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PubMed1995

[Investigation of the role of acetazolamide-reactive mechanism in autoregulation].

PATIENTS AND METHODS: The cerebral blood flow (CBF) and mean stump pressure (MSTP) of 25 preoperative patients were measured during a 15 minute test occlusion of the ipsilateral internal carotid artery (ICA). CBF measurements were carried out by the Xenon/CT system adapted to the Toshiba 20A scanner with 4 min wash-in and 6 min wash-out of 30% Xe. Intra-arterial Xe concentration was calculated from endotidal tube-scanning. We selected two areas: the one fed by the middle cerebral artery (MCA), and the other defined as a unilateral cerebral hemisphere on the axial CT slice through the foramen of Monroe, to obtain CBF. We assessed the asymmetry ratio (AR) of CBF (AR = CBF in occlusion side/CBF in contralateral side) and investigated the correlation and regression of MSTP and AR in 25 cases. Furthermore, in 10 of the 25 patients, we measured the CBF with occlusion of the ICA 20 minutes after intravenous administration of acetazolamide. We evaluated the differences between before and after acetazolamide administration in MSTP and AR (paired t test), and investigated the correlation of and regression between MSTP and AR before and after acetazolamide administration again in these 10 patients. RESULTS: A) In 25 cases; In the cases where MSTP was below 40 mmHg, a straight correlation with significant correlation and regression coefficients (MCA: r = 0.834, P = 0.020; Hemisphere: r = 0.840, P = 0.018) between MSTP and AR recognized. However, this statistical correlation was not seen in the cases where MSTP exceeded 40 mmHg, indicating that relationship could be expressed as horizontal line. B) In 10 cases; (1) AR was found to be significantly decreased after acetazolamide administration (MCA: P = 0.007; Hemisphere: P = 0.004, paired t test), although MSTP remained unchanged. (2) Although the relationship between MSTP and AR could be expressed as horizontal lines without a significant regression coefficient before acetazolamide administration, after that their relationship became a straight correlation with a significant regression coefficient (MCA: r = 0.698, P = 0.025; Hemisphere: r = 0.826, P = 0.003). CONCLUSION: These results suggest that 40 mmHg of MSTP in the cases considered as almost normal is the lower limit of the autoregulatory range. In addition, an acetazolamide reactive mechanism might have a role in autoregulation, and in the lower range down to the lower limit of that the compensated CBF by this mechanism would increase as a progressive reduction of MSTP.

Acetazolamide↗
PubMed1996

[Comparison of cerebral vasoreactivity to acetazolamide in normal volunteer among 123I-IMP, 99mTc-ECD and 99mTc-HMPAO].

We studied the difference in the cerebral vasoreactivity to acetazolamide among three cerebral blood flow tracers, N-isopropyl-p-123I-iodoamphetamine (123I-IMP), 99mTc-ethyl cysteinate dimer (99mTc-ECD), 99mTc-hexamethylpropylene amine oxime (99mTc-HMPAO). Subjects were 4 healthy male adult volunteers at ages respectively of 30, 30, 35 and 41 years. Each subject underwent SPECT total 6 times. The three tracers were each used in the tests during rest and during acetazolamide loading, which were performed on different days. At least three days were allowed to intervene between one test and another, and all tests were completed within 2 months. The blood flow was calculated on the microsphere model with 123I-IMP, and Patlak plot method with 99mTc-ECD and 99mTc-HMPAO, to perform quantitative assessment. In the acetazolamide loading test, 1 g acetazolamide was intravenously administered, and each tracer was administered at 15 minutes after that. mCBF and BPI data on total 8 sides, one side representing the right or left side of each subject, were statistically analyzed. For rCBF, the region of interest was set up on the right and left sides of the frontal, temporal and occipital lobes on the slice passing through the third ventricle. The percent increase in mCBF with IMP was 29.3 +/- 10.5% (Mean +/- SD), significantly higher than 10.4 +/- 3.9% (p < 0.05) with ECD or 8.9 +/- 6.9% (p < 0.02) with HMPAO. The percent increase in rCBF with IMP was 30.8 +/- 13.4%, significantly higher than 14.3 +/- 13% (p < 0.001) with ECD or 8.7 +/- 14.8% (p < 0.001) with HMPAO. The percent increase in rCBF with ECD was higher than that with HMPAO, but not significantly. The percent increase in BPI calculated by Patlak plot method with ECD (26.4 +/- 14.3%) was higher than that with HMPAO (13.9 +/- 12.8%), but not significantly. It has been pointed out that 99mTc-ECD and 99mTc-HMPAO underestimate blood flow in the high blood flow area, which seemed to account for the underestimation of acetazolamide reactivity. The extent of underestimation in the high blood flow area is less with 99mTc-ECD than with 99mTc-HMPAO, while the stability of the preparation under acetazolamide is maintained, which seemed to explain difference in the reactivity.

Acetazolamide↗
PubMed1996

[Noninvasive quantitative measurements of regional cerebral blood flow using technetium-99m-L, L-ECD SPECT activated with acetazolamide].

To evaluate noninvasive regional cerebral blood flow (CBF) measurements using technetium-99m-L, L-ethyl cysteinate dimer (99mTc-ECD), radionuclide angiography, resting- and acetazolamide-activating-SPECT studies were performed during about one hour. Forty-four cases with diagnosis of cerebral ischemic disorders were studied. For 36 cases (Group "Acz"), radionuclide angiography was performed immediately after intravenous bolus injection of 300 MBq of 99mTc-ECD, followed by the consecutive SPECT studies. In the midst of the first SPECT study, acetazolamide was administered. Just after the completion of the first SPECT study, another 300 MBq of 99mTc-ECD was added and the second SPECT study was started. For the remaining 8 cases (Group "Placebo"), physiological saline was administered instead of acetazolamide. Quantitative flow-mapping image was calculated from the qualitative SPECT image by the application of Patlak plot graphical analysis and Lassen's correction. Group "Placebo" showed no increase of mean CBF (mCBF) between the resting- and the placebo-challenged-SPECT image (2nd mCBF/1st mCBF; 98 +/- 5%). Group "Acz" showed 124 +/- 15% increase of mCBF under acetazolamide activation. By use of these quantitative flow-mapping images, acetazolamide-activated CBF increase was recognized clearly and easily. This noninvasive method is easy to perform and may be helpful to measure cerebral perfusion changes in the acetazolamide test.

Acetazolamide↗
PubMed1997

[Efficacy of acetazolamide treatment of patients with hypercapnia and superimposed metabolic alkalosis].

BACKGROUND: Metabolic alkalosis usually complicates the evolution of patients with hypercapnia under diuretic or steroid therapy. The objective of this study was to analyze the efficiency of therapy with acetazolamide, a reversible carbonic anhydrase inhibitor, in this condition. PATIENTS AND METHODS: Prospective study conducted at our hospital from June 1994 to March 1996, with 45 patients who had chronic respiratory acidosis and metabolic alkalosis. After a previous stabilization of the patient and eventually the discontinuation of diuretic or corticosteroid drugs fro 24-48 hours, 500 or 750 mg of acetazolamide were administered daily for 48 hours. Later, variations both in arterial gasometry and venous electrolytes were analyzed by comparing two means of paired data. RESULTS: After therapy with acetazolamide a clinical improvement was observed in patients, a decrease in PaCO2, pH and CO3H (p < 0.001) and an increase in PaO2 (p < 0.001). Hypochloremia (82.2%) and hypopotassemia (33.3%) were the most common electrolytic abnormalities before therapy. Both abnormalities improved significantly after the administration of acetazolamide. In five patients (11.1%) acetazolamide was discontinued when metabolic acidosis appeared, which only in three cases was associated with acidemia. No secondary effects were observed. CONCLUSIONS: Acetazolamide is an efficient alternative for treatment of patients with respiratory acidosis and metabolic alkalosis, particularly when other more common measures in this condition (discontinuation of diuretics and/or volemic replacement) have failed or are contraindicated. On the other hand, the emergence of relevant secondary effects is unlikely.

Acetazolamide↗
PubMed1997

Acetazolamide challenge and technetium-99m-ECD versus iodine-123-IMP SPECT in chronic occlusive cerebrovascular disease.

UNLABELLED: We compared the acetazolamide challenge test using 99mTc-ECD SPECT and 123I-IMP SPECT images in patients with chronic occlusive cerebrovascular disease. We also evaluated the usefulness of linearization correction for acetazolamide challenge test of 99mTc-ECD SPECT. METHODS: Twenty patients with unilateral chronic occlusive cerebrovascular disease (10 patients had middle cerebral arterial lesion and 10 had internal carotid lesion) were included in the study. Split-dose (a dose fractioning was 1:2), and sequential SPECT technique was used for 99mTc-ECD SPECT studies while only acetazolamide challenge test studies for 123I-IMP SPECT were performed. Permeability surface area product model (PS model) and back-diffusion model (Lassen's correction) were used for linearization correction of acetazolamide challenge with 99mTc-ECD SPECT. RESULTS: Six of 16 patients with reduced vasodilatory capacity in 123I-IMP SPECT were underestimated by 99mTc-ECD SPECT acetazolamide challenge test. Relative ECD uptake normalized by cerebellar uptake compared with IMP uptake showed a nonlinear relationship, indicating relatively less uptake in high flow range. The underestimations of limited vasodilatory capacity observed in 99mTc-ECD SPECT without linearization correction was modified by linearization algorithm. However, the effect of correction based on PS model was superior than that of Lassen's correction. The corrected 99mTc-ECD uptake ratio, based on PS model, and IMP uptake ratio demonstrated a better linear relationship than that of Lassen's correction. CONCLUSION: Technetium-99m ECD SPECT corrected based on the PS model is a better method of linearization for evaluating cerebrovascular reserve using acetazolamide challenge.

Acetazolamide↗
PubMed1997

[Quantitative measurements of regional cerebral blood flow using technetium-99m-L,L-ECD SPECT activated with acetazolamide: fundamental study of measurement's accuracy, comparison with 123I-IMP ARG method].

We measured regional cerebral blood flow before and after acetazolamide administration using a serial noninvasive method with 99mTc-ECD developed by Matsuda and Takeuchi et al., and compared the accuracy of measured values with those obtained by the conventional 123I-IMP ARG method. When the regional cerebral blood flow was measured for 80 brain regions in 5 subjects without scatter correction, a differential of 0.5 +/- 8.4% was obtained between values measured before and after physiological saline administration as a placebo. A differential of -0.2 +/- 12.6% was obtained when the same regions were measured with scatter correction. These findings indicated that placebo administration did not affect measured values, regardless of whether scatter correction was performed. When 64 regions in 4 subjects at rest were measured on two successive days, a differential of -1.1 +/- 9.0% was obtained between the values measured on the two days. A differential of -4.0 +/- 11.7% was obtained for the same regions following acetazolamide administration. These findings showed that measurements were reproducible both when subjects were at rest and when they were administered acetazolamide. The above two methods were used for measurement of 80 brain regions in the same 5 subjects for comparison. Measurements of subjects at rest and with acetazolamide administration were performed on separate days. The regression line y = 0.99x + 1.47, r = 0.80, was obtained for the subjects at rest, and y = 0.86x + 7.76, with r = 0.76, for the subjects following acetazolamide administration. These findings demonstrated a good correlation between the values obtained using the two methods. The values obtained using the method of Matsuda and Takeuchi et al., before and after acetazolamide administration were thus consistent with those reported previously using the conventional method, and the former method proved to be both simple and reliable.

Acetazolamide↗
PubMed1998

rCBF SPECT and the acetazolamide test in the evaluation of dementia.

BACKGROUND: The diagnostic potential of 99mTc-HMPAO following systemic administration of the cerebral vasodilator acetazolamide (acetazolamide test) was evaluated using regional-cerebral-blood-flow (rCBF) SPECT in patients with Alzheimer's disease (AD) or with vascular-type of dementia (VD). METHODS: An initial, high-resolution SPELT study was performed with 99mTc-HMPAO, and after 2 days patients were re-evaluated with 99mTc-HMPAO following systemic administration of acetazolamide. Reconstructed SPELT slices were evaluated visually and semiquantitatively by a semiautomatic rCBF map method. RESULTS: Using 99mTc-HMPAO alone, a bilateral hypoperfusion was found in the temporal and/or parietal regions in 33% (6/18) of VD patients and in 70% (23/33) of AD patients. The vascular reserve capacity, as determined with the acetazolamide test, was not impaired in 22% of the VD patients but in 76% of the AD patients. The differences in the perfusion patterns between VD and AD patients were statistically different (p < 0.01, Fischer's exact test). Of the 6 VD patients with hypoperfusion (bilateral temporal and/or parietal), 4 had a decreased vascular reserve capacity as determined in the acetazolamide test. Decreased reserve capacity was found in only 4 out of 25 patients with AD. CONCLUSIONS: The acetazolamide test is helpful in rCBF SPECT to differentiate VD from AD.

Journal Article↗
PubMed1998

Cerebral blood flow assessed by brain SPECT with 99mTc-HMPAO utilising the acetazolamide test in systemic lupus erythematosus.

BACKGROUND: Cerebrovascular diseases are one of the most important complications of systemic lupus erythematosus (SLE). The diagnostic imaging of neuropsychiatric SLE complications presents many problems. This study was undertaken to investigate cerebral blood flow char s and its reactivity to hypercapnia by means of acetazolamide test in SLE patients. METHODS: Brain SPELT studies using 99mTc-HMPAO were performed in 50 patients with SLE. Acetazolamide test was performed in 35 patients 3 days after the baseline study by means of repetitive scanning 20 min after i.v. injection of 1.0 g of acetazolamide. RESULTS: Significant interhemispheric hypoperfusion areas were shown in 76.3% of all patients, 83.8% symptomatic and 63.1 % asymptomatic. Patients with antiphospholipid syndrome showed multifocal perfusion deficits. The reaction of cerebral perfusion to acetazolamide was heterogenous and showed increase, decrease, no change or mixed reaction of baseline-study-found focal hypoperfusion. Acetazolamide test revealed hypoperfusion in two patients with normal baseline study. MRI scanning revealed cerebral lesions in 41 % of patients. CONCLUSIONS: CBF asymmetries in symptomatic and asymptomatic patients with SLE are frequent. Regional CBF alterations seem to be different in patients with and without antiphospholipid syndrome. The part of the patients with SLE shows no or paradoxically inversed reaction to acetazolamide.

Journal Article↗
PubMed1984

Effect of acetazolamide on insulin sensitivity in myotonic disorders.

Acetazolamide is effective treatment for myotonia in certain patients with myotonia congenita. Since potassium metabolism may be abnormal in myotonia congenita, we studied the effect of acetazolamide administration on potassium regulation and glucose disposal, using the euglycemic insulin clamp technique in patients with myotonic disorders and in normal subjects. Glucose disposal was normal in patients with myotonia congenita; administration of acetazolamide increased glucose disposal in normal subjects and in patients with myotonia congenita. By contrast, patients with myotonic dystrophy showed insulin resistance and decreased glucose disposal that was not improved by acetazolamide administration. Patients with myotonia congenita had elevated potassium levels in the basal state and a greater fall in potassium level during the insulin clamp procedure than controls. Patients with myotonic dystrophy had normal or low basal potassium levels and a subnormal decrease in potassium level during the insulin clamp procedure. Administration of acetazolamide did not alter these abnormalities in potassium metabolism in patients with either myotonia congenita or myotonic dystrophy.

Acetazolamide↗
PubMed1984

Betaxolol and acetazolamide. Combined ocular hypotensive effect.

To determine the combined ocular hypotensive effect of topical betaxolol hydrochloride and oral acetazolamide, we conducted a three-week clinical trial of the concurrent administration of the two drugs. One drop of betaxolol hydrochloride 0.5% every 12 hours effected a mean reduction in outflow pressure from baseline of 27.3%. When given topically to both eyes of a patient pretreated with oral acetazolamide (500 mg every 12 hours), betaxolol caused an additional mean outflow pressure decrease of 17.6%. Acetazolamide, 500 mg orally every 12 hours, produced a mean outflow pressure reduction from baseline of 42.5%. When added to the therapy regimen of a patient already receiving topical betaxolol, oral acetazolamide caused an additional mean outflow pressure decrease of 35.1%. Our study supports the clinical usefulness of concurrent administration of betaxolol and acetazolamide to lower intraocular pressure.

Acetazolamide↗
PubMed1998

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

Exposure to high altitude results in significant physiologic changes and may precipitate mountain sickness, ranging from mild symptoms above 2,500 m to severe symptoms above 4,000 m. In a previous study, changes in the pharmacokinetics of meperidine were observed after exposure to high altitude. This study was conducted to investigate whether similar changes occur for acetazolamide, which is prescribed for prophylaxis of acute mountain sickness. Acetazolamide 250 mg was administered orally to young, healthy male volunteers in groups of 12 each: those residing at sea level (group L), these same volunteers on the day after arrival at high altitude (4,360 m, group HA), and volunteers living at high altitude for 10 months or longer (group HC). Serial blood samples were collected for 24 hours and acetazolamide concentrations were measured in whole blood, plasma, and plasma water. The elimination rate constant (lambda z) was significantly increased in group HA compared with group L. Clearance uncorrected for bioavailability (Cl/F) increased significantly in group HA compared with group L, and further increased in group HC. Apparent volume of distribution (Vz/F) was decreased by 17% in group HA compared with group L, and increased by 37% in group HC compared with group HA. Mean residence time (MRT) was significantly decreased in group HA compared with groups L and HC. Erythrocyte (RBC) uptake increased significantly after a significant increase in RBC count in group HC compared with group L. The extent of protein binding (EPB), however, was significantly decreased in group HA compared with groups L and HC. Free acetazolamide concentrations were significantly lower in group HC than in group L 12 hours after administration. Based on these observations, it is suggested that patients travelling to high altitude, especially altitudes above 4,000 m, should be closely monitored and acetazolamide dosage adjusted as necessary.

Acetazolamide↗
PubMed1987

Reduction of uterine blood flow by phenylephrine, an alpha-adrenergic agonist, in the day 11 pregnant rat: relationship to potentiation of acetazolamide teratogenesis.

We have demonstrated previously that phenylephrine, a selective postsynaptic alpha-1-adrenergic agonist, significantly potentiates the incidence of acetazolamide-induced right forelimb ectrodactyly in a dose-response manner. As reported herein, phenylephrine also decreases maternal uterine blood flow in a dose-response manner as measured by radioactive microsphere methodology. At the potentiative dose of 12.5 mg/kg phenylephrine decreases uterine blood flow by 86.8% when compared to control. In turn, pretreatment with prazosin, a selective postsynaptic alpha-1-adrenergic antagonist, prevents this large decrease in uterine blood flow and abolishes the potentiation of acetazolamide teratogenesis by phenylephrine. Although the effects of acetazolamide or acetazolamide + phenylephrine on uterine blood flow were not measured the data suggest a correlation between decreased uterine blood flow and potentiation of acetazolamide teratogenesis.

Acetazolamide↗
PubMed1992

Axial skeletal malformations induced by acetazolamide in rabbits.

In order to evaluate the teratogenic potential of acetazolamide in rabbits, three groups of 18 artificially inseminated females were treated orally with 50, 100, or 150 mg/kg/day of acetazolamide on days 6-18 of gestation. These doses induced maternal acidosis and electrolyte changes, consistent with those reported in rats and considered to be a result of carbonic anhydrase inhibition, as well as reductions in maternal body weight gain. At cesarean sections, average fetal body weights in the acetazolamide groups were dose-dependently decreased compared with controls. There were no effects of acetazolamide on embryonic survival or external morphology of live fetuses. In the fetal skeletal examination, thoracic and lumbar vertebral malformations occurred in 0.7%, 3.9%, and 6.1% of fetuses in the 50, 100, and 150 mg/kg/day groups, respectively, compared with none in the control group. In addition, missing vertebra was seen in a small number of fetuses in the 100 and 150 mg/kg/day groups. These axial skeletal malformations were, in some cases, associated with costal malformations. These results indicate that acetazolamide at maternotoxic doses can produce axial skeletal malformations in the rabbit.

Acetazolamide↗
PubMed2000

Acetazolamide and enalapril combination offers complete protection from nitric oxide-deficient stroke in stroke-prone spontaneously hypertensive rats.

Chronic oral administration of l -NAME precipitates stroke in stroke-prone spontaneously hypertensive rats (SHRSP). The present study investigated whether acetazolamide (an acidotic agent) given alone or in combination with an angiotensin blocker (enalapril maleate) offers any protection from NO-deficient stroke in SHRSP. We also examined whether protection from NO-deficient stroke involves activation of K(+)channels. Five-week-old SHRSP drank saline (group I), l -NAME (group II), l -NAME+enalapril (group III), l -NAME+acetazolamide (group IV), and l -NAME+enalapril+acetazolamide (group V). Within a few hours following onset of stroke, rats were attached to a blood pressure recorder. In subsequent experiments, to investigate the involvement of K(+)channels, glibenclamide and BaCl(2)(K(+)channel blockers) were included in the drinking solutions that were given to the SHRSP groups receiving l -NAME, acetazolamide and enalapril. Group I of SHRSP did not develop stroke. Group II, III and IV developed stroke in 12+/-2, 29+/-2 and 20+/-2 days, respectively. SHRSP from group V did not develop stroke. However, they died in 70+/-2 days. The glibenclamide and BaCl(2)administration failed to prevent this protection from stroke. In conclusion, concurrent administration of acetazolamide and enalapril prevents onset of NO-deficient stroke in SHRSP. These stroke-protective effects are independent of reductions in mean or systolic blood pressures and do not involve an activation of K(+)channels.

Acetazolamide↗
PubMed1997

Assessment of vasoreactivity in brain edema by acetazolamide activation SPECT and PET.

Our study was performed to find out cerebrovascular reactivity post acetazolamide administration in patients with peritumoral edema. Adult patients (n = 9) underwent CBF measurement by 99mTc-HMPAO SPECT pre and post 1 gram i.v. acetazolamide. In all patients, this procedure was repeated once again within 10 days of performing tumor removal. Five of these patients also underwent CBF measurement pre and post 1 gram i.v. acetazolamide post surgery only using oxygen-15 labeled H2O PET. Asymmetry index (AI) was calculated as ratio of ROI counts in the peritumoral edematous area and symmetrical ROI on the contralateral normal hemisphere. The AI increased after acetazolamide in edematous gray matter post operatively though the resting AI remained almost same post operatively. AI in edematous white matter showed non-significant increase post operatively both at rest and after acetazolamide. Good linear correlation of AI between PET and SPECT was observed both in gray and white matter. The improvement of vascular reactivity in edematous gray matter after tumor removal suggests that mass effect not only reduces CBF but also suppresses vascular reactivity. White matter vascular reactivity in early post operative period is little improved, possibly due to factors other than mass effect i.e. excess water accumulation in white matter perivascular space.

Acetazolamide↗
PubMed1982

Cardiovascular performance and oxyhemoglobin dissociation after acetazolamide in metabolic alkalosis.

In patients with metabolic alkalosis, compensatory alveolar hypoventilation may induce hypercapnia and hypoxemia. In edematous or normally-hydrated patients without electrolyte deficiencies, acetazolamide--a carbonic anhydrase inhibitor--has been advocated to correct the primary acid-base disturbance, thereby preventing hypoxemia. The hemodynamic consequences and the effect on oxyhemoglobin dissociation of acetazolamide, were studied. Twelve critically ill patients with metabolic alkalosis were given 15 mg/kg body wt. acetazolamide intravenously. Cardiovascular performance was completely unchanged. The P50 was 26.6 mm Hg at the beginning and the end of the study, indicating that hemoglobin-oxygen affinity is unaffected by acetazolamide. In six patients, investigated after open-heart surgery, the arterial oxygen tension increased by 10-45%. This was probably related to the combined effects of slight reductions in total body oxygen consumption or shunting of venous blood through the lungs. Eight of the 12 patients were on controlled ventilation. After acetazolamide there was a mean increase in mixed venous carbon dioxide tension (PvCO2) of 4.5 mm Hg, with no increase in arterial carbon dioxide tension (PaCO2), indicating only a limited interference with carbon dioxide uptake and release of the carbonic anhydrase inhibition. No other adverse reactions were observed.

Acetazolamide↗
PubMed1989

Effect of acetazolamide on cerebral artery blood velocity and regional cerebral blood flow in normal subjects.

The effect of intravenous acetazolamide 1 g on cerebral artery blood velocity and regional blood flow (rCBF) was investigated in eight normal subjects. Blood velocity was measured with 2 MHz pulsed Doppler in the proximal segments of the middle, anterior and posterior cerebral artery (MCA, ACA, and PCA) and in the distal extracranial internal carotid artery (ICA). The rCBF in the regions of interest tentatively corresponding to the perfusion territories of these vessels was estimated using 133Xe inhalation and a rapidly rotating single photon emission computer tomograph. Both blood velocity and rCBF increased after acetazolamide. There was no significant difference between the percentage ICA blood velocity increase (22 +/- 12%) and the percentage rCBF increase in the ICA region of interest (25 +/- 9%). In the MCA, ACA, and PCA, however, blood velocity increased more (mean increase 36-42%) than the rCBF in the corresponding regions of interest (mean increase 24-26%). These differences were highly significant suggesting a direct and site specific effect of acetazolamide in narrowing the lumen of the proximal MCA, ACA, and PCA, but not of the extracranial ICA. We also propose that the effect of acetazolamide induces reciprocal changes in the extent of adjacent perfusion territories in individual brain hemispheres. Data compiled from all subjects investigated at two very different perfusion levels (before and after acetazolamide) revealed a significant positive correlation between blood velocity and rCBF.

Acetazolamide↗
PubMed2007

Perfusion MRI before and after acetazolamide administration for assessment of cerebrovascular reserve capacity in patients with symptomatic internal carotid artery (ICA) occlusion: comparison with 99mTc-ECD SPECT.

INTRODUCTION: Impaired cerebral vascular reserve (CVR) in patients with symptomatic internal carotid artery (ICA) occlusion is regarded as a possible indication for performing extra-/intracranial (EC/IC) bypass surgery. As perfusion MR imaging (MRI) can demonstrate cerebral haemodynamics at capillary level, our hypothesis was that perfusion MRI could be used in these patients for the evaluation of CVR following acetazolamide challenge in a similar way to single photon emission CT (SPECT) and might provide additional information. METHODS: Enrolled in the study were 12 patients (mean age 61.3 years; 11 male, 1 female) with symptomatic unilateral ICA occlusion proven by angiography. Both perfusion MRI and 99m-technetium-ethyl-cysteinate dimer ((99m)Tc-ECD) SPECT were performed before and after injection of acetazolamide (Diamox ,1000 mg i.v.). CVR parameters including regional cerebral blood flow (rCBF) and volume (rCBV), and mean transit times (MTT) were measured by perfusion MRI. RESULTS: The patients with impaired CVR proven by SPECT (n = 9) had a negative mean rCBF increment (-46.52%), negative rCBV increment (-13.5%) and delayed MTT (mean +2.98 s), respectively, on the occluded side (Student's t-test all P < 0.05). The patients with sufficient CVR (n = 3) had a mean rCBF increment of 1.2%, a decrement of rCBV of 10.46%, and a mean MTT shortening of 0.27 s following the acetazolamide injection. CONCLUSIONS: Perfusion MRI before and after acetazolamide administration compares favourably with (99m)Tc-ECD SPECT for the detection of impaired CVR. The impact that perfusion MRI studies (before and after acetazolamide administration) might have on the treatment decision in patients with ICA occlusion has yet to be determined by a prospective study.

Acetazolamide↗