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NEUROSURGICAL ANESTHESIA

Isoflurane Increases Brain Oxygen Reactivity in Dogs

Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois

Address correspondence and reprint requests to William E. Hoffman, PhD, Department of Anesthesiology, M/C 515, University of Illinois at Chicago, 1740 West Taylor Street, Chicago, IL 60612. Address e-mail to whoffman{at}uic.edu

We tested the possibility that large-dose isoflurane will produce a loss of brain tissue oxygen regulation in dogs. A total of 12 dogs were anesthetized with isoflurane, a craniotomy was performed, and a probe was inserted to measure brain tissue oxygen pressure (PtO₂), carbon dioxide, and pH. Baseline measures were made during 1.5% end-tidal isoflurane with 30% oxygen ventilation, followed by 95% oxygen ventilation. Six dogs (Group 1) were treated with 3% isoflurane and 30% oxygen, followed by a second oxygen challenge with 95% O₂. Six dogs (Group 2) received propofol to produce a similar suppression of the electroencephalogram as in Group 1, followed by 95% oxygen ventilation. Brain tissue oxygen reactivity was calculated by the increase in PtO₂ divided by the increase in arterial PO₂. During 1.5% isoflurane and propofol anesthesia, PtO₂ increased from 42 to 62 mm Hg with oxygen ventilation, and brain tissue oxygen reactivity was 0.14% per mm Hg^-1. Brain tissue oxygen reactivity did not change during propofol anesthesia. With 3% isoflurane, PtO₂ increased from 52 to 113 mm Hg and brain tissue oxygen reactivity was 0.36% per mm Hg^-1 (P < 0.05). These results suggest that the cerebrovasodilator and vasoplegic effects of large-dose isoflurane attenuate brain oxygen regulation.

Implications: We evaluated the ability of oxygen ventilation to increase brain tissue oxygen pressure in dogs anesthetized with 1.5% and 3% isoflurane and propofol. Increases in tissue oxygen were significantly greater during 3% isoflurane compared with 1.5% isoflurane and propofol.