ORIGINAL ARTICLE Effect of Propofol and Clonidine on Cerebral Blood Flow Velocity and Carbon Dioxide Reactivity in the Middle Cerebral Artery Hasan Mirzai, Idil Tekin, Serdar Tarhan, Gulay Ok, and Cihan Goktan Abstract: This study was designed to evaluate the effects of propo- fol alone and propofol-clonidine combination on human middle ce- rebral artery blood flow velocity (Vmca) and cerebrovascular carbon dioxide (CO 2 ) response by using transcranial Doppler ultrasonogra- phy. Mean Vmca in response to changes in arterial partial pressure of CO 2 (PaCO 2 ) was determined under the following conditions: awake (group 1), propofol anesthesia (group 2), and combined propofol- clonidine anesthesia (group 3). Normocapnic, hypercapnic, and hy- pocapnic values of heart rate, mean arterial pressure, partial end-tidal CO 2 pressure, PaCO 2 , and Vmca were obtained. The mean Vmca in groups 2 and 3 was significantly lower than that in group 1 at each level of PaCO 2 . The calculated Vmca at each level of PaCO 2 was not different between groups 2 and 3. There was a correlation between PaCO 2 and Vmca in all groups, but in the anesthetized groups the ef- fect of PaCO 2 on Vmca was attenuated. The present data demonstrated that clonidine-propofol does not change CO 2 reactivity compared with propofol alone, but both anesthetics attenuate cerebral blood flow compared with awake controls. Key Words: propofol, clonidine, cerebral blood flow velocity, car- bon dioxide vasoreactivity, transcranial Doppler (J Neurosurg Anesthesiol 2004;16:1–5) P ropofol is an intravenous anesthetic agent often used for neurosurgical procedures because of its inherent ability to reduce increased intracranial pressure (ICP). 1,2 This decrease in ICP is presumed to reflect propofol’s cerebral vasoconstric- tive effects by decreasing cerebral blood volume. The effects of propofol on cerebral blood flow (CBF) and its response to changes in arterial partial pressure of carbon dioxide (PaCO 2 ) have been studied. PaCO 2 is a potent modulator of the cerebro- vascular tone, and hyperventilation is often used in patients with increased ICP to reduce CBF. 3–5 Alpha-2 agonists are central hypotensive drugs that cause constriction of cerebral arteries, which in turn decreases CBF. 6–11 Despite considerable interest regarding the effect of clonidine on CBF, there are only a few human studies exam- ining the effect of alpha-2 agonists on cerebral CO 2 vasoreac- tivity. 12 Clonidine, an alpha-2 agonist, has been reported to de- crease CBF and to reduce CO 2 reactivity, 8,12 which, given an additive or synergistic effect, might make it deleterious in combination with propofol. The present study was designed to evaluate the effects of propofol anesthesia alone and propofol- clonidine combination anesthesia on human middle cerebral artery blood flow velocity (Vmca) and cerebrovascular CO 2 response by using transcranial Doppler ultrasonography. MATERIALS AND METHODS The study was approved by the Ethics Committee of Celal Bayar University. Informed consent was obtained from 48 patients (ASA physical status I-II) scheduled for nonneuro- logic elective surgery. Inclusion criteria included a negative history for cardiac or cerebrovascular disease. Patients were instructed to abstain from the use of alcohol, caffeine, and to- bacco for 24 hours before the study. The patients were not pre- medicated. One hour before admission to the operating room, the patients were placed in the supine position and a peripheral intravenous catheter was inserted. Total fluid deficit was cal- culated, and the first half of it was started with a balanced elec- trolyte solution. In the operating room, a radial artery catheter was introduced for direct arterial blood pressure measurement and arterial blood gas sampling. Electrocardiography, heart rate (HR), mean arterial pressure (MAP), peripheral O 2 satu- ration (SpO 2 ), tympanic membrane temperature, and partial end-tidal CO 2 pressure (PETCO 2 ) were measured (Criticare 1100). Body temperature was maintained at 36°C to 37°C by using a warming blanket. Vmca was measured continuously using pulsed 2-mHz transcranial Doppler Ultrasonography (TCD) (TC2-64B; EME, Uberlingen, Germany). The Doppler probe was posi- tioned at the right temporal scalp surface and was fixed at the site of best insonation. TCD signals of the middle cerebral ar Received for publication December 9, 2002; accepted July 28, 2003. From the Departments of Neurosurgery, Anesthesiology, and Radiology of Medical Faculty of Celal Bayar University, Manisa, Turkey. Reprints: Dr. Hasan Mirzai, 2040 sk, Pamukkale 4/60, D:67, Mavisehir, TR 35540, Izmir, Turkey. (e-mail: hmirzai@yahoo.com). Copyright © 2003 by Lippincott Williams & Wilkins J Neurosurg Anesthesiol • Volume 16, Number 1, January 2004 1