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PubMed1996

Haemodynamic effects of acetazolamide in patients with cardiovascular disorders: correlation with calculated cerebral perfusion reserve.

Individual responses of cerebral blood flow to acetazolamide are highly variable. We hypothesized that this may be due to interactions with cardiovascular diseases and medication. Therefore, we measured the haemodynamic effects of acetazolamide in patients with various cardiovascular disorders and evaluated whether these had any correlation with calculated cerebral perfusion reserve. Ten male patients aged 58 +/- 9 years (mean +/- S.D.) were studied with first-pass radionuclide ventriculography and echocardiography before and 20 min after the administration of 1 g acetazolamide. Systolic blood pressure fell from 133 +/- 21 to 128 +/- 19 mmHg (P < 0.05) and the cardiac output to total blood volume ratio increased from 0.85 +/- 0.18 to 0.92 +/- 0.11 (P = 0.05), indicating a 14% reduction in peripheral vascular resistance. In a further study, 15 patients aged 60 +/- 7 years (22 studies) were studied simultaneously with a nuclear stethoscope and 99Tc(m)-hexamethylpropyleneamine oxime single photon emission tomography before and after acetazolamide administration. The cardiac output ratio increased from 0.81 +/- 0.17 to 0.89 +/- 0.17 (P < 0.05) and showed a significant inverse correlation with calculated cerebral perfusion reserve. In conclusion, acetazolamide increases the cardiac output ratio and reduces systolic blood pressure, indicating reduced peripheral vascular resistance in patients with various cardiovascular diseases and medication. The increase in the cardiac output ratio is inversely related with calculated cerebral perfusion reserve. This helps to explain the high individual variability in calculated cerebral perfusion reserve.

Acetazolamide↗
PubMed1998

Acetazolamide treatment prevents in vitro endotoxin-stimulated tumor necrosis factor release in mouse macrophages.

We previously showed that incubation in carbon dioxide (CO2), but not air or helium (He), markedly decreased macrophage intracellular pH (pHi) and resulted in reversible inhibition of lipopolysaccharide- (LPS) stimulated tumor necrosis factor (TNF) and interleukin-1 release. We sought to determine whether carbonic anhydrase inhibition with acetazolamide would prevent CO2-mediated inhibition of LPS-stimulated TNF release. Murine peritoneal macrophages were treated with acetazolamide for 1 h under control atmosphere (95% air/5% CO2) and then switched to incubator modules containing: 1) 80% CO2/20% O2, 2) 80% He/20% O2, or 3) 100% air. Before transfer to experimental atmospheric conditions the macrophages were stimulated with 0 or 1 microg/mL of LPS (Escherichia coli 0111 B4). Supernatant TNF was measured 4 h later by bioassay. In parallel experiments LPS-stimulated cytokine mRNA was estimated using reverse transcriptase polymerase chain reaction (RT-PCR) 2 h after LPS stimulation. Viability was determined using dye uptake. Incubation in CO2 or helium had no effect on TNF production in the absence of LPS. In the absence of acetazolamide CO2 produced marked inhibition of LPS-stimulated TNF release, but this was not blocked by the presence of acetazolamide. This CO2-mediated inhibition of TNF was associated with normal levels of TNF mRNA. In acetazolamide-treated macrophages, LPS resulted in a dose-dependent inhibition of TNF release when the cells were incubated in air or helium. Maintenance of normal intracellular pH is required for TNF release, but not TNF mRNA induction by LPS. Factors that alter intracellular pH regulation may modulate LPS-stimulated cytokine production.

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PubMed2003

BOLD and perfusion response to finger-thumb apposition after acetazolamide administration: differential relationship to global perfusion.

The authors studied the effects of altering global cerebral blood flow on both blood oxygen level-dependent (BOLD) response and perfusion response to finger-thumb apposition. A PICORE/QUIPSS II protocol was used to collect interleaved BOLD-weighted and perfusion-weighted images on eight finger-thumb apposition trials. Subjects were studied on a drug-free day and on a day when acetazolamide was administered between the second and third trials. After acetazolamide administration, resting cortical perfusion increased an average of 20% from preadministration levels, whereas the BOLD response to finger-thumb apposition decreased by an average of 35% in the S1M1 hand area. Contrary to predictions from the exhausted cerebrovascular reserve hypothesis and the oxygen limitation model, an effect of acetazolamide on cerebral blood flow response in the S1M1 hand area was not observed. Across the acetazolamide trials, BOLD response was inversely correlated with resting cortical perfusion for individual subject data. These results suggest that resting perfusion affects the magnitude of the BOLD response and is thus an important confounding factor in fMRI studies, and that the physiologic systems that increase cerebral blood flow in response to acetazolamide administration and systems that increase cerebral blood flow in response to altered neural activity appear to have additive effects.

Acetazolamide↗
PubMed1990

Acetazolamide-associated aplastic anaemia.

Eleven cases of acetazolamide-associated aplastic anaemia were reported in Sweden during a 17-year period. There were six women and five men with a median age of 71 years (range 63-85 years). The median dose of acetazolamide was 500 mg, and the median duration of treatment was 3 months (range 2-71 months). Ten of the eleven patients died, all within 8 weeks after detection of their aplastic anaemia. The relative risk of developing aplastic anaemia when taking acetazolamide was 13.3 (95% confidence limits (CL); 6.8-25.3). The estimated incidence of reported acetazolamide-associated aplastic anaemia is approximately one in 18,000 patient years. The results strongly indicate that acetazolamide treatment is associated with a substantial increase in the risk of developing aplastic anaemia.

Acetazolamide↗
PubMed2001

Low-dose acetazolamide reduces CO(2)-O(2) stimulus interaction within the peripheral chemoreceptors in the anaesthetised cat.

1. Using the technique of end-tidal CO(2) forcing, we measured the effect of the carbonic anhydrase inhibitor acetazolamide (4 mg kg(-1), I.V.) on the CO(2) sensitivities of the peripheral and central chemoreflex loops both during hyperoxia and hypoxia in 10 cats anaesthetised with alpha-chloralose-urethane. 2. In the control situation, going from hyperoxia (arterial P(O2) (P(a,O2)) 47.40 +/- 3.62 kPa, mean +/- S.D.) into moderate hypoxia (P(a,O2) 8.02 +/- 0.30 kPa) led to an almost doubling of the peripheral CO(2) sensitivity (S(P)): a rise from 0.09 +/- 0.07 to 0.16 +/- 0.06 l min(-1) kPa(-1). After acetazolamide, however, lowering the P(a,O2) from 46.95 +/- 5.19 to 8.02 +/- 0.66 kPa did not result in a rise in S(P), indicating the absence of a CO(2)-O(2) stimulus interaction. 3. In hypoxia, acetazolamide reduced S(P) from 0.16 +/- 0.06 to 0.07 +/- 0.05 l min(-1) kPa(-1). In hyperoxia, however, the effect on S(P) was much smaller (an insignificant reduction from 0.09 +/- 0.07 to 0.06 +/- 0.05 l min(-1) kPa(-1)). 4. Acetazolamide reduced both the hyperoxic and hypoxic sensitivities (S(C)) of the central chemoreflex loop: from 0.45 +/- 0.16 to 0.27 +/- 0.13 l min(-1) kPa(-1) and from 0.40 +/- 0.16 to 0.26 +/- 0.13 l min(-1) kPa(-1), respectively. In hyperoxia, the apnoeic threshold B (X-intercept of the ventilatory CO(2) response curve) decreased from 2.91 +/- 0.57 to 0.78 +/- 1.9 kPa (P = 0.005). In hypoxia, B decreased from 1.59 +/- 1.22 to -0.70 +/- 2.99 kPa (P = 0.03). 5. Because acetazolamide abolished the CO(2)-O(2) interaction, i.e. the expected increase in S(P) when going from hyperoxia into hypoxia, we conclude that the agent has a direct inhibitory effect on the carotid bodies. The exact mechanism by which the agent exerts this effect will remain unclear until more detailed information becomes available on the identity of the carbonic anhydrase iso-enzymes within the carotid bodies and their precise subcellular distribution.

Acetazolamide↗
PubMedDate not supplied

Correlation between effects of acute acetazolamide administration to mice on electroshock seizure threshold and maximal electroshock seizure pattern, and on carbonic anhydrase activity in subcellular fractions of brain.

The relationships between inhibition of carbonic anhydrase (CA) activity in cytoplasmic, microsomal, and myelin subcellular fractions obtained from cerebral cortex, subcortex, and cerebellum and electroshock seizure threshold (EST) and modification of the extension/flexion (E/F) ratio following maximal electroshock seizures (MES) were ascertained in Swiss-Webster mice given 40 and 200 mg/kg acetazolamide. The parameters were determined at 1, 4, and 24 h after administration of acetazolamide. The results showed that changes in the E/F ratio induced by acetazolamide correlated linearly (r = 0.90) with changes in CA activity in the cytoplasm of the subcortex. However, there was an inverse power function correlation (r = 0.92) between EST and CA activity in the myelin fraction of the cerebral cortex. The time course of acetazolamide inhibition of CA activity in these two fractions also paralleled the time course of its effects on EST and E/F ratio. Thus, acetazolamide decreases susceptibility to seizures (raises EST) by inhibiting myelin CA and prevents spread of seizure activity by inhibiting CA in the cytoplasm of glial cells. The CO2 that accumulates as a result of CA inhibition in these two fractions causes profound changes in brain function.

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PubMed1986

Carbonic anhydrase isoenzymes in the rat kidney. Effects of chronic acetazolamide treatment.

Biochemical, immunocytochemical and histochemical methods were used to study the effect of chronic acetazolamide treatment on carbonic anhydrase (CA) isoenzymes in the rat kidney. Male inbred rats (Lew/Mol) were treated with 15 mg kg-1 day-1 acetazolamide s.c. by Alzet minipump during 2-9 weeks; some animals had a drug-free period of 1-4 weeks before being killed. The renal content of CA II was higher in the acetazolamide-treated rats than in the controls, 178 +/- 10 vs 144 +/- 4.8 micrograms enzyme protein g-1 tissue (mean +/- SE). The distribution of CA isoenzymes did not change during or after chronic acetazolamide treatment. Thus, only CA II was detected in the kidney tubules by immunofluorescence using specific antisera against CA I, CA II and CA III. All animals showed a similar staining pattern, with intense cytoplasmic CA II staining in intercalated cells of collecting ducts, moderate staining in descending thin limbs of Henle, and weak cytoplasmic staining in proximal tubules and chief cells of collecting ducts. All animals also showed histochemical staining of cell membranes in proximal and distal tubules and thick limbs of Henle, suggesting the presence of a membrane-bound isoenzyme (CA IV). The only difference noted by histochemistry and immunocytochemistry was that the intercalated cells appeared bulkier and protruded more markedly into the tubular lumen in treated than in untreated animals. The functional importance of this finding is unclear. The observed changes in CA cannot alone explain why the effect of acetazolamide, in causing loss of bicarbonate and sodium, is self-limited on continued administration.

Acetazolamide↗
PubMed1990

Cardiorespiratory effects induced by acetazolamide on the ventromedullary surface of the cat.

1. Inhibition of carbonic anhydrase by acetazolamide in alpha-chloralose-anaesthetized cats, in a region of the brain stem co-extensive with the glycine-sensitive area, intermediate chemosensitive area, and probably C1 catecholaminergic neurones produces hypotension, bradycardia and depression of the central respiratory drive. 2. These responses are concentration dependent, and can still be observed when the enzyme substrate (CO2) is elevated. Therefore, in both the hypercapnic and the normocapnic condition, similar responses in arterial blood pressure, heart rate and respiratory rate are observed when acetazolamide is topically applied to the glycine-sensitive area. 3. To investigate further the contribution of peripheral baro-, chemo- and cardiopulmonary receptors to these responses, acetazolamide was topically applied to the glycine-sensitive area under three different conditions: intact gallamine-paralysed (5 mg kg-1 h-1) and artificially ventilated (A), sinoaortic denervated (B), and sinoaortic denervated plus bilaterally vagotomized cats (C). Under all conditions, similar responses were observed. The fall in arterial blood pressure was 75 +/- 11 (A), 90 +/- 13 (B), and 75 +/- 9 mmHg (C). Changes in heart rate during acetazolamide application were -23 +/- 6, -20 +/- 8, and -26 +/- 6 beats min-1, respectively. The decreases in respiratory rate were 9 +/- 2 (A), 11 +/- 2 (B), and 11 +/- 2 breaths min-1 (C). 4. The data indicate that the responses to topical application of acetazolamide are mainly due to its central action at the glycine-sensitive area and are not influenced by peripheral baroreceptor and chemoreceptor inputs.

Acetazolamide↗
PubMed1996

The effect of low-dose acetazolamide on the ventilatory CO2 response curve in the anaesthetized cat.

1. The effect of 4 mg kg-1 acetazolamide (I.V.) on the slope (S) and intercept on the Pa,CO2 axis (B) of the ventilatory CO2 response curve of anaesthetized cats with intact or denervated carotid bodies was studied using the technique of dynamic end-tidal forcing. 2. This dose did not induce an arterial-to-end-tidal PCO2 (P(a-ET),CO2) gradient, indicating that erythrocytic carbonic anhydrase was not completely inhibited. Within the first 2 h after administration, this small dose caused only a slight decrease in mean standard bicarbonate of 1.8 and 1.7 mmol l-1 in intact (n = 7) and denervated animals (n = 7), respectively. Doses of acetazolamide larger than 4 mg kg-1 (up to 32 mg kg-1) caused a significant increase in the P(a-ET),CO2 gradient. 3. In carotid body-denervated cats, 4 mg kg-1 acetazolamide caused a decrease in the CO2 sensitivity of the central chemoreflex loop (Sc) from 1.52 +/- 0.42 to 0.96 +/- 0.32 l min-1 kPa-1 (mean +/- S.D.) while the intercept on the Pa,CO2 axis (B) decreased from 4.5 +/- 0.5 to 4.2 +/- 0.7 kPa. 4. In carotid body-intact animals, 4 mg kg-1 acetazolamide caused a decrease in the CO2 sensitivity of the peripheral chemoreflex loop (Sp) from 0.28 +/- 0.18 to 0.19 +/- 0.12 l min-1 kPa-1. Se and B decreased from 1.52 +/- 0.55 to 0.84 +/- 0.21 l min-1 kPa-1, and from 4.0 +/- 0.5 to 3.0 +/- 0.6 kPa, respectively, not significantly different from the changes encountered in the denervated animals. 5. It is argued that the effect of acetazolamide on the CO2 sensitivity of the peripheral chemoreflex loop in intact cats may be caused by a direct effect on the carotid bodies. Both in intact and in denervated animals the effects of the drug on Sc and B may not be due to a direct action on the central nervous system, but rather to an effect on cerebral vessels resulting in an altered relationship between brain blood flow and brain tissue PCO2.

Acetazolamide↗
PubMed1977

Comparison of ocular hypotensive effects of acetazolamide and atenolol.

The ocular hypotensive effect of single oral doses of (a) atenolol (50 mg), (b) acetazolamide (500 mg), (c) atenolol (50 mg) and acetazolamide (500 mg) in combination, and (d) vehicle (inert tablets) were compared in 8 patients with glaucoma. In this single-dose, double-masked trial the combination was observed as most effective in reducing ocular tension. Both the combination and atenolol performed markedly better than vehicle. That acetazolamide did not reduce ocular tension significantly more than vehicle is probably explained by relatively low initial ocular tensions. There was no evidence of interaction between atenolol and acetazolamide in this study. Acetazolamide probably remains the first-choice oral medication for glaucoma. It is cautiously suggested that beta-blocking drugs may have a future therapeutic role, but longer-term studies on larger numbers will be required to establish this.

Acetazolamide↗
PubMed1975

Action of acetazolamide on the chick embryo during late development.

Acetazolamide was injected into chick embryos on the 14th or 15th day of incubation. Doses ranging between 5 and 10 mg per egg produced a retardation in the growth of long bones. The affected bones contained a normal proportion of mineral as determined by ashing and presented a normal histological picture. On the basis of these findings, it is suggested that the alterations were not due to a specific direct effect of the drug on bones. The incorporation of 131-I by the thyroid glands of acetazolamide-injected embryos was analyzed radioautographically and quantitated on the same 6 mu-paraffin sections, with a thin window Geiger counter. The incorporation appeared notably reduced 3 h after the injection of acetazolamide and the reduction persisted for a least 24 h.the electron microscopical observation of thyroid follicular cells from similarly treated embryos showed that the cytological characteristics indicating an active protein synthesis were unmodified with respect to those found in control embryos. These results may indicate that acetazolamide inhibits the iodination of the throid hormone without interfering with the synthesis of the globulin. It is suggested that the growth retardation observed in the embryos treated with acetazolamide may be secondary to the action of the drug on the thyroid gland, although this action appears to be a transitory one.

Acetazolamide↗
PubMed2004

Carotid perfusion CT with balloon occlusion and acetazolamide challenge test: feasibility.

Carotid balloon test occlusion (BTO) is used to assess the collateral circulation and cerebrovascular reserve in patients in whom carotid artery occlusion is contemplated. Eight patients in whom the test was successful were evaluated with perfusion computed tomography (CT) in the resting state and after acetazolamide challenge. Three of the patients showed symmetric blood flow and normal response to acetazolamide. One of them underwent permanent carotid occlusion and did not develop any delayed ischemic stroke. The remaining five patients showed asymmetric blood flow. One of them had markedly low blood flow and abnormal response to acetazolamide. The patient developed ipsilateral hemispheric stroke following permanent carotid occlusion after the superficial temporal artery to middle cerebral artery bypass graft occluded. In the other four patients, the steal phenomenon was seen in ipsilateral and contralateral hemispheres. Although definitive quantitative values for perfusion CT are not yet standardized, it may be feasible to predict that the patients with symmetric blood flow and normal acetazolamide-enhanced challenge test results will do well after permanent carotid occlusion. Patients with asymmetric blood flow and abnormal response to the acetazolamide challenge test may require a revascularization procedure to protect them from delayed ischemic stroke.

Acetazolamide↗
PubMed1977

Ouabain, acetazolamide, and Cl-flux in isolated frog skin: evidence for two distinct active Cl-transport mechanisms.

Two distinctly different mechanisms for active Cl- transport in epithelia may exist: one, ouabain-sensitive and cation-dependent, and the other, acetazolamide-sensitive and cation-independent. As a test of this hypothesis the three active Cl- transport systems in isolated short-circuited skin of Rana pipiens were examined. Sensitivity to ouabain (10(-4) M) and acetazolamide (5 X 10(-3) M) and dependence on Na+ and K+ in the medium were ascertained. The first system, net chloride influx in ordinary Ringer, exhibited specific ouabain sensitivity and acetazolamide insensitivity. As we have previously shown this system to be clearly dependent on Na+ on the cis and K+ on the trans side, cation dependence was not re-studied. The second system, isoproterenol-stimulated net Cl- outflux, was also ouabain-sensitive and acetazolamide-insensitive. It was dependent on the presence of Na+ on the cis side, but the K+ dependence was less clear. In contrast to the first two, the third system (net influx in low Cl- medium sulfate Ringer containing 2.4 mM Cl-) was largely ouabain-insensitive, completely acetazolamide-sensitive and independent of both Na+ and K+. Thus, the hypothesis of two distinct mechanisms seems to hold for the three active Cl- transport systems in frog skin. Data from various other Cl- transporting epithelia are examined, and the general applicability of such a scheme of categorization for active Cl- transport mechanisms is discussed.

Acetazolamide↗
PubMed1978

Slow postcapillary changes in blood pH in vivo: titration with acetazolamide.

A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.

Acetazolamide↗
PubMed2006

Mechanisms of action of acetazolamide in the prophylaxis and treatment of acute mountain sickness.

Acetazolamide, a potent carbonic anhydrase (CA) inhibitor, is the most commonly used and best-studied agent for the amelioration of acute mountain sickness (AMS). The actual mechanisms by which acetazolamide reduces symptoms of AMS, however, remain unclear. Traditionally, acetazolamide's efficacy has been attributed to inhibition of CA in the kidneys, resulting in bicarbonaturia and metabolic acidosis. The result is offsetting hyperventilation-induced respiratory alkalosis and allowance of chemoreceptors to respond more fully to hypoxic stimuli at altitude. Studies performed on both animals and humans, however, have shown that this explanation is unsatisfactory and that the efficacy of acetazolamide in the context of AMS is likely due to a multitude of effects. This review summarizes the known systemic effects of acetazolamide and incorporates them into a model encompassing several factors that are likely to play a key role in the drug's efficacy. Such factors include not only metabolic acidosis resulting from renal CA inhibition but also improvements in ventilation from tissue respiratory acidosis, improvements in sleep quality from carotid body CA inhibition, and effects of diuresis.

Acetazolamide↗
PubMed2006

Comparative efficacy of acetazolamide and apraclonidine in the control of intraocular pressure following phacoemulsification.

PURPOSE: The purpose of our study was to compare the effects of systemically administered acetazolamide and topical apraclonidine 0.5% in the control of intraocular pressure (IOP) following phacoemulsification of senile cataracts. SETTING: The study was conducted on patients affected by cataract and followed at the Department of Ophthalmology. METHODS: Seventy-eight eyes in 78 patients were selected. Twenty-six eyes were randomly assigned to postoperative treatment with topical apraclonidine 0.5%, 26 received oral acetazolamide and the remaining 26 received no hypotensive treatment (control group). Statistical analyses were performed mainly by means of analyis of variance. RESULTS: IOPs measured 24 h after surgery were significantly (p = 0.01) lower in the apraclonidine group compared to the control group. CONCLUSIONS: Our double-blind prospective study conducted on patients randomly assigned to treatment with apraclonidine or acetazolamide shows that the former drug is undoubtedly effective in the prevention of IOP increases following phacoemulsification. IOPs recorded in patients treated with this drug were lower than those observed in the acetazolamide and the control groups. Considering the lower risk of toxicity associated with topical administration, apraclonidine 0.5% seems to be preferable to oral acetazolamide in this postoperative setting.

Acetazolamide↗
PubMed1985

Role of carbonic anhydrase in bone: plasma acetazolamide concentrations associated with inhibition of bone loss.

Earlier reports from our laboratory have indicated that the carbonic anhydrase inhibitor acetazolamide blocks the hypercalcemic response to parathyroid hormone. In addition, we have reported that acetazolamide when administered by several routes partially prevents denervation-induced bone loss in a rat model of disuse osteoporosis. Continuous subcutaneous infusion required the least daily dose (8 mg/kg). The present study extends these earlier findings in several ways. It was found that in partially preventing denervation-induced bone loss: (1) incorporation of 1 M THAM [tris(hydroxymethyl)aminoethane] enhanced the potency of acetazolamide such that it was effective at daily doses of 0.6 mg/kg; (2) acetazolamide in the presence of 1 M THAM was effective at plasma concentrations as low as 50 ng/ml which are more than 500-fold less than peak plasma concentrations normally encountered in the human when acetazolamide is being used as a therapeutic agent; and (3) another inhibitor, benzolamide, was also effective by continuous subcutaneous infusion.

Acetazolamide↗
PubMed1995

Assessment of cerebral vasomotor reactivity by transcranial Doppler ultrasound and breath-holding. A comparison with acetazolamide as vasodilatory stimulus.

BACKGROUND AND PURPOSE: Evaluating cerebrovascular vasomotor reactivity seems to be of prognostic relevance for patients with occlusive internal carotid artery disease. To evaluate its clinical usefulness, the recently introduced breath-holding maneuver as a carbon dioxide-dependent vasodilatory stimulus was compared with the acetazolamide challenge by means of transcranial Doppler ultrasound and stable xenon-enhanced computed tomography. METHODS: In a total of 134 middle cerebral arteries of 74 patients (mean +/- SD age, 62 +/- 9 years) with unilateral or bilateral occlusive carotid artery disease, vasomotor reactivity was estimated by the increase of middle cerebral artery mean blood velocity by transcranial Doppler ultrasound, comparing the breath-holding maneuver and 1 g IV acetazolamide as vasodilatory stimuli. The carotid artery findings were classified as normal, stenosis of 50% to < 70%, 70% to < 90%, 90% to 99%, and occlusion. Eighteen of the 74 patients additionally underwent stable xenon-enhanced computed tomography to calculate the increase of mean cortical regional cerebral blood flow in the middle cerebral artery territory after acetazolamide stimulation. RESULTS: The percentage of mean regional cerebral blood flow changes (n = 36 hemispheres) correlated best with the absolute mean blood velocity changes while breath-holding (P = .007, r = .4332). The absolute mean regional cerebral blood flow changes correlated best with the percentage of mean blood velocity changes after acetazolamide stimulation (P = .004, r = .4580). On all 134 middle cerebral arteries, both vasodilatory stimuli correlated highly significantly (P < .0001) when comparing increases in absolute (r = .5448) or relative (r = .3516) mean blood velocity. Both stimulation techniques similarly indicated significantly reduced vasomotor reactivity with increasing degree of internal carotid artery lesions (P < or = .01). However, the acetazolamide challenge differentiated more accurately between the various groups of internal carotid artery findings. CONCLUSIONS: The assessment of vasomotor reactivity by transcranial Doppler ultrasound correlates with cerebral blood flow changes even when different vasodilatory stimuli are used. In cooperative patients the breath-holding maneuver as vasodilatory stimulus seems clinically useful for a first estimation of cerebral vasomotor reactivity.

Acetazolamide↗