a variety of cerebral pathologic states, including stroke and seizure disorders. The usefulness of technetium-99m-labeled cysteinate dimer as a marker in the measurement of regional cerebral blood flow was tested in five cynomolgus monkeys. To expand the range of blood flow to beyond the normal limits, 40 mg/kg i.v. of the carbonic anhydrase inhibitor acetazolamide was administered. Regional cerebral blood flow in all five monkeys was measured using radiolabeled microspheres (before and after acetazolamide) and the marker (after acetazolamide) in 60-70 samples from 12 brain regions. Acetazolamide significantly increased the mean +/- SEM regional cerebral blood flow measured using microspheres from 0.56 +/- 0.21 to 1.71 +/- 0.9 ml/min/g (p less than 0.01 for each region). A significant positive correlation was found between regional cerebral blood flow values calculated using microspheres and the marker after normalizing the values to those in the cerebellum (r = 0.773, p less than 0.0001). The mean +/- SEM regional cerebral blood flow determined using the marker in a single monkey (1.21 +/- 0.04 ml/min/g) did not differ significantly from that determined in the same monkey using microspheres (1.13 +/- 0.04 ml/min/g). These data support the potential use of this new brain perfusion imaging agent to assess regional cerebral blood flow over a clinically relevant range of blood flows.

Acetazolamide↗
PubMed1993

Dynamic computed tomographic imaging of regional cerebral blood flow and blood volume. A clinical pilot study.

BACKGROUND AND PURPOSE: The advent of faster computed tomography scanners has evoked considerable interest in using this technology as a more practical method of regional cerebral hemodynamic evaluation than the currently available positron emission and single-photon emission computed tomography. The theoretical concepts have been worked out and validated in the laboratory by several groups. The aim of the present study was the development of a clinically useful system. METHODS: Software was developed for dynamic computed tomography-based calculation and color-coded representation of regional cerebral blood flow and blood volume. Normal values, reproducibility, and sensitivity to acetazolamide challenge were established in 13 volunteers. The method was applied to an additional three patients with internal carotid artery occlusion and known decreased vascular reserve capacity as diagnosed by transcranial Doppler ultrasonography. RESULTS: Normal regional cerebral blood flow was determined as 50 +/- 13 ml/100 ml per minute and normal fractional cerebral blood volume as 58 +/- 12 ml/1,000 ml (mean +/- SD). In five volunteers, two examinations were performed within 15 minutes for determination of reproducibility. Intermeasurement variability of hemispheric blood flow and blood volume was determined as +/- 23% and +/- 16%, respectively. Intravenous administration of 1 g acetazolamide resulted on the average in a 75% increase of blood flow and a 65% increase of fractional blood volume. In the patients with decreased cerebrovascular reserve capacity, baseline fractional blood volume in the ischemic hemispheres was significantly increased. Baseline regional cerebral blood flow in the ischemic territories was overestimated. Reactivity to acetazolamide of both regional blood flow and fractional blood volume was clearly reduced in the ischemic hemispheres. CONCLUSIONS: The present results demonstrate that the method is a simple and effective means of determining regional cerebral blood volume. Spatial resolution is superior to that of the radioactive tracer methods. Hemodynamic evaluation of ischemic conditions can be performed on the basis of increased resting cerebral blood volume and a diminished increase after acetazolamide. Accuracy of cerebral blood flow measurements, on the other hand, is affected by abnormal cerebral blood volume, and corresponding adjustments need to be made in pathological conditions.

Acetazolamide↗
PubMed1993

Effects of carbonic anhydrase inhibition on ventilation-perfusion matching in the dog lung.

Lung carbonic anhydrase (CA) permits rapid pH responses when changes in regional ventilation or perfusion alter airway and alveolar PCO2. These pH changes affect airway and vascular resistances and lung compliance to optimize the balance of regional ventilation (VA) and perfusion (Q) in the lung. To test the hypothesis that these or other CA-dependent mechanisms contribute to VA/Q matching, we administered acetazolamide (25 mg/kg intravenously) to six anesthetized and paralyzed dogs and measured VA/Q relationships before and after CA inhibition by the multiple inert gas elimination technique. Four other groups of dogs were studied to control for possible confounding effects of time under anesthesia and nonselective CA inhibition by acetazolamide: (a) saline placebo as a control for duration of anesthesia, (b) 4% CO2 inhalation to mimic systemic CO2 retention, (c) 1 mg/kg benzolamide (a selective renal CA inhibitor) or 0.5 meq/kg HCl to mimic systemic metabolic acidosis, and (d) 500 mg/kg 4,4'-dinitrostilbene-2,2'-disulfonate (an inhibitor of red cell band 3 protein) to mimic the respiratory acidosis arising from an intracapillary block to rapid mobilization of plasma HCO3- in CO2 exchange. Acetazolamide increased VA/Q mismatch and reduced arterial PO2 measured at equilibrium but these did not occur in the control group. There was no deterioration in VA/Q matching when systemic respiratory acidosis produced either by CO2 inhalation or 4,4'-dinitrostilbene-2,2'-disulfonate or metabolic acidosis (benzolamide or HCl) were imposed to mimic the effects of acetazolamide apart from its inhibition of lung CA. These results support the concept that lung CA subserves VA/Q matching in the normal lung.

Acetazolamide↗
PubMed1977

On the lack of specificity of the cobalt-bicarbonate method for carbonic anhydrase.

Data are presented that support a nonenzymic mechanism for the staining obtained with the cobalt-bicarbonate method. The biochemically inactive apocarbonic anhydrase and Cu+2 apocarbonic anhydrase stain positively and this stain is inhibited by acetazolamide. The staining of the acetazolamide resistant carbonic anhydrase of male rat liver is inhibited by 10-6 M acetazolamide, at which concentration no biochemical inhibition is observed. There is no correlation between the biochemical and histochemical inhibitory potencies of a number of sulfonamides. The nonsulfonamide inhibitor, KCNO, does not inhibit staining. When incubations are performed in media exposed to atmospheres of increasing CO2 content, staining is not abolished until the atmospheric pCO2 approaches that generated by the medium itself. This finding renders the carbonic anhydrase catalyzed dehydration of HCO3- an improbable reaction for the staining. Studies with modified media show differences in staining patterns and in sensitivity to acetazolamide inhibition which question the specificity of the method for carbonic anhydrase.

Acetazolamide↗
PubMed1982

Carbonic anhydrase activity in skeletal muscle fiber types, axons, spindles, and capillaries of rat soleus and extensor digitorum longus muscles.

Carbonic anhydrase (CA) activities were studied in soluble extracts and cryostat sections of skeletal muscles from prepubertal and postpubertal rats. Acetazolamide inhibition was utilized to distinguish between activities of the acetazolamide-sensitive (CA I and II) and acetazolamide-resistant (CA III) forms of the enzyme. The inhibition studies indicated that fast-twitch oxidative-glycolytic muscle fibers contained both the sensitive and resistant forms of CA. Acetazolamide-sensitive activity was localized within muscle fibers, axons, myelin, and capillaries. Axoplasmic staining was restricted to subpopulations of myelinated axons in both the dorsal and ventral roots. Soleus muscles exhibited significantly greater activity of CA III than extensor digitorum longus muscles at all ages examined. CA III was richest in slow-twitch oxidative and intrafusal fibers. During puberty, soleus muscle fibers matured and converted from fast-twitch oxidative-glycolytic to slow-twitch oxidative fibers. There was a shift from the sensitive to the resistant form of CA; CA III activity increased about sevenfold. This activity peaked earlier in the muscles of female rats than male rats. These results demonstrated a complex distribution of CA isozymes in the neuromuscular system and pointed out that isozyme content depends on both the type of muscle and the age and sex of the animal.

Acetazolamide↗
PubMed2002

Enzyme replacement reverses abnormal cerebrovascular responses in Fabry disease.

BACKGROUND: Fabry disease is a lysosomal X-linked enzyme deficiency of alpha-galactosidase A associated with an increased mortality and morbidity due to renal failure, cardiac disease and early onset stroke. METHODS: We examined the functional blood flow response of the brain after visual stimulation (reversing checkerboard pattern), and cerebral vasoreactivity following acetazolamide (15 mg/kg) with [15O]H2O and positron emission tomography (PET) in Fabry disease. Twenty-six hemizygous patients (age range 19-47 years) were enrolled in a randomized double-blind placebo-controlled 6-month trial of enzyme replacement therapy administered by intravenous infusion every two weeks. Regional cerebral blood flow (rCBF) was measured with PET at the beginning and end of the trial. RESULTS: Fabry patients had a significantly greater increase in rCBF following visual stimulation and acetazolamide challenge compared to controls. Visual reactivity was normal. The time for recovery of the cerebral vasculature following acetazolamide was prolonged in Fabry patients compared to controls. The abnormal rCBF response induced by visual stimulation and acetazolamide decreased significantly following enzyme replacement therapy, as did the prolonged recovery of the cerebral vasculature. CONCLUSIONS: Enzyme replacement therapy reverses the exaggerated cerebrovascular response in Fabry disease.

Acetazolamide↗
PubMed1981

Ontogenesis of gastric acid secretion in fetal rat.

The pH of gastric fluid was measured in rat fetuses during the last 3 days of gestation. On day 19, the gastric pH was close to neutral. During the night of day 20, the pH was clearly lowered (6.11 +/- 0.15 units), this decrease becoming more marked on the following day. At birth (day 22), just before the first feeding, the pH of gastric fluid reached the mean value of 2.98 +/- 0.14 units. This drop in gastric pH was concomitant with an increase in chloride concentration whereas the gastric PCO2 remained constant. These results imply that in term rat fetuses, the gastric mucosa secretes fixed acid, very likely hydrochloride acid. The administration of acetazolamide (inhibitor of carbonic anhydrase) to 20-day-old fetuses did not suppress the spontaneous acidification of gastric fluid, although the enzyme activity was reduced by approximately 80%. Moreover, the gastric pH in acetazolamide-injected fetuses was markedly lower than in the noninjected littermates. The administration of NaCl solution (acetazolamide vehicle) had no effect on the carbonic anhydrase activity but clearly decreased the pH of gastric fluid. Thus, the drop of gastric pH produced by injection of acetazolamide or saline solution alone probably results from a stress effect of puncture. In fetuses from adrenalectomized, metopirone-treated mothers, the injection of NaCl solution no longer had effect on the pH of gastric fluid whereas triamcinolone injection produced a clear decrease in the gastric pH 3 hr latter.

Acetazolamide↗
PubMed1979

Acute therapeutic modalities for experimental vasogenic edema.

Experimental vasogenic cerebral edema was created in rabbits with a cold-induced left occipital cortical lesions. Intracranial pressure (ICP), intracranial elastance (Em), water content, hemispheric brain tissue volume, electrolytes, electroencephalograms, behavior, and gross pathology were studied. Various therapeutic modalities were employed alone or in combination to reduce ICP acutely: acetazolamide, furosemide, mannitol, pentobarbital, lorazepam, and dexamethasone. All therapies except dexamethasone were effective in reducing ICP. Peak ICP reduction occurred at 27 +/- 9.8 (SD) minutes with mannitol and at 71.4 +/- 15.5 minutes with acetazolamide, with the remaining agents and combinations falling between these two extreme values. Em improved by 31.7 +/- 17.02% in all therapuetic trials except those employing acetazolamide and lorazepam. With therapy, there was a reduction in the water content of the hemispheres, but the difference from that in the untreated, lesioned animals was not statistically significant. In the lesioned left hemisphere, sodium content was increased by acetazolamide (p less than 0.005), furosemide (p less than 0.025), pentobarbital (p less than 0.05), and the combination of dexamethasone, pentobarbital, and mannitol (p less than 0.005). Significant reduction was noted in the lesioned group for the potassium content of the left hemisphere in the dexamethasone (p less than 0.05), pentobarbital (p less than 0.025), and combination groups containing these agents (p less than 0.005 to 0.025). (Neurosurgery, 5: 656--665, 1979).

Acetazolamide↗
PubMed1999

Does gill boundary layer carbonic anhydrase contribute to carbon dioxide excretion: a comparison between dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss).

In vivo experiments were conducted on spiny dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss) in sea water to determine the potential role of externally oriented or gill boundary layer carbonic anhydrase in carbon dioxide excretion. This was accomplished by assessing pH changes in expired water using a stopped-flow apparatus. In dogfish, expired water was in acid-base disequilibrium as indicated by a pronounced acidification (delta pH=-0.11+/-0.01; N=22; mean +/- s.e.m.) during the period of stopped flow; inspired water, however, was in acid-base equilibrium (delta pH=-0.002+/-0.01; N=22). The acid-base disequilibrium in expired water was abolished (delta pH=-0.005+/-0.01; N=6) by the addition of bovine carbonic anhydrase (5 mg l-1) to the external medium. Addition of the carbonic anhydrase inhibitor acetazolamide (1 mmol l-1) to the water significantly reduced the magnitude of the pH disequilibrium (from -0.133+/-0.03 to -0.063+/-0.02; N=4). However, after correcting for the increased buffering capacity of the water caused by acetazolamide, the acid-base disequilibrium during stopped flow was unaffected by this treatment (control delta [H+]=99.8+/-22.8 micromol l-1; acetazolamide delta [H+]=81.3+/-21.5 micromol l-1). In rainbow trout, expired water displayed an acid-base disequilibrium (delta pH=0.09+/-0.01; N=6) that also was abolished by the application of external carbonic anhydrase (delta pH=0.02+/-0.01). The origin of the expired water acid-base disequilibrium was investigated further in dogfish. Intravascular injection of acetazolamide (40 mg kg-1) to inhibit internal carbonic anhydrase activity non-specifically and thus CO2 excretion significantly diminished the extent of the expired water disequilibrium pH after 30 min (from -0.123+/-0.01 to -0.065+/-0.01; N=6). Selective inhibition of extracellular carbonic anhydrase activity using a low intravascular dose (1.3 mg kg-1) of the inhibitor benzolamide caused a significant reduction in the acid-base disequilibrium after 5 min (from -0.11+/-0.01 to -0.07+/-0. 01; N=14). These results demonstrate that the expired water acid-base disequilibrium originates, at least in part, from excretory CO2 and that extracellular carbonic anhydrase in dogfish may have a significant role in carbon dioxide excretion. However, externally oriented carbonic anhydrase (if present in dogfish) plays no role in catalysing the hydration of the excretory CO2 in water flowing over the gills and thus is unlikely to facilitate CO2 excretion.

Acetazolamide↗
PubMed1977

Effects of diuretics on calcium excretion and Ca2+-activated ATPase in rat kidney.

Effects of three diuretics on the urinary Ca2+ excretion and on the microsomal Ca2+-activated ATPase were examined in the rat kidney. Furosemide and bumetanide increased Na+, K+, and Ca2+ excretion in the rats. Acetazolamide increased Na+ and K+ excretion but not Ca2+. Urinary inorganic phosphate excretion was not affected during the administration of acetazolamide. It is suggested that acetazolamide inhibits Na+ transport without affecting Ca2+ reabsorption in the rat nephron. Microsomal ATPase of the rat kidney cortex was stimulated by Ca2+ or Mg2+ alone and an additive effect of the two cations was not observed. Microsomal ATPase activated by Ca2+ or Mg2+ was not inhibited by furosemide, bumetanide, and acetazolamide. These data suggest that the inhibitory effect of furosemide and bumetanide on the Ca2+ reabsorption is not related to the inhibition of Ca2+-activated ATPase.

Acetazolamide↗
PubMed1989

[Measurement of cerebral blood flow by single photon emission computed tomography in cases of internal carotid artery occlusion].

Cerebral blood flow (CBF) was measured with 133xenon inhalation and single photon emission computed tomography in 33 cases of internal carotid artery occlusion, in the resting state and 25 minutes after acetazolamide (Diamox) administration. The patient population consisted of 24 males and nine females with a mean age of 57 years, who presented with transient ischemic attacks or stroke. Acetazolamide inhibits carbonic anhydrase, and CBF increases as a result of dilatation of cerebral arteries due to CO2 accumulation. The mean CBF was 46 ml/100/g/min on the affected hemisphere and 56 ml/100/g/min on the unaffected hemisphere. The mean CBF value obtained by the same method in 10 normal volunteers was 55 ml/100/g/min. Thus, in the patients, CBF decreased on the affected side. The average increase in CBF after acetazolamide administration was 9% on the affected side and 17% on the unaffected side. The average increase in 10 normal volunteers was 32%. The reduced cerebral arterial reactivity to acetazolamide administration was bilateral in the patient group, which suggests that the cerebral arteries were dilated in order to maintain normal CBF. Extra-intracranial (EC-IC) bypass surgery was performed in nine patients. Preoperatively, the mean CBF was 48 ml/100 g/min on the affected side and 57 ml/100 g/min on the unaffected side; the postoperative CBF was 48 ml/100 g/min on the affected side and 56 ml/100 g/min on the unaffected side. Thus, there was no notable change in CBF on either side after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1996

Cerebral blood flow in normal brain tissue of patients with intracranial tumors.

Pre- and postoperative cerebral blood flow (CBF) changes in the normal brain tissue of 17 patients with intracranial tumors were studied to determine the value for planning therapeutic strategy. The tumors included eight astrocytomas, seven meningiomas, one metastasis, and one arachnoid cyst. The patients were divided into two groups based on the mass effect seen on computed tomography (CT) scans. Group A comprised six patients with midline shift or evidence of herniation; Group B, 11 patients with no mass effect or local compression only. CBF and vasoresponse to acetazolamide were measured in the bilateral hemispheres, cortices, and thalami using xenon-enhanced CT, excluding the area of tumor extension, before and 2-3 weeks after tumor excision. Preoperative CBF was reduced bilaterally but more markedly ipsilateral to the tumor. The CBF reduction was significantly greater in Group A than in Group B. Acetazolamide caused CBF to increase by 70.5-99.1% in Group B but only increase by 1.7-9.6% or paradoxically decrease in Group A. Postoperatively, the CBF tended to recover partially in Group A but persisted or deteriorated in Group B. The more pronounced CBF reduction and poor or paradoxical response to acetazolamide preoperatively and postoperative CBF restoration in Group A may indicate that ischemia was more important than metabolic depression in these patients. In contrast, the excessive response to acetazolamide and the postoperative CBF deterioration in Group B may indicate that CBF reduction was secondary to metabolic depression. Mass effect is a key predictor for functional recovery following surgical decompression of intracranial tumors.

Acetazolamide↗
PubMed1979

Re-examination of the dose-reponse relationship for the renal effect of acetozolamide.

To examine the effect of acetazolamide on tubular reabsorption of bicarbonate, plasma concentrations of bicarbonate, potassium and PCO2 were kept constant in volume expanded dogs. Intravenous infusion of acetazolamide reduced glomerular filtration rate (GFR) at all dose levels; after a dose of 30 mg/kg body wt GFR was reduced by about 30% and was not reduced further by increasing the infused dose of acetazolamide up to 500 mg/kg body wt. When control GFR was restored by raising systemic blood pressure, increments in filtered and excreted bicarbonate were not significantly different. At control GFR a linear relationship was obtained between bicarbonate reabsorption and log dose when acetazolamide was administered intravenously in doses ranging between 0.3 and 500 mg/kg body wt (r = 0.93). We conclude that a log dose-reponse relationship applies over a 25 times larger dose range than previously assumed.

Absorption↗
PubMed1995

Percutaneous transluminal angioplasty in the treatment of atherosclerotic disease of the anterior cerebral circulation and hemodynamic evaluation.

Nineteen patients between 56 and 76 years of age with clinically symptomatic atherosclerotic stenotic lesions at or distal to the C-5 segment in the carotid arterial system underwent percutaneous transluminal angioplasty (PTA). The 19 patients had a total of 19 stenotic lesions, including two lesions in the C-5 segment, three in the C-4 segment, and three in the C-2 segment of the carotid artery, six in the M1 segment and three in the M2 segment of the middle cerebral artery, and two in the A2 segment of the anterior cerebral artery. Both prior to and more than 6 months after PTA, angiograms were performed and cerebral perfusion was measured using 99mTc-hexamethyl-propyleneamine-oxime single-photon emission computerized tomography, before and after the administration of 10 mg/kg acetazolamide. Percutaneous transluminal angioplasty could be performed in 13 (68.4%) of the 19 patients. The mean degree of stenosis (+/- standard deviation) was 83.1% +/- 8.6% before PTA, but only 35.8% +/- 17.3% on the follow-up angiograms. Restenosis was detected in follow-up angiograms in five (38.5%) of the 13 patients. Seven of the 13 patients exhibited improvement in their neurological condition after PTA and had shown subnormal cerebral perfusion and subnormal vasodilatory response to administration of acetazolamide prior to undergoing PTA. On the other hand, the remaining six patients exhibited no improvement in neurological condition after PTA, and four of these patients (66.7%) had shown normal perfusion and five (83.3%) had shown normal vasodilatory response to administration of acetazolamide prior to undergoing PTA. These findings suggest that PTA may be indicated for patients with atherosclerotic stenotic lesions in the anterior cerebral circulation who have subnormal cerebral perfusion and low vasodilatory response to administration of acetazolamide.

Acetazolamide↗