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Absence of Autoregulation of Cerebral Blood Flow During Halothane and Enflurane Anesthesia

DAVID J. MILETICH, PhD^*, ANTHONY D. IVANKOVICH, MD, RONALD F. ALBRECHT, MD, CHARLES R. REIMANN, MD, RONALD ROSENBERG, MD^||, and EVERETT D. McKISSIC, MD^**

*Assistant Professor of Anesthesiology, Pritzker School of Medicine, Michael Reese Medical Center, Chicago, Illinois 60616. Associate Professor of Anesthesiology, Pritzker School of Medicine, The University of Chicago, Michael Reese Medical Center, Chicago, Illinois 60616. Professor of Anesthesiology, Pritzker School of Medicine, The University of Chicago; Chairman, Department of Anesthesiology, Michael Reese Medical Center, Chicago, Illinois 60616. Research Associate, Department of Anesthesiology, Michael Reese Medical Center. ||Associate Professor of Anesthesiology, Pritzker School of Medicine, The University of Chicago, Chicago, Illinois 60616. **Assistant Professor of Anesthesiology, Pritzker School of Medicine, The University of Chicago.Chicago, Illinois 60616.

Abstract

The effects of halothane and enflurane anesthesia under conditions of normo-, hyper-, and hypocarbia on the autoregulation of cerebral blood flow (CBF) in the goat were evaluated. The goat was selected because of its unique arterial blood supply to the head and the development of a method by which CBF may be continuously measured. The study revealed that 1 MAC of halothane or enflurane anesthesia at normocarbia abolished cerebral autoregulation, CBF increasing or decreasing with increasing or decreasing peripheral blood pressure. Reduction of anesthesia to 0.5 MAC partially restored cerebral autoregulatory capability. The effect of 1 MAC and 0.5 MAC anesthesia on cerebral autoregulation of blood flow was potentiated by hypercarbia and antagonized by hypocarbia, indicating that the vascular response to blood CO₂ fluctuations remained intact.

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