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Anesth Analg 2001;93:45-52
© 2001 International Anesthesia Research Society


CARDIOVASCULAR ANESTHESIA

Reduced Regional and Global Cerebral Blood Flow During Fenoldopam-Induced Hypotension in Volunteers

Richard C. Prielipp, MD, FCCM*, Michael H. Wall, MD*, Leanne Groban, MD*, Joseph R. Tobin, MD, FCCM*, Frederic H. Fahey, DSc{dagger}, Beth A. Harkness, MS{dagger}, David A. Stump, PhD*, Robert L. James, MS*, Mark A. Cannon, MD*, Judy Bennett, RN*, and John Butterworth, MD*

Departments of *Anesthesiology (Sections of Critical Care and Cardiothoracic Anesthesiology) and {dagger}Radiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina

Address correspondence and reprint requests to Richard C. Prielipp, MD, Department of Anesthesiology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1009. Address e-mail to prielipp{at}wfubmc.edu

Dopamine has a wide spectrum of receptor and pharmacologic actions that may affect cerebral blood flow (CBF). A new, selective dopamine-1 agonist, fenoldopam, is a potent systemic vasodilator with moderate {alpha}2-receptor affinity. However, the effects of fenoldopam on the cerebral circulation are undefined. We therefore hypothesized that infusion of fenoldopam would decrease mean arterial blood pressure (MAP) and might concurrently decrease CBF via vascular {alpha}2-adrenoreceptor activation in awake volunteers. We studied nine healthy normotensive subjects, using positron emission tomography to measure CBF in multiple cortical and subcortical regions of interest. In addition, bioimpedance cardiac output and middle cerebral artery blood flow velocity were determined during fenoldopam-induced hypotension. Three men and four women, aged 25–43 yr, completed the study. Fenoldopam infused at 1.3 ± 0.4 µg · kg-1 · min-1 (mean ± SD) reduced MAP 16% from baseline: from 94 (89–100) mm Hg (mean [95% confidence interval]) to 79 [74–85] mm Hg (P < 0.0001). During the fenoldopam infusion, both cardiac output (+39%), and heart rate (+45%) increased significantly, whereas global CBF decreased from baseline, 45.6 [35.6–58.5] mL · 100 g-1 · min-1, to 37.7 [33.9–42.0] mL · 100 g-1 · min-1 (P < 0.0001). Despite restoration of baseline MAP with a concurrent infusion of phenylephrine, global CBF remained decreased relative to baseline values at 37.9 [34.0–42.3] mL · 100 gm-1 · min-1 (P < 0.0001). Changes in middle cerebral artery velocity did not correlate with positron emission tomography-measured changes of CBF induced by fenoldopam, with or without concurrent phenylephrine.

Implications: In awake volunteers with (presumably) intact cerebral autoregulation,fenoldopam-induced hypotension significantly decreased global cerebral bloodflow (CBF). Clinicians should be aware of these pharmacodynamic effects whenchoosing a vasodilator to control blood pressure, especially in situationswhere control of CBF, cerebral blood volume, and intracranial pressure aretherapeutic priorities.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2001 by the International Anesthesia Research Society.