(Stroke. 1995;26:1234-1239.)
© 1995 American Heart Association, Inc.
Articles |
Evaluation of the Acetazolamide Test
Vasoreactivity and Cerebral Blood Volume
From the Department of Neurosurgery, Juntendo University, Tokyo, Japan.
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Abstract |
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Background and Purpose We evaluated the potential usefulness of the acetazolamide test by investigating whether acetazolamide vasoreactivity reflected the change in resting cerebral blood volume caused by compensatory vasodilation due to a decline in cerebral perfusion pressure.
Methods We measured resting and acetazolamide-activated cerebral blood flow with a stable xenon-enhanced CT system and resting cerebral blood volume with the subtraction technique using contrast-enhanced CT in 30 patients with various diseases. These parameters were measured in the anterior, middle, and posterior cerebral arterial territories of both hemispheres separately. We evaluated the statistical relationships between resting cerebral blood volume and vasoreactivity in these three territories, and the significance of the correlations was tested by ANOVA/ANCOVA to adjust for the double entries.
Results Significant negative linear relationships were demonstrated between the resting cerebral blood volume and the change in cerebral blood flow, expressed as a percentage induced by acetazolamide activation, for the anterior (r=-.607, P=.0004), middle (r=-.551, P=.0015), and posterior (r=-.523, P=.0078) cerebral arterial territories and between the resting cerebral blood volume and the increase in cerebral blood flow (absolute values) for the anterior (r=-.512, P=.0164) and middle (r=-.523, P=.0001) but not the posterior (r=-.571, P=.0563) cerebral arterial territories.
Conclusions The acetazolamide test appears to be useful for the investigation of compensatory vasodilation: the vasoreactivity can be calculated as the increased cerebral blood flow expressed as a percentage or an absolute value, which both reflect cerebral blood volume directly.
Key Words: acetazolamide • cerebral blood flow • cerebral blood volume • tomography
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The hemodynamic changes due to a decline in cerebral perfusion pressure (CPP) have been studied by many investigators to gain an understanding of hemodynamic compromise. Experiments in animals have shown that a progressive reduction of the CPP leads to an initial increase in the cerebral blood volume (CBV),1 which is followed by a reduction in the cerebral blood flow (CBF) and finally a decrease in oxygen metabolism.2 These changes have been demonstrated to occur in humans. Positron emission tomography (PET) studies demonstrated that in the hemisphere with a reduced CPP, the CBV increased significantly, but the CBF was almost normal.3 4 When the reduction in CPP is so severe that autoregulation fails, the CBF falls relative to the cerebral oxygen metabolism, and the oxygen extraction fraction increases.3 5 6 7 Furthermore, a correlation between a low CBF and low cerebral oxygen metabolism has been demonstrated in some patients,3 4 resulting from selective neuronal loss induced by ischemia.8 9 Therefore, measurement of the CBF in the resting state alone is considered inadequate for the evaluation of hemodynamic compromise,7 and a rise in CBV is thought to be an initial sensitive indicator of a fall in CPP and probably reflects compensatory vasodilation within the autoregulatory range.
Previous studies in experimental animal models have shown that a reduction in the CPP decreases the vasoreactivity to CO2 because CO2-reactive arterioles dilate progressively in the low autoregulatory range.10 11 It was suggested that the so-called lower limit of autoregulation would be determined by the maximal dilation of these arterioles.11 In clinical studies, Pistolese et al12 observed poor vasoreactivity to hypercapnia in patients whose CBF was maintained during carotid clamping. Furthermore, in patients with reduced CBF, they found a paradoxical reversed vasoreactive response to hypercapnia that resulted in further CBF reduction, which presumably was due to intracerebral steal, since maximal vasodilation had already occurred in the region with reduced CBF. Dyken13 and Norrving et al14 also showed that patients with reduced CPP had impaired CO2 responses. In summary, in light of these results, a decline in the CPP would be expected to evoke compensatory vasodilation to maintain the CBF, with a consequent increase in the CBV and reduction in the response of cerebral vasculature to CO2.
On the assumption that this is the case, trials of acetazolamide administration, which is believed to induce vasodilation in a manner similar to CO2, have been carried out to investigate decreased CPP and estimate the extent of compensatory vasodilation that occurs by measuring the reserve vasodilatory capacity. If the vasodilatory reserve, obtained by measuring the vasoreactivity to acetazolamide, does reflect compensatory vasodilation substantially, then it should reflect the CBV, which would be changed by compensatory vasodilation.
In this study, we measured the acetazolamide vasoreactivity by measuring the CBF using stable xenon-enhanced CT (Xe-CT), and we determined the CBV in the resting state with the CT scanning subtraction technique to establish whether acetazolamide vasoreactivity reflected the CBV, to evaluate the potential usefulness of the acetazolamide test.
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Subjects and Methods |
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We investigated 30 patients with various diseases to evaluate their hemodynamic conditions (Table 1
). None of these
patients had large areas of brain damage, such as major cerebral
infarction, that might possibly lead to reduced microvasculature
density (at least in the standardized slice, which is discussed later).
The necessity for precise CBF measurement by stable Xe-CT was
determined on the basis of the presence of symptoms and signs thought
to be due to ischemia or results of other imaging modalities
routinely performed at our hospital, such as conventional and MR
angiography and single-photon emission CT. We explained to all the
patients or their parents the necessity for and significance of CBF
measurement and acetazolamide testing with stable Xe-CT as well as the
purpose of this trial.
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We selected a standardized slice that passed through the basal ganglia
and included the midsection of the anterior horns of the lateral
ventricles, caudate, putamen, thalamus, and pineal body for
investigation. For each patient, we identified the bilateral regions of
each vascular territory, ie, the areas fed by the anterior (ACA),
middle (MCA), and posterior (PCA) cerebral arteries and measured the
CBF and CBV in both sides separately (Fig 1). In
patients with arachnoid cysts, a slice 10 to 15 mm below the
standardized slice was scanned to investigate the focal region adjacent
to each cyst; therefore, these slices did not include the entire PCA
territory. In patients with Sturge-Weber syndrome, it was possible that
the CBV in the occipital lobes had increased beyond the physiological
range because vascular abnormalities, mainly dilated veins, that were
not considered to result from hemodynamic compromise were demonstrated
angiographically. Overall, we studied 60 regions involving both the ACA
and MCA vascular territories and 54 regions in the PCA territory.
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CBF Measurement
The CBF studies were performed using an Xe study system adapted
from the Toshiba 20A scanner (Toshiba). Scanning of each standardized
slice was carried out 13 times per period (256x256 pixels, 276 MAS)
during wash-in for 4 minutes and washout for 6 minutes with a 30% Xe
delivery system (AZ-721, ANZAI). The chamber into which the sampler
selectively delivered the end-tidal gas exhaled by a patient each time
he or she breathed was scanned together with the patient's head. The
CT density of the end-tidal Xe gas in the chamber was measured and
converted into the Xe concentration to obtain the curve of Xe
concentration in arterial blood against time. The CBF was calculated
from the curves of the Xe concentrations in the brain and arterial
blood against time (2x2 pixels). We monitored the tidal volume and
respiration rates and coached the patient as necessary to breathe in
his or her natural manner. The arterial CO2 tension was
measured intermittently with an electrode measurement system (IL BGE,
Instrumentation Laboratory). The acetazolamide-activated CBF was
measured 20 minutes after an intravenous bolus injection of
acetazolamide (20 mg/kg body wt). We obtained the resting and
acetazolamide-activated CBF values and calculated 
CBF as
acetazolamide-activated CBF-resting CBF and %CBF as
([acetazolamide-activated CBF-resting CBF]/resting CBF)x100%.
CBV Measurement
Penn et al15 measured the CBV by subtracting the CT
density measurements taken before an intravenous infusion of a contrast
medium from those taken after infusion. Our method was based on theirs,
but we corrected the CBV according to the hematocrit in the brain and
measured it in the same standardized slice as that in which the CBF was
measured. First, we scanned without contrast medium enhancement and
then scanned the same slice with enhancement. A preliminary dynamic CT
study showed that the curve of iopamidol concentration in blood from
the straight sinus against time had a initial high peak about 15
seconds after the bolus injection, followed by a low peak approximately
30 seconds after injection. After the second peak, the concentration
stabilized, and the concentration time curve was virtually flat 1
minute after the injection. Therefore, to obtain a stable concentration
in the blood, we injected 100 mL iopamidol (612.4 mg/mL) over 2 minutes
and scanned 4 minutes after starting the injection. We obtained the
mean density, which indicated the average density change per pixel,
in each vascular territory bilaterally from the subtracted image (Fig 2), and the CBV (milliliters per 100 g) was calculated
as (mean density in each vascular
territory/[1-0.85xhematocrit])x100/(mean density in straight
sinus/[1-hematocrit]). We verified the one-to-one correspondence of
the percentage concentration of iopamidol to percentage density in a
preliminary phantom study.
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With patients in the resting state, the CBF and then the CBV were measured. The acetazolamide-activated CBF was measured approximately 1 hour later to avoid any effects of the injected contrast medium on the CBF measurement.
Statistical Treatment
To investigate the relationships between resting CBV and CBF
and %CBF, a linear regression analysis was performed on 60 CBF
and CBV measurements (30 patientsx2 hemispheres) in the ACA and MCA
territories and on 54 CBF and CBV measurements (27 patientsx2
hemispheres) in the PCA territory. In general, when several
measurements are taken for the same patient, they tend to be correlated
with each other. Because a preliminary evaluation showed correlations
in the CBV and acetazolamide vasoreactivity between the two
hemispheres, the univariate linear model was not considered
appropriate. If a measurement can be thought of as a response to the
value of an experimental factor of interest, the correlation can be
taken into account by performing ANOVA/ANCOVA. This analysis
adjusts the correlation bias depending on double entries (two
measurements per patient) because the effect of the independent term
for each patient is used in the model as follows.
The ANOVA/ANCOVA model was given as
Yij=µ0+Ti+rXij+
ij,
where i=1 (30 patients), j=1 (2 hemispheres), µ0 is the
overall mean, Ti is the effect of each patient
level, r is a regression coefficient for the relationship
between Y and X, ij is the value
of the error term, Yij is the value of the
dependent variable, and Xij is the value of the
independent variable. Testing for linearity of regression involves the
same alternatives as those for ANOVA models: for Ho,
r equals zero; for H1, r is not equal
to zero. In our model, the CBF and %CBF were used as dependent
variables, and the resting CBV was used as the independent variable;
analysis was performed using a statistical analysis package,
ANALYST (Fujitsu Ltd). To evaluate the results of the
analysis, the significance criterion for a correlation (two-tailed
test) was adjusted for multiple observations (ie, P=.05, for
3 correlations=.0167).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Resting and Acetazolamide-Activated CBF and Resting CBV
The values obtained for resting and acetazolamide-activated CBF and resting CBV are presented in Table 2
. As a
result of acetazolamide activation, CBF was increased by 11.5±8.0
(mean±SD) mL/100 g per minute or 34.9±25.9% in the ACA territory,
14.7±10.5 mL/100 g per minute or 39.2±30.3% in the MCA territory,
and 15.0±8.4 mL/100 g per minute or 47.3±28.9% in the PCA
territory.
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Relationship Between Resting CBV and CBF
The relationships between the resting CBV and CBF in the ACA
and MCA territories after acetazolamide activation were negative and
linear, and ANOVA/ANCOVA showed they were significant. Letting
y=CBF (mL/100 g per minute) and x=resting CBV
(mL/100 g), for the ACA, y=23.2-2.6x,
r=-.512, P=.0164; for the MCA,
y=38.4-4.1x, r=-.523,
P=.0001. In the PCA territory this relationship failed to
reach significance (y=30.6-3.1x,
r=-.571, P=.0563).
Relationship Between Resting CBV and %CBF
The relationships between the resting CBV and %CBF in each
territory also were negative and linear (Fig 3) and were
shown by ANOVA/ANCOVA to be significant (for the ACA,
r=-.607, P=.0004; for the MCA,
r=-.551, P=.0015; and for the PCA,
r=-.523, P=.0078).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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CBV Measurement
Precise measurement of CBV has proven difficult. Few studies have been carried out in humans, in whom normal CBV values of 3 to 4 mL/100 g have been obtained using different methods.16 17 18 19 Recent studies yielded CBV values measured by PET of 4.3±0.4 mL/100 g3 and 3.4±0.3 mL/100 g4 in normal control subjects. Our method of CBV measurement was based on that reported by Penn et al,15 and our CBV values were similar to or slightly higher, especially in the MCA territory, than those reported in normal control subjects. There are several possible explanations for the difference. First, there are subject differences. We measured CBF and CBV only in patients requiring hemodynamic investigation. In view of the pathophysiological response to a fall in CPP, the CBV values in our subjects would have been greater than those in normal control subjects. Second, there are differences in the nature of the regions. Grubb et al19 reported significant differences between CBV values of scanned slices measured by PET. They attributed the differences to the different ratios of gray to white matter, since gray matter has a denser microvasculature than white matter.20 The CBV values we obtained were the mean CBVs of the vascular territories in the standardized CT slice. Although the ACA and PCA territories included only the convexity cortex and white matter, the MCA territory included the convexity, temporal lobe medial, and insular cortices, and it therefore would have had a higher ratio of gray to white matter. Because each vascular territory in the standardized slice had a different gray to white matter ratio, this may account for the different CBV values. Third, there may have been methodological problems. Eichling et al21 and Phelps et al22 used a plasma tracer and pointed out the possibility of overestimating the CBV when damage to the blood-brain barrier was suspected. Furthermore, we corrected for the small vessel or tissue hematocrit, which we took as 85% of the large vessel hematocrit.19 Rosenblum23 cautioned that acute diseases of the brain, such as ischemic infarction, may cause changes in local tissue hematocrit. Because all the patients in whom we measured the CBV were in the late phases of their diseases, we think they were unlikely to have had blood-brain barrier damage and large tissue hematocrit differences. However, it is possible that the contrast medium itself may have induced some arteriolar vasodilation, since peripheral arterial vasodilation after contrast medium injection has been reported.24 Considering the CBV values in patients with carotid occlusions, 5.08±1.30 mL/100 g6 and 3.9 to 8.2 mL/100 g4 , we speculate that the values we obtained could be correct, although we cannot rule out the possibility that the CBV was overestimated as a result of methodological problems.
Acetazolamide Vasoreactivity
Acetazolamide penetrates the blood-brain barrier slowly and
inhibits carbonic anhydrase, which has been detected widely in cerebral
tissue,25 thus inducing acidosis26 27 28 with
resulting blockade of the vasoreaction to
CO2.29 30 Therefore, acetazolamide
administration induces a considerable increase in CBF similar to that
evoked by CO2 inhalation, which reaches about 70% of that
in normal control subjects,31 and can be attributed to
vasodilation of small arterioles11 32 due to a decrease in
tissue pH.31 33
Although the acetazolamide test is performed to evaluate the decrease in CPP through the investigation of the reserve vasodilatory capacity, which is thought to reflect compensatory vasodilation, very few studies have demonstrated that the reserve vasodilatory capacity, ie, acetazolamide vasoreactivity, directly reflects the decreased CPP or parameter changes due to a decline in CPP. Accordingly, the method for estimating acetazolamide activation has not been assessed yet definitively. In some studies,31 33 34 acetazolamide activation was assessed with methods based on the laterality of the CBF, that is the asymmetry, because of the rather wide range of acetazolamide vasoreactivity in normal control subjects31 33 ; it was found that the asymmetry was correlated with angiographic findings in patients with unilateral carotid diseases. We investigated all of the present cases using ordinary methods including angiography, but in the majority of cases (excluding those of stenosis or occlusion of internal carotid artery) we were unable to determine the predominant side. Therefore, such assessments were impossible in this study.
Ideally, assessments based on the asymmetry of CBF are made by assuming
normal acetazolamide vasoreactivity on the contralateral side. It has
been indicated that unilateral occlusion might decrease the
vasoreactivity on the contralateral side in some cases.31
Also, Moyamoya disease, as an example of a bilateral disease, would
show severe hemodynamic compromise on both sides, similar to that in
cases of bilateral carotid occlusion.3 Therefore, we think
that an assessment based on CBF asymmetry or difference might provide
an underestimation in some cases considered to be due primarily to
unilateral disease and that it would not be applicable to cases of
bilateral disease. Furthermore, in an investigation of Sturge-Weber
syndrome in which the primarily affected side can be determined easily
by radiology, we found a correlation between clinical progression and
acetazolamide vasoreactivity expressed as CBF on the contralateral
side and not on the affected side, although the CBF asymmetry in both
resting and acetazolamide-activated conditions showed no
correlation.35 We therefore chose CBF and %CBF in
each hemisphere and evaluated the acetazolamide activation by
investigating their relationships with CBV independently of the
laterality of the pathological condition, using high-resolution stable
Xe-CT.
If the degree of acetazolamide vasoreactivity does reflect the extent
of compensatory vasodilation resulting from a decrease in the CPP, then
poor acetazolamide vasoreactivity should reflect the increased CBV due
to compensatory vasodilation directly. We obtained statistically
significant relationships between CBV and CBF in the ACA and MCA,
but not the PCA territories, and between CBV and %CBF in all three
territories. Although the relationship between CBV and CBF in the
PCA territory failed to reach significance, it tended to be similar to
relationships in the other territories. As the PCA territory is located
near the basal surface of the brain in our standardized slice, its CBV
values would include the CBV in the draining veins, which was not
related to compensatory vasodilation, to a greater extent than those in
other territories. We speculate that this special condition caused by
the location of the PCA led to the lack of significance of the
relationship between the CBV and CBF of the PCA territory.
On the basis of our finding that CBF and %CBF do reflect the CBV
of both hemispheres directly, we consider that acetazolamide activation
can be used to estimate compensatory vasodilation, which should lead to
a change in the CBV secondary to a decrease in the CPP, by calculating
the CBF or %CBF in the bilateral hemispheres independently.
A recent study indicated that the total length of the microvascular
network including arterioles would decrease after ischemic
insults and that recovery of the microcirculation after prolonged
ischemia would be partial.36 Therefore, it is
possible that the number, or total length, of arterioles that react to
acetazolamide may be reduced under pathological conditions such as
incomplete infarction, as proposed by Lassen et al8 who
showed that a low resting CBF correlated with low metabolism due to the
brain having been damaged by prolonged ischemia. Even if
residual arterioles under such conditions are able to react
appropriately to acetazolamide administration, CBF would be
expected to be smaller than that in the normal vascular network. Under
such conditions, a small CBF value may not always indicate a large
compensatory vasodilation and may actually only reflect the severity of
the initial ischemic insult. Therefore, we suggest that the
calculation of %CBF evoked during the acetazolamide activation is a
better parameter than CBF for the evaluation of CPP decreases in the
autoregulatory range.
We intend to investigate the precision of the estimation yielded by the acetazolamide test, especially in patients with conditions that result in an abnormally low residual acetazolamide vasoreactivity.
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Acknowledgments |
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We thank S. Ohtsuki of the Biostatistics Group, Kureha Chemical Industry Co Ltd, for support with statistical analysis and K. Nambu of CT Systems Engineering Department, Toshiba Nasu Works, for technical support. Dr D.B. Douglas assisted with the preparation of the manuscript.
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Footnotes |
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Reprint requests to Yojiro Okudaira, MD, Department of Neurosurgery, Tokyo Metropolitan Hiroo General Hospital, 2-34-10 Ebisu, Shibuya-ku, Tokyo 150, Japan.
Received April 18, 1994; revision received April 10, 1995; accepted April 10, 1995.
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References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Grubb RL Jr, Phelps ME, Raichle ME, Ter-Pogassian MM. The effect of arterial blood pressure on the regional cerebral blood volume by x-ray fluorescence. Stroke. 1973;4:390-399.
2. Grubb RL Jr, Raichle ME, Phelps ME, Ratcheson RA. Effects of increased intracranial pressure on cerebral blood volume, blood flow and oxygen utilization in monkey. J Neurosurg. 1975;43:385-398. [Medline] [Order article via Infotrieve]
3. Gibbs JM, Leeders KL, Wise RJS, Jones T. Evaluation of cerebral perfusion reserve in patients with carotid artery occlusion. Lancet. 1984;1:310-314. [Medline] [Order article via Infotrieve]
4. Leblanc R, Tyler JL, Mohr G, Meyer E, Dilsic M, Yamamoto L, Taylor L, Gauthier S, Hakim A. Hemodynamic and metabolic effects of cerebral revascularization. J Neurosurg. 1987;66:529-535. [Medline] [Order article via Infotrieve]
5.
Baron JC, Bousser MG, Rey A, Guillard A, Comar D,
Gastaigne P. Reversal of focal `misery-perfusion syndrome' by
extracranial-intracranial arterial bypass in hemodynamic cerebral
ischemia: a case study with 15O positron emission
tomography. Stroke. 1981;12:454-459.
6. Powers WJ, Grubb RL, Raichle ME. Physiological responses to focal cerebral ischemia in humans. Ann Neurol. 1984;16:546-552. [Medline] [Order article via Infotrieve]
7.
Powers WJ, Raichle ME. Positron emission
tomography and its application to the study of cerebrovascular disease
in man. Stroke. 1985;16:361-376.
8. Lassen NA, Olsen TS, Hojgaard K, Skriver E. Incomplete infarction: a CT negative irreversible ischemic brain lesion. J Cereb Blood Flow Metab. 1983;3(suppl 1):602-603.
9.
Metter EJ, Mazziotta JC, Itabashi HH, Mankovich NJ,
Phelps ME, Kuhl DE. Comparison of glucose metabolism, x-ray CT,
and postmortem data in patients with multiple cerebral
infarcts. Neurology. 1985;35:1695-1701.
10. Harper AM, Glass HI. Effect of alternation in the arterial carbon dioxide tension on the blood through the cerebral cortex at normal and low flow arterial blood pressure. J Neurol Neurosurg Psychiatry. 1965;28:449-452.
11.
Kontos HA, Wei EP, Navari RM, Levasseur JE, Rosenblum
WI, Patterson Jr JL. Responses of cerebral arteries and
arterioles to acute hypotension and hypertension. Am J
Physiol. 1978;234:H371-H383.
12. Pistolese GR, Faraglia V, Spartera C, Tata MV, Lauri D, Agnoli A. Relationship between different levels of CBF and reactivity to physiological stimuli (CO2 and MABP). In: Langfitt TW, McHenry LC Jr, Reivich M, Wollman H. Cerebral Circulation and Metabolism. New York, NY: Springer-Verlag; 1975:272-275.
13. Dyken ML. Intracranial `steal' in complete occlusion of the internal carotid artery. Eur Neurol. 1971;6:301-305. [Medline] [Order article via Infotrieve]
14.
Norrving B, Nilsson B, Riesenberg J. rCBF in
patients with carotid occlusion: resting and hypercapnic flow related
to collateral pattern. Stroke. 1982;13:155-162.
15.
Penn RD, Walser R, Ackerman L. Cerebral blood
volume in man: computed analysis of a computerized brain
scan. JAMA. 1975;234:1154-1155.
16.
Kuhl DE, Reivich M, Alavi A, Nyary I, Staum MM.
Local cerebral blood volumes determined by three-dimensional
reconstruction of radionuclide scan data. Circ
Res. 1975;36:610-619.
17.
Grubb RL, Phelps ME, Ter-Pogossian MM. Regional
cerebral blood volume in humans: x-ray fluorescence studies.
Arch Neurol. 1973;28:38-44.
18. Mathew NT, Meyer JS, Bell RL, Johnson PC, Neblett CR. Regional cerebral blood flow and volume measured with the gamma camera. Neuroradiology. 1972;4:133-140. [Medline] [Order article via Infotrieve]
19. Grubb RL, Raichle ME, Higgins CS, Eichling JO. Measurement of regional cerebral blood volumes by emission tomography. Ann Neurol. 1978;4:322-328. [Medline] [Order article via Infotrieve]
20.
Weiss HR, Buchweitz E, Murtha TJ, Auletta M.
Quantitative regional determination of morphometric indices of
the total and perfused capillary network in the rat brain.
Circ Res. 1982;51:494-503.
21. Eichling JO, Gado MH, Grubb RL Jr, Larson KB, Raichle ME, Ter-Pogossian MM. Potential pitfalls in the measurement of regional cerebral blood volumes. In: Harper M, Jennet B, Miller D, Rowan J, eds. Blood Blow and Metabolism in the Brain: Proceedings of the 7th International Symposium on Cerebral Blood Flow and Metabolism. Edinburgh/London, UK: Churchill Livingstone Inc; 1975:7.15-7.19.
22. Phelps ME, Kuhl DE. Pitfall in the measurement of cerebral blood volume with computed tomography. Radiology. 1976;121:375-377. [Abstract]
23.
Rosenblum WI. Can plasma skimming or inconstancy
of regional hematocrit introduce serious error in regional cerebral
blood flow measurement of their interpretation?
Stroke. 1972;3:248-254.
24. Alguacil LF, Gonzales C, Bohle F, Jimenez I, Alamo C, Martin JL. Contrast media algogenic potential in peripheral arteriography: potentiation of bradykinin-induced pain in the rat. Invest Radiol. 1994;29:294-300. [Medline] [Order article via Infotrieve]
25. Ridderstrale Y, Hanson M. Histochemical study of the distribution of carbonic anhydrase in the cat brain. Acta Physiol Scand. 1985;124:557-564. [Medline] [Order article via Infotrieve]
26. Hauser D, Astrup J, Lassen NA, Betz E. Brain carbonic acid acidosis after acetazolamide. Acta Physiol Scand. 1975;93:385-390. [Medline] [Order article via Infotrieve]
27. Severinghaus JW, Cotev S. Carbonic acidosis and cerebral vasodilatation after Diamox. Scand J Clin Lab Invest Suppl. 1968;102:I:E.
28. Vorstrup S, Henriksen L, Paulson OB. Effect of acetazolamide on cerebral blood flow and cerebral metabolism rate for oxygen. J Clin Invest. 1984;74:1634-1639.
29. Gotoh F. Carbonic anhydrase inhibition and cerebral venous blood gases and ions in man. Arch Intern Med. 1966;11:39-46.
30. Meyer JS. Interaction of cerebral hemodynamics. Neurology. 1961;11:46-65.
31. Sullivan HG, Kingsbury TB IV, Morgan ME, Jeffcoat RD, Allison JD, Goode JJ, McDonnel DE. The rCBF response to Diamox in normal subjects and cerebrovascular disease patients. J Neurosurg. 1987;67:525-534. [Medline] [Order article via Infotrieve]
32. Gotoh F, Muramatsu F, Fukuuchi Y, Amano T. Dual control of cerebral circulation: separate sites of action in vascular tree in autoregulation and chemical control. Stroke. 1973;4:327. Abstract.
33.
Vorstrup S, Brun B, Lassen NA. Evaluation of the
cerebral vasodilatory capacity by the acetazolamide test before EC-IC
bypass: surgery in patients with occlusion of the internal carotid
artery. Stroke. 1986;17:1291-1298.
34. Schroeder T. Cerebrovascular reactivity to acetazolamide in carotid artery disease: enhancement of side-to-side CBF asymmetry indicates critical reduced perfusion pressure. Neurol Res. 1986;8:231-236. [Medline] [Order article via Infotrieve]
35. Sato K, Okudaira Y, Arai H. Hemodynamics in Sturge-Weber syndrome, observed by means of stable xenon CT. Childs Nerv Syst. 1994;10:408. Abstract.
36. Yoshimine T, Kato A, Hayakawa T, Ushio Y, Mogami H. Deterioration and recovery of microcirculation during cerebral ischemia and recirculation: automated morphometric analysis. J Cereb Blood Flow Metab. 1987;7(suppl 1):S337. Abstract.
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 M. Wiart, Y. Berthezene, P. Adeleine, P. Feugier, P. Trouillas, J.-C. Froment, and N. Nighoghossian Vasodilatory Response of Border Zones to Acetazolamide Before and After Endarterectomy : An Echo Planar Imaging-Dynamic Susceptibility Contrast-Enhanced MRI Study in Patients With High-Grade Unilateral Internal Carotid Artery Stenosis Stroke, July 1, 2000; 31(7): 1561 - 1565. [Abstract] [Full Text] [PDF]
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 D. G. Nabavi, A. Cenic, R. A. Craen, A. W. Gelb, J. D. Bennett, R. Kozak, and T.-Y. Lee CT Assessment of Cerebral Perfusion: Experimental Validation and Initial Clinical Experience Radiology, October 1, 1999; 213(1): 141 - 149. [Abstract] [Full Text]
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R. Brilla, D. G. Nabavi, G. Schulte-Altedorneburg, V. Kemeny, D. Reichelt, S. Evers, U. Schiemann, and I.-W. Husstedt Cerebral Vasculopathy in HIV Infection Revealed by Transcranial Doppler : A Pilot Study Stroke, April 1, 1999; 30(4): 811 - 813. [Abstract] [Full Text] [PDF]
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P. T. Ulrich, S. Kroppenstedt, A. Heimann, O. Kempski, and B. G. Lyeth Laser-Doppler Scanning of Local Cerebral Blood Flow and Reserve Capacity and Testing of Motor and Memory Functions in a Chronic 2-Vessel Occlusion Model in Rats • Editorial Comment Stroke, November 1, 1998; 29(11): 2412 - 2420. [Abstract] [Full Text] [PDF]
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Y. Okudaira, H. Arai, and K. Sato Cerebral Blood Flow Alteration by Acetazolamide During Carotid Balloon Occlusion : Parameters Reflecting Cerebral Perfusion Pressure in the Acetazolamide Test Stroke, April 1, 1996; 27(4): 617 - 621. [Abstract] [Full Text]
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