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PubMed2000

Assessment of blood flow velocity and diameter of the middle cerebral artery during the acetazolamide provocation test by use of transcranial Doppler sonography and MR imaging.

BACKGROUND AND PURPOSE: Our purpose was to show changes in the diameter of the M1 segment of the middle cerebral artery (MCA) by using high-resolution MR imaging in patients with chronic internal carotid artery occlusion after IV administered acetazolamide challenge. Changes in blood flow velocity of the basal cerebral arteries are thought to correlate with changes of cerebral blood flow. Changes in the diameter of the basal cerebral arteries, however, might influence the validity of transcranial Doppler measurements. METHODS: Eight patients with internal carotid artery occlusion who were undergoing acetazolamide testing for assessment of cerebrovascular vasomotor reactivity were included in the study. Blood flow velocities of both MCAs were measured with transcranial Doppler sonography before and 25 minutes after the administration of acetazolamide. Before and 15 minutes after the administration of medication, MR imaging was performed contralateral to the occlusion side. A T2-weighted turbo-gradient spin-echo sequence was chosen to show a cross section of the M1 segment in high resolution (pixels, 0.27 x 0.29 mm). Based on interpolated data, the smallest and greatest MCA diameters were determined. RESULTS: We did not find changes in the diameter of the MCA after acetazolamide provocation testing with high-resolution MR imaging in patients with occlusive extracranial carotid artery disease. CONCLUSION: The results of our study support the hypothesis that changes in MCA flow velocity measured by transcranial Doppler sonography reflect relative changes in cerebral blood flow after acetazolamide provocation testing.

Acetazolamide↗
PubMed2001

Indomethacin activates carbonic anhydrase and antagonizes the effect of the specific carbonic anhydrase inhibitor acetazolamide, by a direct mechanism of action.

OBJECTIVES: In this paper we investigated the effect of indomethacin, acetazolamide and their combination in vitro and in vivo on carbonic anhydrase (CA) isozymes. METHOD: In vitro experiments followed the effect of the two substances at concentrations between 10(-8)-10(-4) M on purified human red cell CA I and II as well as on human gastric mucosa CA IV using dose-response relationships. Kinetic studies were also performed. The effects of single and combined administration of indomethacin and acetazolamide on red cell CA and on gastric acid secretion were studied in vivo. RESULTS: Indomethacin, in vitro and in vivo. induces an increase in erythorcyte CA I and CA II activity. Acetazolamide, a specific inhibitor of CA, reduces the activity of CA I and CA II from red cells. Indomethacin completely antagonizes CA activity, i.e. abolishes the inhibitory effect of acetazolamide on CA. In humans, an increase or decrease in erythrocyte CA II activity is correlated with an increase or decrease in gastric acid secretion. CONCLUSIONS: Our results show that indomethacin, a known cyclooxygenase (COX) inhibitor, is also an activator of CA. Our data also prove that indomethacin is not only an activator of CA but also antagonizes the effect of acetazolamide, a specific inhibitor of this enzyme. In view of the role of CA in acid-base balance as well as the fact that an increase or decrease in its activity is accompanied by an increase or decrease in intra- and extracellular pH, our results suggest that: firstly, CA activation induced by indomethacin might cause changes in COX activity; secondly, PGs are synthetized as a consequence of the changes in COX activity, a hypothesis that requires further study.

Acetazolamide↗
PubMed2002

Acetazolamide suppresses tumor metastasis and related protein expression in mice bearing Lewis lung carcinoma.

AIM: To study the suppressing effect of acetazolamide on tumor metastasis in vivo and observe the protein alteration of lung in mice bearing Lewis lung carcinoma. METHODS: The functional role of aquaporin-1 (AQP1) was investigated in tumor tissues by SDS-PAGE and Western blot. The effect of acetazolamide on tumor metastasis was analyzed by Lewis-lung-carcinoma model. Differential protein was identified by SDS-PAGE, isoelectrofocusing (IEF) methods, and peptide mass fingerprinting (PMF). RESULTS: Acetazolamide (40 mg/kg/d po for 21 d) dramatically reduced the numbers of lung metastasis after sc inoculating Lewis lung carcinoma. The inhibition rate of lung metastases was 83.9 %. Simultaneously, the AQP1 protein level and actin-cytoplasmic in lungs containing metastatic tumor deposits were found to be higher than that in the normal tissue. After treated with acetazolamide for 21 d, the expression of AQP1 was obviously inhibited. CONCLUSION: Acetazolamide can suppress tumor metastasis, at least in part, by inhibiting the expression of AQP1. AQP1 and actin-cytoplasmic may be new prognostic molecules as well as new therapeutic targets for the prevention and treatment of metastatic tumor.

Acetazolamide↗
PubMed2002

[The effect of rhodiola and acetazolamide on the sleep architecture and blood oxygen saturation in men living at high altitude].

OBJECTIVE: To study the changes of sleep architecture and blood oxygen saturation (SaO(2)) during sleep in men living at high altitude, and to investigate the effect of rhodiola and acetazolamide on these sleep indexes. METHODS: Twenty-four men aged 18 to 21 years who had stayed at high altitude (5 380 m above sea level) for 1 year were randomly divided into groups A (treated with oral rhodiola), B (treated with oral acetazolamide) and C (treated with rhodiola + acetazolamide). Their sleep architecture and SaO(2) were recorded for 24 days before and after taking the medicines. RESULTS: Compared with baseline, the waking SaO(2) (WSaO(2)), the lowest SaO(2) (LSaO(2)) and the mean SaO(2) (MSaO(2)) were increased significantly after treatment for 24 days (P < 0.01), and the times of oxygen desaturation >/= 4% per hour (DI4) and the percentage of time spent at SaO(2) below 80% (SIT(80)) were decreased significantly (P < 0.01). After treatment, the NREM I and II was shortened, and III + IV and REM sleep were prolonged (P < 0.01): the total waking time (TWT) was shortened, and the sleep efficiency index (SEI) was markedly increased (P < 0.01). Compared with group A's, groups B's and C's SIT(80) were increased (P < 0.05). CONCLUSION: Both rhodiola and acetazolamide were effective in modulating the sleep architecture and improving the sleep quality in young men living at high altitude, but there was no synergistic effect between rhodiola and acetazolamide.

Acetazolamide↗
PubMed2003

Quantitative measurement of regional cerebrovascular reactivity to acetazolamide using 123I-N-isopropyl-p-iodoamphetamine autoradiography with SPECT: validation study using H2 15O with PET.

UNLABELLED: A simplified technique using (123)I-N-isopropyl-p-iodoamphetamine ((123)I-IMP) autoradiography (ARG) with SPECT has been proposed recently for quantifying regional cerebral blood flow (rCBF). To validate the accuracy of (123)I-IMP-ARG for quantifying regional cerebrovascular reactivity (rCVR) to acetazolamide, we compared rCVR determined using (123)I-IMP-ARG with that determined using H(2)(15)O PET. METHODS: Thirty-nine patients with chronic stenoocclusive disease in a unilateral major cerebral artery underwent SPECT and PET studies before and after intravenous administration of acetazolamide. The rCBF images in the 4 conditions in each patient were calculated according to the ARG method. The same standard input function and the same distribution volume of 35 mL/mL were used in the calculation of rCBF images using the (123)I-IMP-ARG method at resting state and with acetazolamide challenge. One large cortical region of interest (ROI) for a unilateral middle cerebral artery territory was bilaterally determined on each standardized summed rCBF image. On the basis of the rCBF values in each ROI, rCVR to acetazolamide was calculated as follows: rCVR (%) = ([acetazolamide challenge rCBF - resting rCBF]/resting rCBF) x 100. RESULTS: Significant correlation was observed between rCVR values obtained using (123)I-IMP-ARG and H(2)(15)O PET methods in the 78 ROIs examined in the 39 patients (r = 0.820; P < 0.0001). When a rCVR lower than the mean - 2 SD of values obtained in healthy volunteers (18.4% for (123)I-IMP-ARG and 18.2% for H(2)(15)O PET) was defined as reduced, and when the H(2)(15)O PET method was assumed to represent the true determinant of rCVR, (123)I-IMP-ARG was 90% sensitive and 92% specific and displayed an 87% positive predictive value for detecting patients with reduced rCVR. CONCLUSION: These findings demonstrate that (123)I-IMP-ARG methods accurately quantify rCVR and can adequately define subgroups of patients with reduced rCVR.

Acetazolamide↗
PubMed2004

Acetazolamide inhibits aquaporin-1 protein expression and angiogenesis.

AIM: To study effects of acetazolamide on aquaporin-1 (AQP(1)) protein expression and angiogenesis. METHODS: Establishing Lewis-lung-carcinoma model, the localization of AQP(1) in tumor tissues was investigated by immunohistochemical methods; The biological activity of acetazolamide was detected by endothelial cells proliferation test (MTT) assay and chorioallantoic membrane (CAM) vascular inhibition test. RESULTS: Immunohistochemical localization of AQP(1) in mice tumor was labeled in capillaries, post capillary venules endothelial cells. After being treated with acetazolamide, the number of capillaries and post capillary venules was significantly decreased in tumor tissue. Acetazolamide showed significant inhibitory effect on angiogenesis in CAM and endothelial cell proliferation. CONCLUSION: Acetazolamide might be identified and developed as one of potential lead compounds for a new therapeutic intervention in inhibiting cancer angiogenesis.

Acetazolamide↗
PubMed1992

The acute effect of oral acetazolamide on macular blood flow.

Acetazolamide has been shown to be beneficial in the treatment of macular edema. To investigate whether this effect is associated with changes in the retinal circulation, the acute effect of oral acetazolamide on macular blood flow was studied in 20 healthy volunteers. The blue-field simulation technique, a noninvasive method enabling the quantitation of the number (N) and mean velocity (Vm) of leukocytes flowing in the subject's own macular capillaries was used in this study. On two different occasions, separated by 3 or more days, 20 subjects adjusted Vm and N of computer-simulated leukocytes moving on a video screen to match those of their own entoptically perceived leukocytes before and 3 hr after a double-blind, randomized administration of 500 mg acetazolamide or placebo capsules. Ten trials were done, and the velocities were averaged. After acetazolamide ingestion, there was a nonsignificant average change from baseline in Vm (2.5 +/- 23% [+/- one standard deviation]; P greater than 0.1, by paired student t-test) and N (6.9 +/- 25%, P greater than 0.1). After placebo ingestion, the average changes from baseline in Vm and N also were not statistically significant (-1 +/- 18% and 14.9 +/- 30.3%, respectively). Furthermore, when compared with the changes measured after placebo intake, acetazolamide ingestion was associated with a nonsignificant 4.3 +/- 28.7% change in Vm (P greater than 0.1) and a -8 +/- 30.9% change in N (P greater than 0.1). With 20 subjects tested, the calculated average minimum change in leukocyte velocity that could have been detected with this technique (P less than 0.05, by paired student t-test) is about 9%.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMedDate not supplied

A new method for monitoring the cerebrovascular response to acetazolamide using 99mTc-DTPA-HSA.

We developed a new method for monitoring the cerebrovascular response to acetazolamide using technetium-99m diethylenetriaminepentaacetic acid human serum albumin (99mTc-DTPA-HSA). We infused 740 M Bq (20 mCi) of 99mTc-DTPA-HSA intravenously and carried out dynamic scanning of the anterior view of the head for 50 minutes. Ten minutes after the start of scanning, 1,000 mg of acetazolamide was injected intravenously. In three normal volunteers, the radioactivity in brain increased for an average of 8 minutes after the injection of acetazolamide and then remained relatively stable. The average of dilatation index [(peak count/the count just before acetazolamide injection-1)x 100] was 16.1. Our method enabled us to observe vasodilation caused by acetazolamide straight, and may be of value in assessing cerebral perfusion reserve easily and quantitatively.

Acetazolamide↗
PubMed1991

Stability of acetazolamide in suspension compounded from tablets.

The stability of acetazolamide in an extemporaneous suspension compounded from tablets was studied. Acetazolamide 25-mg/mL suspension was prepared by levigating the comminuted 250-mg tablets with 70% sorbitol solution. The mixture was incorporated into a suspension vehicle containing magnesium aluminum silicate and carboxymethylcellulose sodium. Appropriate sweeteners, flavoring agents, preservatives, humectants, and pH adjusters were then added. The suspension was stored in amber glass bottles at 5, 22, 30, 40, and 50 degrees C. Samples were analyzed for the concentration of acetazolamide by stability-indicating high-performance liquid chromatography on days 3, 7, 11, 18, 24, 32, 42, 54, and 79. For batches stored at 5, 22, and 30 degrees C, the initial acetazolamide concentration was maintained during the entire 79 days of the study. However, the concentrations in the batches stored at 40 and 50 degrees C were below 90% of the initial value after 79 and 32 days, respectively. The Arrhenius plot was used to predict a shelf life of the suspension at room temperature of 371 days. Acetazolamide oral suspension 25 mg/mL was stable for at least 79 days at 5, 22, and 30 degrees C. The formulation should be maintained at pH 4-5 and stored in amber glass bottles.

Acetazolamide↗
PubMed1991

Acetazolamide or dexamethasone use versus placebo to prevent acute mountain sickness on Mount Rainier.

Eighteen climbers actively ascended Mount Rainier (elevation 4,392 m) twice during a randomized, double-blind, concurrent, placebo-controlled, crossover trial comparing the use of acetazolamide, 250 mg, dexamethasone, 4 mg, and placebo every 8 hours as prophylaxis for acute mountain sickness. Each subject was randomly assigned to receive placebo during one ascent and one of the active medications during the other ascent. Assessment of acute mountain sickness was performed using the Environmental Symptoms Questionnaire and a clinical interview. At the summit or high point attained above base camp, the use of dexamethasone significantly reduced the incidence of acute mountain sickness and the severity of symptoms. Cerebral and respiratory symptom severity scores for subjects receiving dexamethasone (0.26 +/- 0.16 and 0.20 +/- 0.19, respectively) were significantly lower than similar scores for both acetazolamide (0.80 +/- 0.80 and 1.20 +/- 1.05; P = 0.25) and placebo (1.11 +/- 1.02 and 1.45 +/- 1.27; P = .025). Neither the use of dexamethasone nor that of acetazolamide measurably affected other physical or mental aspects. Compared with placebo, dexamethasone appears to be effective for prophylaxis of symptoms associated with acute mountain sickness accompanying rapid ascent. The precise role of dexamethasone for the prophylaxis of acute mountain sickness is not known, but it can be considered for persons without contraindications who are intolerant of acetazolamide, for whom acetazolamide is ineffective, or who must make forced, rapid ascent to high altitude for a short period of time with a guaranteed retreat route.

Acetazolamide↗
PubMedDate not supplied

Impaired cerebral vasoreactivity after embolization of arteriovenous malformations: assessment with serial acetazolamide challenge xenon CT.

Embolization of a portion of the nidus of an arteriovenous malformation not only may alter hemodynamics within the nidus, but also may change blood flow dynamics in adjacent normal vessels. Sequential acetazolamide-challenge xenon CT cerebral blood flow studies were performed in eight patients before and after embolization of arteriovenous malformations to assess the hemodynamic effects on the major vascular territories supplying the malformation. Acetazolamide is a potent cerebral vasodilator, and its administration combined with cerebral blood flow studies allows assessment of cerebral vasoreactivity. In seven of the eight patients, one or more parenchymal areas exhibited a normal cerebral blood flow augmentation response to acetazolamide before embolization, but diminished acetazolamide flow augmentation was seen after embolization, indicating abnormal vasoreactivity. We found that the decrease in vasoreactivity peaked 6-10 days after embolization. In one of the eight patients, a temporary delayed neurologic deficit developed during a period of impaired cerebral vasoreactivity following embolization. Our results suggest that embolization of an arteriovenous malformation can induce vasoreactivity changes in adjacent normal vessels. Because these changes appear to be somewhat time-dependent, an appropriate interval should be observed between embolization stages or before surgical resection of an arteriovenous malformation following embolization to allow hemodynamic equilibration to occur. Acetazolamide challenge combined with serial cerebral blood flow studies following embolization enables determination of this hemodynamic equilibration.

Acetazolamide↗
PubMedDate not supplied

[Effect of acetazolamide on Menière's disease].

The effect of acetazolamide was assessed in 25 patients with Menière's disease. During the test session hearing threshold and plasmatic osmolality were monitored along with fluctuations in hearing loss, fullness, tinnitus and balance. A single, 250 mg dose of acetazolamide was administered to all patients via os early in the morning on an empty stomach. Hearing was tested prior to administration and every hour for five hours thereafter. Plasmatic osmolality was also assessed during the same session. In 52% of this group an improvement in the threshold was seen. The greatest shift was observed two hours after administration of acetazolamide at 250 Hz, whereas the smallest threshold shift corresponded to 2000 Hz. In all cases, plasmatic osmolality remained constant throughout. Of the patients 44% presented an improvement of all or one of the symptoms: hearing loss, tinnitus, fullness, balance. The data were compared with data obtained for a control group (9 patients) which received a placebo while following the same testing criteria. The results of this study suggest that acetazolamide can have a positive effect on endolymphatic hydrops. It should be stressed, therefore, that acetazolamide could be introduced in the diagnostic and therapeutic strategies applied in Menière's disease.

Acetazolamide↗
PubMed1985

Inhibitory effect of acetazolamide on renal tubular reabsorption of NaHCO3 and NaCl in dogs varies inversely with plasma pH.

To examine the effect of carbonic anhydrase inhibition on proximal tubular electrolyte reabsorption, plasma pH was altered before and after acetazolamide administration in six volume-expanded dogs during continuous infusion of ethacrynic acid to inhibit transcellular NaCl reabsorption. Plasma pH was altered by changing PCO2, keeping plasma bicarbonate concentration and glomerular filtration rate constant. Linear inverse relationships were obtained between electrolyte reabsorption and plasma pH. Before acetazolamide administration, a change in plasma pH of 0.1 unit from pH 7.4 altered bicarbonate reabsorption by about 10% and sodium and chloride reabsorption remaining during ethacrynic acid infusion by about 6.5%. Administration of acetazolamide (30 mg/kg b.wt.) caused a reduction in electrolyte reabsorption at all plasma pH levels examined. A further reduction occurred after increasing the dose to 100 mg/kg b.wt. The absolute inhibitory effects were almost twice as large during hypercapnia as during hypocapnia whereas the reduction in fractional reabsorption was the same at all plasma pH levels. Both variations in plasma pH and administration of acetazolamide altered the reabsorption of bicarbonate, chloride and sodium in molar ratios of about 1:2:3. Hence, acetazolamide inhibits a constant fraction of the NaHCO3 reabsorption and the associated NaCl reabsorption in the proximal tubules independent of changes in plasma pH.

Absorption↗
PubMed1981

Acetazolamide in control of acute mountain sickness.

As part of a double-blind trial slow-release acetazolamide (500 mg daily) or placebo was given to 20 men ascending to 5000 m. In the 18 who attained this altitude, those on acetazolamide had fewer symptoms of acute mountain sickness (AMS) than those on placebo (p < 0.02). 10 of the men had been to 5400 m on a previous expedition. 5 of these men took acetazolamide and 5 took placebo. Those on the drug performed better than those on placebo (p < 0.005). Furthermore, the performance of the 5 men on acetazolamide during the second expedition had improved more than that of the men on placebo (p < 0.01). In the group as a whole the symptoms of AMS were negatively correlated with arterial oxygen tensions (p < 0.001) which were higher in the drug group (p < 0.001). Acetazolamide probably had its effect by causing a metabolic acidosis with a resultant increase in respiratory drive and arterial oxygen tension.

Acetazolamide↗
PubMed1984

Adverse interaction between acetazolamide and anticholinesterase drugs at the normal and myasthenic neuromuscular junction level.

At skeletal neuromuscular junction level in vivo and in vitro experiments have revealed an adverse reversible interaction between acetazolamide and anticholinesterase drugs. Acetazolamide (500 mg, i.v.) prevented the increase in amplitude induced by edrophonium (5 mg, i.v.) on the action potentials derived by surface electrodes from the opponens pollicis muscle of patients affected by myasthenia gravis, when the median nerve was stimulated at the wrist by low frequency repetitive pulses (5/s). Similarly, acetazolamide significantly reduced the contractile force potentiation induced by neostigmine on the rat phrenic-diaphragm preparation, indirectly stimulated by means of low frequency repetitive pulses on the motor nerve. Under such experimental conditions acetazolamide did not show any significant action of its own, but it counteracted the effects of anticholinesterase drugs only when tested before them. It is hypothesized that the effect of acetazolamide on the skeletal neuromuscular junction may occur at presynaptic and/or postsynaptic sites by a mechanism only partly ascribable to the well-known carbonic anhydrase inhibitory activity of this drug.

Acetazolamide↗
PubMed1995

[Cerebral blood flow increase and P300 latency prolongation by intravenous injection of acetazolamide--investigation in lacunar cerebral infarction and healthy subjects].

The cerebral blood flow and the P300 were measured before and 20 minutes after intravenous injection of 17 mg/kg acetazolamide in 15 cases of lacunar cerebral infarction and 10 healthy subjects. In cerebral infarction, the study was performed within 2 weeks after the onset. The cerebral blood flow except the infarcted area was increased significantly by the intravenous injection of acetazolamide in the lacunar cerebral infarction group and the healthy subject group. The blood flow decrease around the infarcted area (intracerebral steal phenomenon) by the intravenous injection of acetazolamide was not observed in any case. The N200 latency and the P300 latency were prolonged significantly by the intravenous injection of acetazolamide in the lacunar cerebral infarction group and in the healthy subject group but the N100 latency and the P200 latency did not show any significant changes. Despite the increase in cerebral blood flow, cerebral function may be decreased by intravenous injection of acetazolamide.

Acetazolamide↗
PubMedDate not supplied

Assessment of the cerebrovascular response to acetazolamide using 99mTc-DTPA-HSA: methodological considerations.

We have reported methods of assessing the cerebrovascular response to acetazolamide using 99mTc-DTPA-HSA and their usefulness in evaluating cerebral hemodynamics. Several problems of this technique were investigated in 10 normal subjects. Following 99mTc-DTPA-HSA injection, dynamic imaging of the anterior head view was performed for 25 to 50 minutes, and 10 minutes after the beginning of imaging, 1,000 mg of acetazolamide was infused intravenously. Venous blood samples were obtained during the imaging period to estimate the blood retention of 99mTc-DTPA-HSA. Radioactivity in the head increased for about 10 minutes following acetazolamide infusion, then decreased slowly. The declining phase almost disappeared after correction for the blood clearance of 99mTc-DTPA-HSA, indicating stability of the vasodilatory effect of acetazolamide. Dilatation index, the percent increase in activity, was a little smaller after correction, but was closely correlated with the index without correction. There was a high correlation between dilatation indices obtained by two analyses, including ROI setting and visual determination of the peak, of the same data. In conclusion, neither blood clearance of 99mTc-DTPA-HSA nor subjective analysis considerably impairs the reliability of the dilatation index, and blood volume in the head from about 15 to 40 minutes after acetazolamide injection is stable and suitable for SPECT.

Acetazolamide↗
PubMedDate not supplied

SPECT measurements of cerebral blood volume before and after acetazolamide in occlusive cerebrovascular diseases.

Cerebral blood volume before and after acetazolamide was measured by SPECT to evaluate cerebral vasodilatory capacity in eight patients with cerebrovascular disease and five control subjects. Two SPECT measurements were performed serially, and acetazolamide was administered between them. The ratio of increase in hemispheric blood volume was calculated, and it was compared with the results of cerebral blood flow and cerebral blood volume measurements. A cerebral vasodilatory capacity map, the image after acetazolamide minus the baseline image, was also produced. Acetazolamide increased hemispheric blood volume in all unilateral carotid disease than in the uninvolved hemispheres of the patients and control subjects. The ratio of concordance with blood flow and blood volume measurements was approximated at 80%. Cerebral vasodilatory capacity mapping revealed three defects compatible with the clinical data. SPECT measurements of cerebral blood volume after acetazolamide can be performed following baseline SPECT with no additional radiotracer, and may be helpful to assess hemodynamic status.

Acetazolamide↗