Search

Background and Purpose: To improve the assessment of cerebral vasoreactivity using acetazolamide (ACZ), we studied the time course of the response and the relationship between dose, response, and serum concentration., Methods: Blood flow velocities were measured with the use of transcranial Doppler ultrasonography in one of the middle cerebral arteries of 48 healthy subjects after the intravenous administration of 1 to 1.6 g ACZ. In 34 subjects (group 1), velocities were measured every second minute to detect the maximum middle cerebral artery velocity increase. We also measured regional cerebral blood flow using single-photon emission computed tomography in 27 of the subjects in group 1 before and approximately 15 to 20 minutes after the ACZ injection. The serum concentration of ACZ was measured in 15 subjects. In the remaining 14 subjects (group 2), middle cerebral artery velocity measurements were made 10, 25, 30, and 45 minutes after ACZ administration to obtain information regarding the late time course of the response., Results: In group 1 the plateau phase of the velocity response was reached 8 to 15 minutes after ACZ administration. A large range of velocity increase was observed, and a significant correlation was found between the maximum velocity increase and the dose and serum concentration of ACZ. In group 2 subjects, maximum velocities were maintained 30 minutes after the injection, but after 45 minutes velocities had decreased to 68% of their highest level. No significant relationship was found between dose or serum concentration of ACZ and the regional cerebral blood flow increase. The velocity increase after ACZ was similar in both older and younger subjects., Conclusions: This study shows that cerebral vasoreactivity is best assessed 10 to 30 minutes after ACZ administration and that the dose should probably exceed 15 mg/kg if a maximum vasodilatory response in the cerebral circulation is to be obtained.

We studied the effect of acetazolamide on cerebellar blood flow in 11 stroke patients with large, unilateral cerebral hemispheric infarcts and no evidence of cerebellar infarction, but with cerebrocerebellar diaschisis of cerebral blood flow. Blood flow was determined with xenon-133 inhalation and dynamic single-photon emission computed tomography at rest and 20 minutes after the intravenous injection of 1.0 g acetazolamide. After acetazolamide, the mean +/- SD increases in blood flow in the affected and contralateral cerebellar hemispheres were 11.1 +/- 3.7 and 12.0 +/- 5.3 ml/100 g/min, respectively; the difference between hemispheres was not significant. The absolute increase in cerebellar flow in these 11 patients was of the same magnitude as that in 12 healthy controls. We conclude that cerebellar vasoreactivity is intact in stroke patients with crossed cerebrocerebellar diaschisis of cerebral blood flow. Our results lend further support to the concept that reduced cerebellar blood flow is secondary to functional deactivation. Our patients were studied 2 weeks to 5 years after their stroke, indicating that this phenomenon may be persistent.

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.