title: Effect of fentanyl on ischemic depolarization and ischemic neuronal damage of hippocampal CA1 in the gerbil.
abstract: OBJECTIVE
  Temporary brain ischemia occurring during surgery under general anesthesia may induce the death of neuronal cells and cause severe neurological deficits. On the other hand, it is not clear whether μ-opioid receptor agonists promote ischemic brain injury. It is known that duration of ischemic depolarization affects the degree of neuronal damage. However, the effects of fentanyl during brain ischemia on ischemic depolarization have not been investigated. Therefore, in the current study, the effects of fentanyl on ischemic neuronal damage and ischemic depolarization were quantitatively evaluated.
  
  
  METHODS
  Forty-two male gerbils were randomly assigned to a saline-administered group (control group, n = 21) and a fentanyl-administered group (fentanyl group, n = 21). Fentanyl at 50 μg/kg was first administered over a 10-min period and then 50 μg/kg/h was administered continuously for the fentanyl group. Forebrain ischemia was initiated by occlusion of bilateral common carotid arteries and sustained for 3, 5, or 7 min (n = 7 in each group). Direct-current potentials were measured in bilateral CA1 regions, in which histological evaluation was performed 5 days later.
  
  
  RESULTS
  There were no significant differences in onset time, duration of ischemic depolarization, and percentage of neuronal damage between the two groups with any ischemic duration. In the relationships between ischemic time and neuronal damage and those between duration of ischemic depolarization and neuronal damage, there was no significant difference in the percentage of neuronal damage between the two groups.
  
  
  CONCLUSIONS
  Fentanyl at a clinically relevant dose does not affect ischemic depolarization and ischemic neuronal damage.
authors.affiliation: Department of Anesthesiology and Resuscitology, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama, Okayama 700-8558, Japan. shiraken@cc.okayama-u.ac.jp
authors.forename: Kensuke
authors.initials: K
authors.lastname: Shiraishi
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Takeda
authors.forename: Kenichi
authors.initials: K
authors.lastname: Masui
authors.forename: Hideki
authors.initials: H
authors.lastname: Taninishi
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Sasaki
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Danura
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Morita
mesh_terms: D000701:Analgesics, Opioid / Q000097:blood / Q000494:pharmacology*; D000818:Animals; D002545:Brain Ischemia / Q000097:blood / Q000473:pathology*; D056547:CA1 Region, Hippocampal / Q000187:drug effects* / Q000473:pathology; D016923:Cell Death / Q000187:drug effects; D005283:Fentanyl / Q000097:blood / Q000494:pharmacology*; D005849:Gerbillinae; D016015:Logistic Models; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D011897:Random Allocation; D017450:Receptors, Opioid, mu / Q000819:agonists
chemical_list: D000701:Analgesics, Opioid; D017450:Receptors, Opioid, mu; D005283:Fentanyl