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Kofke W. Andrew MD FCCM; Garman, Robert H. DVM; Tom, William C. MD; Rose, Marie E. BA; Hawkins, Richard A. PhD
Anesthesia & Analgesia: December 1992
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We evaluated the effect of alfentanil on hippocampal glucose utilization and histopathology associated with alfentanil-induced seizures. Three separate experiments were performed. First, anesthetized, paralyzed Long-Evans rats (n = 15; 5 rats per group) were mechanically ventilated and randomly assigned to three groups: (a) control, 70% N2O and 30% O2continued for 1 h; (b) low-dose alfentanil (150 μg/kg IV bolus), followed by infusion at 15 μg.kg−1.min−1 for 1 h without N2O; or (c) high-dose alfentanil (1000 μg/kg IV bolus), followed by infusion at 100 μg.kg−1.min−1 for 1 h without N2O. After 1 h, [6-14C]glucose was injected intravenously for autoradiography. With high-dose alfentanil, there was increased glucose utilization in the ventral hippocampus and the lateral septal nucleus. In the second experiment, anesthetized, paralyzed Sprague-Dawley rats (n = 12; 4 rats per group) were mechanically ventilated, underwent insertion of hippocampal depth electrodes, and were randomly assigned to three groups: (a) control, 70% N2O and 30% O2;(b) low-dose alfentanil (150 μ/kg IV bolus), with 70% N2O and 30% O2; or (c) high-dose alfentanil (1000 μg/kg IV bolus), with 70% N2O and 30% O2. An epileptiform pattern was observed on hippocampal and subdermal electroencephalographic recordings in both alfentanil groups. In the third experiment, anesthetized, paralyzed Sprague-Dawley rats (n = 20) were mechanically ventilated and assigned to two groups: (a) control, 70% N2O and 30% O2 (n = 5) or 100% O2 (n = 5) continued for 1 h; or (b) alfentanil (2000 μg/kg IV bolus), followed by infusion at 33.3 μg.kg−1.min−1 for 1 h with 100% O2. After tracheal extubation, the rats recovered overnight. Light-microscopic evaluation revealed hippocampal or amygdaloid damage in 6 of the 10 alfentanil-treated rats. High doses of alfentanil administered to rats can produce limbic system seizure activity with hypermetabolism associated with neuropathologic lesions.

Address correspondence to Dr. Kofke, Department of Anesthesiology/CCM, University of Pittsburgh, Pittsburgh, PA 15261.

© 1992 International Anesthesia Research Society