Effect of Adenosine on Cerebral Blood Flow Velocity Carla Zanferrari, MD, PhD Alexander Y. Razumovsky, PhD Pablo M. Lavados, MD Souvik Sen, MD Stephen M. Oppenheimer, MD, PhD A B S T R A C T Background and Purpose. Evidence suggests that adenosine (ADN) is a potent vasodilator of cerebral vessels. However, the feasibility of manipulating human cerebral vascular resistance with ADN has not been assessed by means of TCD. The pur - pose of this study was to quantitatively estimate the change in middle cerebral artery cerebral blood flow velocity (CBFV) in response to intravenous ADN infusion in humans. Methods. Eleven patients with subacute cerebrovascular events (ischemic stroke, transient ischemic attack, or hemorrhage) undergoing adenosine-thallium stress testing were studied before, during, and after ADN infusion to evaluate the effect of ADN on cerebral blood flow velocity. Continuous blood pressure (BP), heart rate (HR), respiration rate (RR), end-tidal CO 2 (ET-CO 2 ), and trans- cranialDopplerultrasonography monitoring of CBFV and pulsatility index (PI) in both middle cerebral arteries were per- formed. Results.The mean CBFVs were 65.4 ± 19.2 cm/s before, 55.4 ±18.1 cm/s during, and 64.1 ± 22.5 cm/s after ADN infusion, which represents a statistically significant decrease during ADN test compared with both baseline (P = .007) and posttest levels (P = .017). The PI was increased during the test (0.91 ± 0.2) when compared with baseline (0.71 ± 0.1) (P = .007). During ADN injection, mean HR increased (P = .004) and mean ET-CO 2 levels decreased significantly (P = .003). Mean BP and RR did not change significantly. Conclusions. The authors hypothesize that any direct vasodilatory effect of ADN on the distal cerebral peripheral vasculature may be negated by an effect of ADN on depth of respiration resulting in hypocapnia and secondary distal vasoconstriction. Key words: Adenosine, ultrasound, cerebrovascular reactivity. Zanferrari C, Razumovsky AY, Lavados PM, Sen S, Oppenheimer SM. Effect of adenosine on cerebral blood flow velocity. J Neuroimaging 2001;11:272–279. Cerebrovascular reactivity (CVR)reflectschangesin smooth muscle tone in the arterial wall in response to changes in transmural pressure or the arterial partial pres- sure of carbon dioxide (PaCO 2 ). The assessment of CVR can provide information about the reserve capacity of the cerebral circulation and can serve as an indicator of cere- bral blood flow (CBF)autoregulation. Previous studies have suggested that different levels of CVR impairment mightbe related to different degrees ofstroke risk in patients with carotid stenosis and/or occlusion. 1–5 CVR assessment involves the response of CBF to vasoactive substances and allows quantification. Decreased CVR indicates the presence of preexisting vasodilatation and reduced reserve capacity of CBF autoregulation. Transcranial Doppler (TCD)ultrasonography measures cerebral blood flow velocity (CBFV) changes provoked by different stimuli in the basal cerebral arteries. There is a significant correlation between CBFV and CBF in these circumstances. 6–10 Thus, TCD has been proposed as a noninvasive, simple,and inexpensive method to assess cerebral vasoreactivity and can monitor CBFV changes in response to a vasodilatory stimulus such as hypercapnia. 9 In the TCD assessment of CVR, the most commonly used vasodilatory stimuli have been CO 2 3 and acetazolamide. 4 These compounds presumably cause a dilatation of small cerebral resistance arteries and arteri - oles and increase CBF. 11 272 Copyright © 2001 by the American Society of Neuroimaging Received March 29, 2000, in first revised form December 12, 2000, and in second revised form February 12, 2001. Accepted for publication February 17, 2001. From the Institute of Neurology, University of Parma, It - aly (CZ); the Departmentof Anesthesiology/Critical Care Medicine and the Department of Neurology, Johns Hopkins Medical Institutions,Baltimore,MD (AYR, SMO); the Departmentof Neurological Sciences, Alemana Hospital, Santiago, Chile (PML); and the De - partment of Neuroscience, New Jersey Neuroscience In - stitute, Edison, New Jersey (SS). Addresscorrespondence to DrRazumovsky,Neuro- sciences Critical Care Division, Johns Hopkins Medical Institutions, Meyer 8-140, North Wolfe Street, Baltimore, MD 21287-7840. E-mail: arazumov@jhmi.edu.