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(Stroke. 1995;26:1572-1576.)
© 1995 American Heart Association, Inc.

Articles

Effect of Adenosine on Cerebral Blood Flow as Evaluated by Single-Photon Emission Computed Tomography in Normal Subjects and in Patients With Occlusive Carotid Disease

A Comparison With Acetazolamide

Andrea Soricelli, MD; Alfredo Postiglione, MD; Alberto Cuocolo, MD; Simona De Chiara, MD; Antonio Ruocco, MD; Arturo Brunetti, MD; Marco Salvatore, MD Peter J. Ell, MD

From the Nuclear Medicine Unit, Medical School, "Federico II" University, National Cancer Institute "G. Pascale," and Nuclear Medicine Center of the National Council of Research (A.S., A.C., A.B., M.S.), and the Institute of Internal Medicine and Metabolic Diseases, Medical School, "Federico II" University (A.P., S. De C., A.R.), Naples, Italy; and the Institute of Nuclear Medicine, University College and Middlesex School of Medicine, London, UK (P.J.E.).

Correspondence to Andrea Soricelli, MD, Servizio di Medicina Nucleare, Facoltà di Medicina e Chirurgia, Università degli Studi "Federico II," via S Pansini 5, 80131 Naples, Italy.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose Acetazolamide is commonly used with single-photon CT to assess the cerebrovascular reserve in patients with internal carotid artery stenosis or occlusion. In this study we wanted to evaluate the effects of adenosine, a well-known vasodilatatory compound with a short biological half-life, on brain circulation in humans and compare the results with those of acetazolamide.

Methods Acetazolamide (1 g) and adenosine (140 µg/kg per minute) were injected intravenously on different days in 6 normal subjects and 6 patients: 4 with unilateral stenosis, 1 with bilateral stenosis, and 1 with complete occlusion of the internal carotid artery. Changes in regional cerebral blood flow relative to that of the cerebellum (cortico/cerebellar ratios) from resting conditions were evaluated by ^99mTc–hexamethylpropyleneamine oxime and single-photon emission CT.

Results The measured blood flow ratios increased significantly in the normal group 20 minutes after acetazolamide injection in several cortical and subcortical regions, as well as at the 4th minute of a 6-minute adenosine infusion. Regional cerebral blood flow ratio values were higher after adenosine than after acetazolamide in both cortical (frontal and parietal) and subcortical (thalamus and basal ganglia) regions. In 4 of the 6 patients the side-to-side asymmetry increased from the basal resting condition after the injection of acetazolamide and even more so after the injection of adenosine.

Conclusions Adenosine infusion causes vasodilatation of cerebral arteries and can be used for the investigation of cerebrovascular perfusion capacity in patients with carotid occlusive disease. One advantage in the use of adenosine over acetazolamide is the possibility of interrupting the test with reversal of clinical symptoms or patient discomfort within a few minutes.

Key Words: acetazolamide • adenosine • carotid artery diseases • tomography, emission-computed • cerebral blood flow

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Patients with carotid and/or cerebrovascular disease often have hemodynamic impairment of blood supply to the brain with reduced CVRC, which could be evaluated by the intravenous injection of acetazolamide (Diamox, Lederle) at the usual dose of 1 g. In normal subjects the increase of CBF is approximately 50%, although the effect of acetazolamide is fairly slow and appears to be maximal 20 minutes after intravenous administration^{1 2 3} ; in pathological conditions it is possible to demonstrate areas with a reduced CBF response due to reduced vasoreactivity that therefore are at high risk of developing acute ischemia. Acetazolamide injection has to date been used to evaluate CVRC in patients with carotid stenosis,^{3 4} transient ischemic attacks,⁵ cerebrovascular disease,⁶ diabetes mellitus,^{7 8} or before extracranial-intracranial bypass⁹ with the use of nuclear medicine techniques, such as SPECT with ¹³³Xe⁴ or ^99mTc-HMPAO¹⁰ or even transcranial Doppler sonography.^{8 11}

The effects of adenosine on CBF regulation have also been investigated: intravenous infusion of adenosine causes a rapid and marked cerebral vasodilatation^{12 13 14} with increased CBF.¹⁵ Adenosine also demonstrates antithrombotic activity¹⁶ and may also have a neuroprotective effect in cerebral ischemia.¹⁷ However, limited data are available on the effects of adenosine on human brain circulation: in six normoventilated subjects studied by PET under general anesthesia with a mean dose of 337 µg/kg per minute of adenosine, CBF increased by a mean of 55%.¹³

The aims of our study were to assess, with the use of SPECT and ^99mTc-HMPAO, the effects of the intravenous injection of adenosine on brain perfusion at the standard dose of 140 µg/kg per minute for 6 minutes as reported for cardiac stress studies¹⁸ and to compare these effects with those obtained after the intravenous injection of acetazolamide at the standard dose of 1 g. The study was performed in 6 normal subjects and 6 patients: 4 with unilateral stenosis, 1 with bilateral stenosis, and 1 with unilateral occlusion of the internal carotid artery.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Six normal subjects (3 men and 3 women; mean±SD age, 52±8 years) without metabolic or cardiovascular diseases and 6 patients with internal carotid occlusive disease (5 men, 1 woman; mean±SD age, 60±9 years) were studied. All subjects and patients gave their informed consent. CT or MRI of the brain was performed before the SPECT studies, together with ultrasound Doppler examination of the extracranial carotid arteries (Biosound 2000-II).

Three SPECT scans were performed on different days: the first under resting conditions with the eyes open and the ears unplugged without any acoustic, visual, or motor stimulation; the second 20 minutes after the intravenous injection of 1 g acetazolamide (Diamox, Lederle); and the third at the 4th minute of a 6-minute intravenous infusion of 140 µg/kg per minute of adenosine (5 mg/mL, 10.5-mL vials, Middlesex Pharmacy). The second and third studies were always performed randomly under environmental conditions similar to those for the first basal investigation. All subjects and patients had not taken any methylxanthine products (eg, caffeine, theophylline) for at least 24 hours before the adenosine infusion.

Brain perfusion was studied with a brain-dedicated system based on an annular single crystal device (CERASPECT, Digital Scintigraphics Inc). A 30-minute acquisition was performed 15 to 20 minutes after the intravenous injection of 800 MBq of ^99mTc-HMPAO (Ceretec, Amersham); transaxial, sagittal, and coronal images were reconstructed with the use of the back projection method and a Butterworth filter. A semiquantitative method was used for the evaluation of tracer uptake: for normal subjects, a standard set of multiple circular ROIs (10 pixels in diameter, approximately 1.6 cm) was drawn over the cerebellum and at four levels over the supratentorial planes. Irregular ROIs were drawn over the thalamus and basal ganglia. Relative regional perfusion was defined as the ratio between regional and cerebellar activity. In patients with carotid occlusive disease, the side-to-side asymmetry between hypoperfused areas or areas distal to the carotid stenosis and the contralateral normal regions was calculated as follows: (tracer uptake in hypoperfused area)-(tracer uptake in normal contralateral area)/(tracer uptake in normal contralateral area). Before and after the injection of adenosine and acetazolamide, heart rate, systolic and diastolic blood pressures, and possible side effects were monitored in patients and control subjects.

Statistical significance was set at P<.05 with the paired Student's t test with two-tailed analysis. Comparisons of cerebral perfusion ratios were performed between basal and acetazolamide, between basal and adenosine, and between adenosine and acetazolamide changes.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Results in Normal Subjects
No evidence of focal or diffuse abnormality was detected in normal subjects on CT or MRI scans. Carotid arteries were patent without any stenosis or sign of atherosclerosis. The highest CBF ratios were obtained in the subcortical regions, such as the thalamus and basal ganglia, and in the bilateral temporal cortex. The CBF ratios significantly increased 20 minutes after acetazolamide injection in all the ROIs considered: in the cortex the highest values were observed in the frontal and parietal areas, while the lowest were observed in the occipital regions. The ratios in the thalamus also showed a marked bilateral increase 20 minutes after acetazolamide injection. During the adenosine test, the CBF ratios significantly increased even more markedly in all the aforementioned regions. Differences in percentage changes from the basal resting conditions are shown in Table 1. In the cortex the increase of CBF ratios during adenosine injection was greater than 20% in both the parietal and the frontal regions, while a less marked increase was observed at the basal ganglia level. However, in all the ROIs the CBF ratio increase was always higher after the injection of adenosine than after the injection of acetazolamide.

View this table: [in this window] [in a new window]   Table 1. Percent Changes in Blood Flow Ratios After Injection of Acetazolamide and Adenosine in Six Normal Subjects

Results in Patients With Carotid Occlusive Disease
Different hemodynamically significant stenoses or occlusion of the internal carotid arteries were detected by Doppler ultrasonography in all 6 patients. Table 2 shows the asymmetry of CBF ratios between hypoperfused and normal contralateral areas under resting conditions and after both vasodilatatory tests. In 4 patients (2 with unilateral severe stenosis, 1 with bilateral severe stenosis, and 1 with carotid occlusion), the asymmetry index increased after the injection of acetazolamide and even more so after the injection of adenosine. Increase in the CBF ratio occurred in the normally perfused contralateral area with normal CVRC, while the ratios remained unchanged or were even reduced in the areas with lower blood perfusion. Fig 1 shows the SPECT images of patient 2 (a 76-year-old man) before and during the acetazolamide and adenosine tests: the decrease in tracer uptake, already observed distal to the right internal carotid stenosis in basal conditions, was more evident after acetazolamide and further reduced after adenosine. The asymmetry index in this patient changed from -0.09 to -0.19.

View this table: [in this window] [in a new window]   Table 2. Asymmetry Index in Six Patients With Occlusive Carotid Disease Under Basal Conditions and During Acetazolamide and Adenosine Tests

View larger version (0K): [in this window] [in a new window]   Figure 1. SPECT images in patient 2 with 80% stenosis of the right internal carotid artery. A reduction in perfusion in the territory distal to the stenosis is evident after acetazolamide (ACZ) and even more after adenosine (ADN).

In 2 patients with unilateral carotid occlusive disease, the asymmetry index did not change after both tests or even showed an improvement. Fig 2 shows the SPECT images of patient 4 (a 94-year-old woman): the area with reduced tracer uptake in the territory distal to the left internal carotid artery had a satisfactory perfusion capacity, as the asymmetry index changed from -0.09 to -0.03.

View larger version (0K): [in this window] [in a new window]   Figure 2. SPECT studies in patient 4 with 80% stenosis of the left internal carotid artery. The tracer distribution after acetazolamide (ACZ) and adenosine (ADN) infusion is present in the area distal to the stenosis, reflecting a normal perfusion capacity after both tests.

Mean systolic and diastolic blood pressures were not significantly changed during either test. An increase in mean heart rate was observed during the adenosine test (from 73±11 beats per minute to 88±14 beats per minute in the 4th minute, P<.001) but not after acetazolamide injection. The incidence of side effects in both studies is shown in Table 3. Flushing and dyspnea were frequent in all normal subjects and in patients during the adenosine test, and worsening in the electrocardiogram was also observed in one patient who had already reported angina. However, the clinical symptoms and the electrocardiographic modifications resolved spontaneously within 2 minutes after discontinuing the adenosine infusion because of the short half-life of adenosine. The side effects did not require premature interruption of the infusion or drug interventions in any of the patients. Paresthesia and headaches were reported by the same persons during the acetazolamide test, but these side effects were present for a longer period of time.

View this table: [in this window] [in a new window]   Table 3. Reported Side Effects During Acetazolamide and Adenosine Tests in Six Normal Subjects and Six Patients With Cerebrovascular Disease

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Although absolute CBF values cannot be determined with the use of ^99mTc-HMPAO, the use of this tracer has some advantages compared with others, such as ¹³³Xe⁴ or [¹²³I]iodoamphetamine.¹⁹ The use of ¹³³Xe requires a fast-rotating brain-dedicated device and an acquisition time of approximately 5 minutes; therefore, during any pharmacological test the stimulus must be constant. On the other hand, [¹²³I]iodoamphetamine is expensive and not routinely available in most departments of nuclear medicine. On a clinical basis, ^99mTc-HMPAO could be considered an accurate tracer for the assessment of brain perfusion.

Acetazolamide-induced vasodilatation is well known to occur in several pathophysiological conditions and can be used to study patients with extracranial and intracranial disease to evaluate CVRC and the hemodynamic significance of occlusion or narrowing of arteries supplying the brain. The mechanism of action of acetazolamide, an inhibitor of carbonic anhydrase, has been widely investigated in experimental animals and in humans. It causes a decline in the pH of brain tissues,^{20 21} and therefore the consequent acidosis increases CBF in cortical and subcortical regions.^{3 22} On the other hand, studies of the metabolic and hemodynamic effects of adenosine in humans are very limited despite the growing scientific interest in this compound because its derivatives appear to be promising candidates for the development of anticonvulsant, anti-ischemic, analgesic, and neuroprotective agents.²³ In rats the inhibition of adenosine deaminase during hypoxia increases the diameter of pial arteries²⁴ and CBF.²⁵ These effects are counterbalanced by theophylline, an adenosine receptor antagonist.^{24 25} In rats the concentration of adenosine in the cerebrospinal fluid increased 4.2-fold during transient cerebral ischemia and 13.8-fold during the first 5 minutes of reperfusion; the highest arteriolar diameter coincided with the highest adenosine levels.²⁶ During hypotension in piglets²⁷ and during somatosensory stimulation in rats,²⁸ adenosine plays a role in arterial vasodilatation and CBF regulation. These effects of adenosine on the brain circulation have also been demonstrated in rabbits²⁹ and in baboons¹⁵ but not in cats or dogs.³⁰ In humans adenosine infusion has been successfully used in the diagnosis of coronary artery disease at a dosage of 140 µg/kg per minute,^{18 31} and therefore it might also be used in the evaluation of CVRC and the diagnosis of cerebrovascular disease. In humans Sollevi et al¹³ studied the effects of adenosine on cerebral hemodynamics using PET in 6 normoventilated subjects with arteriovenous malformations and found a 55% mean CBF increase.

In our study both acetazolamide and adenosine exerted a significant vasodilatory effect on the cerebral circulation of normal subjects and patients with carotid occlusive disease. In the former group, in which extracranial and intracranial vessels were free of atherosclerotic lesions, the observed increase in the CBF ratios was almost similar in all the regions considered after the infusion of both compounds, indicating that acetazolamide and adenosine act at least in the same vascular territories without any regional difference.

In patients with carotid disease, the usefulness of evaluating CVRC and perfusion changes by ^99mTc-HMPAO SPECT after acetazolamide has already been demonstrated.¹⁰ Of course, if the hemispheric response to acetazolamide is used to assess CVRC in individual cases, it is necessary to evaluate the changes in CBF pattern by calculating the enhancement in side-to-side asymmetry. In fact, the hypoperfused area or the area distal to the carotid disease may have remained unchanged or perfusion may even have been reduced after injection of the dilating agent, while the normoresponsive arteries may physiologically vasodilate and produce an increase in CBF. In this study the asymmetry that was already present in the resting condition between flow patterns in normal areas and contralateral regions distal to the carotid disease increased after acetazolamide and increased even more after adenosine infusion in 4 of 6 patients. It is evident that in these patients adenosine exerted a stronger vasodilatatory effect in normal regions and therefore enhanced the differences in flow pattern between these regions and those areas distal to a hemodynamically significant arterial stenosis. Two patients (1 and 4) had normal perfusion reserve capacity: the asymmetry index decreased after acetazolamide and adenosine in the territory distal to the carotid stenosis. Although vasodilatation occurs similarly in all cerebral territories, the mechanism of action of adenosine is different from that of acetazolamide. It is thought that the pharmacological effect involves activation of purine receptors³² as well as the reduction of cellular calcium uptake and activation of adenylate cyclase.³¹

Unwanted side effects were limited after both tests but were slightly more frequent after adenosine injection. However, all side effects disappeared within 2 minutes because of the very short biological half-life of the compound. One advantage in the use of adenosine over acetazolamide is the possibility of interrupting the infusion if clinical symptoms reverse or the patient experiences discomfort.

In conclusion, adenosine causes vasodilatation of cerebral arteries in humans and increases blood perfusion in territories with normal vasoreactivity. It can be successfully used for the evaluation of CVRC in patients with carotid occlusive disease.

	Selected Abbreviations and Acronyms

 

CBF = cerebral blood flow CVRC = cerebrovascular reserve capacity HMPAO = hexamethylpropyleneamine oxime PET = positron emission tomography ROIs = regions of interest SPECT = single-photon emission CT

Received February 16, 1995; revision received May 9, 1995; accepted May 18, 1995.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Soricelli, A. Articles by Ell, P. J. Search for Related Content PubMed PubMed Citation Articles by Soricelli, A. Articles by Ell, P. J.