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Anesth Analg 1990; 70:624-630
© 1990 International Anesthesia Research Society
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Dexmedetomidine, an {alpha}2-Adrenergic Agonist, Decreases Cerebral Blood Flow in the Isoflurane-Anesthetized Dog

Mark H. Zornow, MD, Jerry E. Fleischer, MD, Mark S. Scheller, MD, Kazuhiko Nakakimura, MD, and John C. Drummond, MD

Department of Anesthesiology, University of California at San Diego, San Diego, and the Anesthesia Service, Veterans Administration Medical Center, San Diego, California.

Abstract

The purpose of this study was to examine the effects of dexmedetomidine, an {alpha}2-adrenergic agonist, on cerebral blood flow and metabolic rate in dogs anesthetized with 0.64% isoflurane. After intubation and institution of mechanical ventilation, arterial, venous, pulmonary artery, and sagittal sinus catheters were inserted. Measurements of cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), mean arterial pressure, cardiac output, and blood gas tensions were made at various levels of isoflurane anesthesia (0.64%, 1.9%, and 2.8%), after the administration of 10 µg/kg of dexmedetomidine (a dose that has been shown to reduce anesthetic requirements in dogs by >90%) and finally after 0.3 mg/kg of the {alpha}2-adrenergic antagonist idazoxan. Despite an increase in arterial pressure, dexmedetomidine caused a marked reduction (>45%, P < 0.05) in CBF when compared with all preceding concentrations of isoflurane. The administration of dexmedetomidine had no effect on the CMRo2. The electroencephalogram showed a loss of high-frequency activity in a pattern similar to that seen with 1.90% isoflurane. Administration of dexmedetomidine was associated with a 57% decrease in cardiac output (to 0.89 L/min). Administration of idazoxan (an {alpha}2-adrenergic antagonist) resulted in an increase in cardiac output and a reversal of the electroencephalogram effects. This experiment indicates that 10 µg/kg of dexmedetomidine in isoflurane-anesthetized dogs is associated with a profound decrease in CBF and cardiac output in the face of an unaltered CMRo2. Despite the large reduction in the CBF/CMRo2 ratio, there was no evidence of global cerebral ischemia.

Key Words: BRAIN, BLOOD FLOW—dexmedetomidine • BRAIN, METABOLISM—dexmedetomidine • SYMPATHETIC NERVOUS SYSTEM, PHARMACOLOGY—dexmedetomidine




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1990 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 1990 by the International Anesthesia Research Society.