J. Charchaflieh et al., THE EFFECT OF FENTANYL ON ELECTROPHYSIOLOGIC RECOVERY OF CA-1 PYRAMIDAL CELLS FROM ANOXIA IN THE RAT HIPPOCAMPAL SLICE, Anesthesia and analgesia, 87(1), 1998, pp. 68-71
Fentanyl is widely used in conditions in which the brain is at risk of
ischemic or anoxic injury. We evaluated the effect of fentanyl on ano
xic injury to CA 1 pyramidal cells in the rat hippocampus. These neuro
ns are extremely sensitive to anoxic injury and are densely populated
with opioid receptors. We prepared hippocampal slices from adult Sprag
ue-Dawley rats and evoked a postsynaptic population spike in the CA 1
pyramidal cell region by stimulating the Schaffer collateral pathway.
The amplitude of this response was used to evaluate the effect of fent
anyl on anoxic injury. Pretreatment with fentanyl (50 or 500 ng/mL) di
d not alter the amplitude of the CA 1 population spike before anoxia,
nor did it alter the recovery of this response after 5, 6, or 7 min of
anoxia. After 5 min of anoxia, the population spike recovered to 76%
of its preanoxic level in the control group and to 87% in the group tr
eated with 500 ng/mL of fentanyl. After 6 min of anoxia, recovery was
45% in the control group, 57% in the group treated with 50 ng/mL of fe
ntanyl, and 58% in the group treated with 500 ng/mL of fentanyl. After
7 min of anoxia, recovery was 5% in the control group and 4% in the g
roup treated with 50 ng/mL of fentanyl. We conclude that fentanyl does
not affect the recovery of the electrophysiological response in rat h
ippocampal neurons subjected to an anoxic insult. Implications: Becaus
e fentanyl is used in large doses during surgical procedures in which
the brain is at increased risk of ischemic or anoxic injury, it is imp
ortant to determine its effect on such injury. Using the rat hippocamp
al slice model, we found fentanyl to be neither neurotoxic nor protect
ive against anoxic injury to neurons when used in concentrations compa
rable to those produced in clinical practice.