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PubMed1985

Effect of Carbonic Anhydrase Inhibitors on Inorganic Carbon Accumulation by Chlamydomonas reinhardtii.

Membrane-permeable and impermeable inhibitors of carbonic anhydrase have been used to assess the roles of extracellular and intracellular carbonic anhydrase on the inorganic carbon concentrating system in Chlamydomonas reinhardtii. Acetazolamide, ethoxzolamide, and a membrane-impermeable, dextran-bound sulfonamide were potent inhibitors of extracellular carbonic anhydrase measured with intact cells. At pH 5.1, where CO(2) is the predominant species of inorganic carbon, both acetazolamide and the dextran-bound sulfonamide had no effect on the concentration of CO(2) required for the half-maximal rate of photosynthetic O(2) evolution (K(0.5)[CO(2)]) or inorganic carbon accumulation. However, a more permeable inhibitor, ethoxzolamide, inhibited CO(2) fixation but increased the accumulation of inorganic carbon as compared with untreated cells. At pH 8, the K(0.5)(CO(2)) was increased from 0.6 micromolar to about 2 to 3 micromolar with both acetazolamide and the dextran-bound sulfonamide, but to a higher value of 60 micromolar with ethoxzolamide. These results are consistent with the hypothesis that CO(2) is the species of inorganic carbon which crosses the plasmalemma and that extracellular carbonic anhydrase is required to replenish CO(2) from HCO(3) (-) at high pH. These data also implicate a role for intracellular carbonic anhydrase in the inorganic carbon accumulating system, and indicate that both acetazolamide and the dextran-bound sulfonamide inhibit only the extracellular enzyme. It is suggested that HCO(3) (-) transport for internal accumulation might occur at the level of the chloroplast envelope.

Journal Article↗

PubMed1976

A method for screening diuretic agents in the mouse: an investigation of sexual differences.

Acetazolamide, aminophyline, frusemide, ethacrynic acid and triamterene were tested for diuretic action at dosages of 3, 10 and 30 mg kg-1 (s.c.) in male and female mice. Each drug significantly raised sodium excretion and all but acetazolamide elevated urine volume and chloride excretion. Potassium excretion was significantly raised by acetazolamide and frusemide. Acetazolamide and triamterene evoked urinary alkalinization whereas frusemide and ethacrynic acid reduced urinary pH. Female mice were markedly more sensitive than males to the diuretic, natriuretic, chloruretic and urinary acidfying actions of ethacrynic acid.

Animals↗

PubMed1980

Effects of sugars, amino acids and inhibitors on electrolyte transport across hen colon at different sodium chloride intakes.

1. The isolated colonic mucosa from adult hens has been studied in vitro under short-circuit conditions. Colonic mucosa was prepared from hens fed either a NaCl-poor or a NaCl-rich diet. 2. The unidirectional transmucosal fluxes of chloride, K and Na were measured. For the high NaCl colon the fluxes of lysine were also measured. The effects of galactose, glucose, leucine, lysine, amiloride (10(-4) M) and acetazolamide (5 X 10(-4) M) on the short-circuit current (Isc) were examined. 3. The Isc of the high NaCl colon was stimulated by galactose, glucose, leucine and lysine in a manner which suggests that these substances were transported by the epithelium in co-transport with Na. The Isc was in most cases insensitive to amiloride (mucosal side), but moderately stimulated by acetazolamide (serosal side). The Isc was closely matched by the sum of the net transmucosal fluxes of chloride, lysine, K and Na. The effects of galactose, leucine and lysine on the Isc were maintained only when glucose was present on the serosal side of the preparations. 4. The Isc of the low NaCl colon depended on the presence of glucose on the serosal (or mucosal) side. It was not stimulated by galactose or by lysine, but leucine did stimulate when added to the mucosal solution. Adding amiloride on the mucosal side invariably eliminated or, in most cases, led to an inversion of the Isc. Acetazolamide markedly stimulated the Isc; and, when added after amiloride, acetazolamide caused the Isc to become positive again. The data on Isc and net fluxes of chloride, lysine, K and Na are consistent with the presence of a process of bicarbonate absorption or H ion secretion. 5. There is a net secretion of K across both the high and the low Na colon, which is highest in the former although both Isc and net absorption of Na are highest in the latter. 6. The results from both types of colon suggest that the transport of chloride differs with the functional status of tissues.

Amiloride↗

PubMed1985

Cl- requirement for saliva secretion in the isolated, perfused rat submandibular gland.

Replacement of perfusate Cl- with Br- reduced by 37% the volume of saliva secreted by isolated, perfused rat submandibular glands exposed to 10(-6) M acetylcholine. Replacement of perfusate Cl- with SO4(2-) reduced fluid secretion by 73%, while replacement of bicarbonate with HEPES or addition of acetazolamide had no effect on salivary flows or volumes. Furosemide (10(-3) M) reduced saliva secretion when added to Cl- -(73%) or Br- -containing (56%) perfusates and also to HEPES- (95%) or acetazolamide-containing (82%) perfusates. Perfusion of the glands with furosemide or SO4- containing perfusates resulted in significantly reduced salivary Cl- concentrations and increased residual anion (Na+-K+-Ca2+-Cl-) concentrations, while perfusion with solutions containing acetazolamide or with HCO3- -free (HEPES) perfusates resulted in opposite changes in salivary anions. Addition of furosemide to HEPES- or acetazolamide-containing perfusates reversed these changes and caused a reduction in salivary Cl- concentrations and an increase in residual anion concentrations. It is concluded that 1) extracellular Cl- is required for saliva secretion in the rat submandibular gland, 2) the required external Cl- enters the salivary cells by a furosemide-sensitive transport system, which is likely to be similar to a Na+-K+-Cl- cotransport system described in other epithelia, 3) HCO3- is not normally required for saliva secretion but can sustain it partially when Cl- transport is inhibited by either furosemide or Cl- replacement, and 4) salivary electrolyte changes induced by Cl- or HCO3- replacement or by furosemide probably represent combined effects on acinar secretion and transductal electrolyte transport.

Animals↗

PubMed1989

Regulation of erythropoietin production is related to proximal tubular function.

Regulation of renal erythropoietin (EPO) production is based on an intrarenal oxygen sensor. Whereas the sensitivity of this oxygen sensor to variations in renal oxygen supply is well established, the influence of changes in renal oxygen consumption has not yet been elucidated. Diuretic drugs, which inhibit active sodium reabsorption, reduce tubular oxygen consumption. We therefore investigated the effects of acetazolamide, furosemide, hydrochlorothiazide, and amiloride, known to preferentially inhibit sodium reabsorption at different segments of the nephron, on hypoxia-induced EPO formation in mice. Those drugs that are considered to act mainly in the loop of Henle, distal tubule, and collecting duct (furosemide, hydrochlorothiazide, and amiloride) did not impair EPO formation. Acetazolamide on the other hand, which is thought to act predominantly at the proximal tubular site, significantly reduced EPO formation in response to normobaric hypoxia (8 and 14% O2) and functional anemia (0.1% carbon monoxide). This inhibitory effect of acetazolamide was dose dependent and correlated with the natriuresis induced. It appeared not to depend on the metabolic acidosis induced by the drug, since the simultaneous administration of sodium bicarbonate, which restored standard bicarbonate levels to normal, did not diminish the inhibitory effect of acetazolamide on EPO production. In conclusion the data suggest that the regulation of EPO production is likely to be related to proximal tubular function.

Animals↗

PubMed1995

[The time required topical carbonic anhydrase inhibitor (MK-507) to take effect on intraocular pressure of normal human eyes].

The effective time course of a topical carbonic anhydrase inhibitor, MK-507, on intraocular pressure (IOP) was studied in 6 normal volunteers. As a baseline study, IOP was determined and aqueous protein concentration was determined by laser flare photometry every half hour for 5 hours with the instillation of a placebo. Then, an examination with the same time course was performed on the same subjects with the instillation of 1% MK-507 or oral administration of acetazolamide at a dose of 250 mg. MK-507 lowered IOP 30 minutes after the instillation, and showed a significant reduction of IOP at 1 hour. Aqueous protein concentration increased significantly 30 minutes after the MK-507 instillation. Acetazolamide lowered IOP 30 minutes after the administration, and showed a significant reduction of IOP at one hour. Aqueous protein concentration increased significantly one hour after the acetazolamide administration. Corneal thickness, anterior chamber depth, anterior chamber volume, and serum protein concentration were not significantly changed by the drug treatment. These results suggest that the inhibition of aqueous humor production causes the rapid reduction of IOP seen in the use of MK-507 as well as acetazolamide.

Administration, Topical↗

PubMed2000

Interactions between carbonic anhydrase and its inhibitors revealed by gel electrophoresis and circular dichroism.

Structural properties, and especially the differential stability, of complexes between carbonic anhydrase (CA) and three sulfonamide inhibitors, acetazolamide, dorzolamide and methazolamide, were investigated by spectroscopic and electrophoretic techniques. These included denaturant gradient gel electrophoresis either across a urea or a steady-state transverse sodium dodecyl sulfate (SDS) gradient. Acetazolamide, the smallest and most hydrophilic of the sulfonamides, forms the most stable complex in the presence of urea, whereas dorzolamide, with a bulky and hydrophobic structure, is most stable against the effects of SDS. At pH 7.4, complexes with dorzolamide show minimal changes in mobility across the SDS gradient, as if unaffected by the detergent, both in the presence and in the absence of excess ligand in the gel. When bound to both acetazolamide and methazolamide, on the other hand, CA displays an increase in mobility above 0.05% SDS, lower in the presence than in the absence of excess ligand. The finding of a distinct pattern for the unliganded enzyme, however, suggests the complexes can still retain the ligand, although binding of the surfactant changes their charge density. Under saturating conditions and in the presence of SDS, the surface charge of all complexes is much lower than for unliganded, denatured CA. Circular dichroism (CD) spectra clearly indicate that the increase in secondary structure and the decrease in tertiary structure brought about in CA by the presence of low concentrations of SDS are largely prevented by complexing with the inhibitors. These observations point out peculiar properties of each CA inhibitor, of potential value in the definition of their biological activities and also in the potential development of novel antagonist molecules.

Acetazolamide↗

PubMed2004

Functional implications of a novel EA2 mutation in the P/Q-type calcium channel.

Episodic ataxia type 2 (EA2) is an autosomal dominant condition characterized by paroxysmal attacks of ataxia, vertigo, and nausea, typically lasting minutes to days in duration. These symptoms can be prevented or significantly attenuated by the oral administration of acetazolamide; however, the mechanism by which acetazolamide ameliorates EA2 symptoms is unknown. EA2 typically results from nonsense mutations in the CACNA1A gene that encodes the alpha1A (Cav2.1) subunit of the P/Q-type calcium (Ca2+) channel. We have identified a novel H1736L missense mutation in the CACNA1A gene associated with the EA2 phenotype. This mutation is localized near the pore-forming region of the P/Q-type Ca2+ channel. Functional analysis of P/Q-type channels containing the mutation show that the H1736L alteration affects several channel properties, including reduced current density, increased rate of inactivation, and a shift in the voltage dependence of activation to more positive values. Although these findings are consistent with an overall loss of P/Q-type channel function, the mutation also caused some biophysical changes consistent with a gain of function. We also tested the direct effect of acetazolamide on both wild-type and H1736L mutated P/Q-type channels and did not observe any direct action on channel properties of this pharmacological agent used to treat EA2 patients.

Acetazolamide↗

PubMed1998

Carbonic anhydrase II plays a major role in osteoclast differentiation and bone resorption by effecting the steady state intracellular pH and Ca2+.

Carbonic anhydrase II (CA II) expression in characteristic for the early stage of osteoclast differentiation. To study how CA II, which is crucial in proton generation in mature osteoclasts, influences the osteoclast differentiation process we performed rat bone marrow cultures. In this model, acetazolamide, a specific CA inhibitor, decreased the 1,25 (OH)2D3-induced formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells, in a dose-dependent manner. We then performed intracellular pH (pHi) and Ca2+ (Cai2+) measurements for cultured osteoclasts and noticed that addition of acetazolamide caused a rapid, transient increase of both parameters. The increase in pHi was dependent neither on the culture substrate nor on the extracellular pH (pHe) but the increase could be diminished by DIDS or by bicarbonate removal. Membrane-impermeable CA inhibitors (benzolamide and pd5000) did not have this effect. Addition of CA II antisense oligonucleotides into the cultures reduced the pHi increase significantly. CA II inhibition was also found to neutralize the intracellular vesicles at extracellular pH (pHe) of 7.4, but at less extent at pHe 7.0. In mouse calvaria cultures, bone resorption was inhibited dose dependently by acetazolamide at pHe 7.4 while inhibition was smaller at pHe 7.0. We conclude that CA II is essential not only in bone resorption but also in osteoclast differentiation. In both processes, however, the crucial role of CA II is at least partially due to the effect on the osteoclast pHi regulation.

Acetazolamide↗

PubMed1995

Regional cerebral hemodynamics in childhood moyamoya disease.

Regional cerebral blood flow (rCBF) and its reactivity to acetazolamide were analyzed in a series of 15 cases of childhood moyamoya disease, using the xenon-133 inhalation method and single photon emission CT (SPECT). Most of the patients had normal mean hemispheric cerebral blood flow (mCBF), comparable to that of age-matched healthy children. However, they had abnormal rCBF distribution and disturbed reactivity to acetazolamide in the territory of the internal carotid artery, especially in the frontal lobe. Surgical revascularization for the anterior circulation, which consisted of STA-MCA anastomosis and indirect synangiosis, dramatically improved these cerebral hemodynamics in the anterior circulation, including the frontal lobe, and reactivity to acetazolamide in the whole brain. These results suggest that surgical revascularization for the anterior circulation should be carried out in order to improve cerebral hemodynamics as widely as possible, especially in the frontal lobe, and may improve cerebral perfusion reserve in the posterior circulation.

Acetazolamide↗

PubMed1978

Phosphate transport in the proximal convolution of the rat kidney. III. Effect of extracellular and intracellular pH.

Inorganic phosphate (Pi) transport was evaluated using the standing droplet method with simultaneous microperfusion of the peritubular capillaries. To evaluate rather small differences in Pi transport and to eliminate the influence of tubular heterogeneity, the technique of crossed paired samples was applied. 1. In chronic PTX rats changing the luminal or both luminal and peritubular pH by varying the HCO-3-concentration between 4 and 50 mmol/l at constant 5% CO2 had no influence on Pi transport. 2. If, however, bicarbonate was omitted from the perfusate and 2 mmol/l phosphate (pH 7.4) was the only buffer, Pi transport was decreased from the control. It was, however, further reduced when the perfusates were gased with 5% CO2 i.e. the starting pH was 5.6. 3. When the solutions contained HEPES buffer (25 mmol/l), Pi transport at pH 8 was much larger than at pH 6.0. 4. Raising the CO2 pressure from 35 to 70 mm Hg did not change the Pi transport when both perfusates had a HCO-3-concentration of 25 mmol/l. It reduced, however, the Pi transport, when the luminal perfusate had only 4 mmol/l bicarbonate. 5. Lowering the CO2 pressure from 38 to 7.6 mm Hg did hardly change the Pi transport when the luminal perfusate contained 4 mmol/l bicarbonate. It lowered, however, the Pi transport significantly when the luminal perfusate had 2k mmol/l bicarbonate. 6. Acetazolamide, 10-4M, lowered the Pi transport when the luminal perfusate contained 4 or 25 mmol/l bicarbonate. At 4 mmol/l luminal HCO-3, raising the pCO2 to 228 mmol/l depressed Pi transport even more. At 25 mmol/l luminal bicarbonate, raising the pCO2 from 38 to 114 mm Hg reversed the acetazolamide inhibition of the Pi transport almost completely. The data indicate that luminal acidosis and intracellular alkalosis inhibits the transtubular Pi transport. A shift of the intracellular pH to a more alkaline value seems to be responsible for the inhibition of Pi transport by acetazolamide, while omission of buffer from the perfusate inhibits Pi transport by effecting an acidic luminal pH.

Acetazolamide↗

PubMed1987

Electrophysiological identification of principal and intercalated cells in the rabbit outer medullary collecting duct.

Intracellular microelectrode techniques were used together with inhibitors of Na+ transport (amiloride) and H+ transport (acetazolamide and SITS) to identify principal cells and intercalated cells in the outer stripe of the rabbit outer medullary collecting duct. The principal cell (n = 9) had a basolateral membrane voltage (Vbl) of -64.7 +/- 3.2 mV, a fractional resistance of the apical membrane (fRa = Ra/Ra + Rbl) of 0.82 +/- 0.02, and a K+-selective basolateral membrane. Luminal amiloride hyperpolarized Vbl by 10.3 +/- 2.1 mV and increased fRa to near unity (n = 7). Bath acetazolamide and SITS were without effect on these parameters. The intercalated cell (n = 5) had a Vbl of -25.0 +/- 3.2 mV, a fRa of 0.99 +/- 0.01, and a Cl(-)-selective basolateral membrane. Bath acetazolamide or SITS hyperpolarized Vbl by 26.4 +/- 8.2 mV. Luminal amiloride did not alter Vbl of this cell. The differential effects of the inhibitors also indicate that the principal and intercalated cells are probably not directly coupled electrically.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1976

H in cortical peritubular capillaries of rat kidney.

The pH of peritubular capillaries was measured by means of antimony microelectrodes, during their perfusion with mammalian Ringer's solutions at different pH, in control and acetazolamide infused rats. In capillaries perfused with a solution more acid than blood, significant alkalinization was observed at increasing distances from the point of perfusion, while during perfusions with more alkaline solutions, acidification was observed. Plotting the pH change observed per micrometer of distance from the perfusion point against the pH of the perfusing solution, the pH in equilibrium with tubular cells was interpolated. A value of 7.51 +/- 0.01 was found for control rats, significantly higher than the mean arterial blood pH of this group, of 7.39. In acetazolamide infused rats an equilibrium pH of 7.44 +/- 0.02 was found, still higher than the blood pH of 7.34. The slope of these lines was significantly greater in control than in acetazolamide treated rats. This slope was shown to evaluate permeability to the ions responsible for acid-base balance. The present data suggest that peritubular alkalinization is reduced after carbonic anhydrase inhibition due to decreased peritubular permeability to the involved ions, which represents a further site of action of these inhibitors.

Acetazolamide↗

PubMed1981

Intracranial hypertension and brain oedema in albino rabbits. Part 2: Effects of acute therapy with diuretics.

Increased intracranial pressure due to brain oedema was produced in albino rabbits by combining a cryogenic lesion in the left hemisphere with the intraperitoneal administration of 6-aminonicotinamide (cytotoxic agent). The most effective reduction in ICP (74%) was achieved when furosemide and mannitol were used in combination. When either mannitol or furosemide was employed alone, the average ICP reduction was approximately 53%. Peak ICP reduction occurred at 45 minutes with furosemide, 30 minutes with mannitol and furosemide combined, and at 60 minutes with a combination of mannitol and acetazolamide. Also studied simultaneously in these animals were investigated elastance (Em), brain water content, hemispheric water volume content, electrolytes, EEG, and gross pathology. Following therapy there was a statistically significance reduction of water content in the left hemisphere (cryogenic lesion) by all therapeutic modalities except with furosemide alone. In the right hemisphere the water content was reduced by furosemide and the furosemide-mannitol combination but not by the association of mannitol with acetazolamide. A significant decrease of brain sodium was noted only for the combination of mannitol and furosemide. This study indicates that effective reduction of cytotoxic-cryogenic brain oedema and intracranial hypertension can be obtained with a variety of diuretic agents. From the standpoint of tissue dehydration, restoration of tissue electrolyte balance, and rate of ICP reduction, the combination of furosemide-mannitol appears to offer advantages over furosemide alone, or acetazolamide-mannitol.

Acetazolamide↗

PubMed1994

Role of carbonic anhydrase in basal and stimulated bicarbonate secretion by the guinea pig duodenum.

The role of carbonic anhydrase in the process of proximal duodenal mucosal bicarbonate secretion was investigated in the guinea pig. In a series of experiments in vivo, the duodenum was perfused with 24 mmol/liter NaHCO3 solution (+ NaCl for isotonicity) to ensure that active duodenal HCO3- secretion against a concentration gradient was measured. Acetazolamide (80 mg/kg) was infused intravenously to examine the role of carbonic anhydrase on basal and agonist-stimulated HCO3- secretion. Acetazolamide abolished basal HCO3- secretion and significantly decreased HCO3- secretion after stimulation with dibutyryl 5'-cyclic adenosine monophosphate (dBcAMP, 10(-5) mol/kg), dibutyryl 5'-cyclic guanosine monophosphate (dBcGMP, 10(-5) mol/kg), prostaglandin E2 (PGE2, 10(-6) mol/kg), PGF2 alpha (10(-6) mol/kg), tetradecanoyl-phorbol-acetate (TPA, 10(-7) mol/kg), glucagon (10(-7) mol/kg), vasoactive intestinal polypeptide (VIP, 10(-8) mol/kg), and carbachol (10(-8) mol/kg). Utilizing a fluorescence technique, we could detect the enzyme carbonic anhydrase in equal amounts in villous and crypt cells of the proximal duodenal epithelium; no activity was demonstrated in tissues pretreated with acetazolamide. In conclusion, carbonic anhydrase is required for both basal and stimulated duodenal HCO3- secretion.

Acetazolamide↗

PubMed1985

Role of carbonic anhydrase in bone resorption induced by 1,25 dihydroxyvitamin D3 in vitro.

The present investigation was undertaken to study the role of carbonic anhydrase in 1,25 dihydroxyvitamin D3-induced bone resorption. Calvaria were removed from 5- to 6-day-old mice and cultured for periods up to 96 h in Dulbecco's Modified Eagle Medium (high glucose, 4,500 mg/dl) supplemented with antibiotics and either heat-inactivated horse and fetal calf sera or bovine serum albumin. The experimental cultures contained 1 X 10(-8) M 1,25 dihydroxyvitamin D3 (1,25(OH)2D3). All cultures were incubated at 37 degrees C in 5% CO2/95% air. Bone resorption was assessed by release of stable calcium into the medium. Bone enzymes (acid and alkaline phosphatases and carbonic anhydrase) were determined following homogenization in 0.25 M sucrose. The effects of 1,25(OH)2D3 were studied in the presence and absence of the carbonic anhydrase inhibitor acetazolamide and its analogue (CL 13,850), which lacks inhibitory activity. Acetazolamide inhibited 1,25(OH)2D3-induced calcium release in a dose-dependent fashion from 10(-5)-10(-4)M. When added to the cultures at a concentration of 1 X 10(-4)M, acetazolamide completely blocked the 1,25(OH)2D3-induced calcium release, a phenomenon not seen with an equimolar concentration of CL 13,850. The most significant finding was that 1,25(OH)2D3-induced calcium release was accompanied by a significant increase in the carbonic anhydrase activity of bone at both 48 (treated/control ratio = 2.05) and 96 (treated/control ratio = 2.59) hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗

PubMed2000

Sodium bromide: effects on different patterns of epileptiform activity, extracellular pH changes and GABAergic inhibition.

Results regarding the anticonvulsant potency of bromide have been questioned, and the mechanisms of its action are unclear. Using combined rat hippocampus-entorhinal cortex slices we analyzed the effects of NaBr on four types of epileptiform discharges in two different models of epilepsy, the low-Ca2+ and the low-Mg2+ model. NaBr concentration-dependently reduced the frequency and finally blocked the low Ca2+-induced discharges. Low Mg2+-induced short recurrent discharges were also reduced in a concentration-dependent manner. In the entorhinal cortex the frequency of seizure-like events was reduced by 3 and 5 mM and the discharges were blocked by 7 mM NaBr. Also, the late recurrent discharges in the entorhinal cortex which do not respond to most clinically employed anticonvulsants were reduced by concentrations of 10 and 15 mM and completely blocked by 30 mM NaBr. Using pH-sensitive microelectrodes different effects of NaBr were seen than those of acetazolamide on extracellular pH under control conditions and after stimulation. Acetazolamide at 1 mM caused a reversible acidification of delta pH: 0.2+/-0.14 at rest whereas no change on extracellular pH was seen with 5 mM NaBr. Acetazolamide increased the transient alkalosis induced by repetitive stimulation of the stratum radiatum in area CA1 and reduced the subsequent acidosis. NaBr also increased the alkalosis but had no effect on the subsequent acidosis. A significant increase in paired-pulse inhibition was seen in a paired-pulse stimulation protocol used to monitor the efficacy of GABAergic inhibition at concentrations of 5 mM NaBr. This finding was confirmed in whole-cell patch clamp recordings from cultured hippocampal neurons showing an increase in inhibitory postsynaptic current amplitude. In summary, our results suggest a broad-spectrum anticonvulsant activity which is likely to be caused by its effects on membrane excitability, by an increase in GABAergic inhibition and is less likely caused by its effects on extracellular pH.

Acetazolamide↗

PubMed2007

Statistical parametric mapping and statistical probabilistic anatomical mapping analyses of basal/acetazolamide Tc-99m ECD brain SPECT for efficacy assessment of endovascular stent placement for middle cerebral artery stenosis.

INTRODUCTION: Statistical parametric mapping (SPM) and statistical probabilistic anatomical mapping (SPAM) were applied to basal/acetazolamide Tc-99m ECD brain perfusion SPECT images in patients with middle cerebral artery (MCA) stenosis to assess the efficacy of endovascular stenting of the MCA. METHODS: Enrolled in the study were 11 patients (8 men and 3 women, mean age 54.2 +/- 6.2 years) who had undergone endovascular stent placement for MCA stenosis. Using SPM and SPAM analyses, we compared the number of significant voxels and cerebral counts in basal and acetazolamide SPECT images before and after stenting, and assessed the perfusion changes and cerebral vascular reserve index (CVRI). RESULTS: The numbers of hypoperfusion voxels in SPECT images were decreased from 10,083 +/- 8,326 to 4,531 +/- 5,091 in basal images (P = 0.0317) and from 13,398 +/- 14,222 to 7,699 +/- 10,199 in acetazolamide images (P = 0.0142) after MCA stenting. On SPAM analysis, the increases in cerebral counts were significant in acetazolamide images (90.9 +/- 2.2 to 93.5 +/- 2.3, P = 0.0098) but not in basal images (91 +/- 2.7 to 92 +/- 2.6, P = 0.1602). The CVRI also showed a statistically significant increase from before stenting (median 0.32; 95% CI -2.19-2.37) to after stenting (median 1.59; 95% CI -0.85-4.16; P = 0.0068). CONCLUSION: This study revealed the usefulness of voxel-based analysis of basal/acetazolamide brain perfusion SPECT after MCA stent placement. This study showed that SPM and SPAM analyses of basal/acetazolamide Tc-99m brain SPECT could be used to evaluate the short-term hemodynamic efficacy of successful MCA stent placement.

Acetazolamide↗

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