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The Effects of Doxapram on Cerebral Blood Flow and Peripheral Hernodynamics in the Anesthetized and Unanesthetized Goat

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

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

Abstract

The effects of doxapram on cerebral blood flow (CBF) and peripheral hemodynamics were evaluated in the goat after direct injection into the cerebral circulation and after peripheral IV administration. Doxapram injected centrally via the temporal artery, in doses too small to affect peripheral circulation, produced an immediate and prolonged decrease in CBF in both anesthetized and unanesthetized goats. The reduction in CBF was considered not to be due to changes in blood CO₂ concentration, since blood flow decreased immediately after injection and as reduction in CBF occurred in the absence of changes in blood CO₂. Peripheral IV administration of doxapram in clinical doses to anesthetized and unanesthetized goats produced a biphasic cardiovascular response. Cerebral blood flow, cardiac output, blood pressure, and heart rate decreased abruptly, but with the exception of CBF, these parameters returned to or exceeded preinjection values within 30 seconds. Cerebral blood flow slowly returned to preinjection values (within 10 minutes) and, in the case of unanesthetized animals and anesthetized animals ventilated with room air, rose substantially above preinjection levels, reaching a peak 20 minutes after injection. The latter observation is thought to be a compensatory reaction to the reduction in CBF; it was not evident in anesthetized animals ventilated with 100% O₂.