title: Pre- or postinsult administration of lidocaine or thiopental attenuates cell death in rat hippocampal slice cultures caused by oxygen-glucose deprivation.
abstract: Lidocaine and thiopental improve recovery when administrated during hypoxia and ischemia; however, the effect of pre- or postinsult treatment alone is unknown. We applied either lidocaine or thiopental to hippocampal slice cultures from 20-day-old rats either before or after 10 min of oxygen-glucose deprivation (OGD). Propidium iodide (PI) fluorescence was used as an indicator of neuronal death for 7 days after OGD. OGD-induced neuronal death, in both the Cornus Ammonis 1 (CA1) and the dentate gyrus regions, peaked the first day after ischemia. Preinsult administration of either lidocaine (10, 100 microM) or thiopental (250, 600 microM) significantly reduced the damage measured on the first and second days after OGD; these drugs also significantly decreased the summed daily post-OGD PI fluorescence in both regions. Postinsult administration of lidocaine (10, 100 microM) or thiopental (250, 600 microM) significantly decreased the PI fluorescence on the first day after OGD; postinsult administration of these drugs also attenuated the summed daily post-OGD PI. These data indicate that the administration of lidocaine or thiopental either before or directly after OGD reduced neuronal damage in this in vitro model of cerebral ischemia. Postischemic administration is frequently the first opportunity for treatment.
  
  
  CONCLUSIONS
  Lidocaine or thiopental applied either 10 min before or 10 min directly after oxygen-glucose deprivation reduced neuronal cell death in rat hippocampal slice cultures. Postinsult administration is often the first opportunity for treatment after stroke; lidocaine and thiopental reduced damage caused by oxygen-glucose deprivation, an in vitro model of stroke.
authors.affiliation: Departments of *Anesthesiology and †Physiology & Pharmacology, State University of New York Downstate Medical Center, Brooklyn, New York; ‡Department of Anesthesiology, Xuzhou Medical College, Jiangsu Province; and §Anesthesiology Department, Second Affiliated Hospital of Wenzhou Medical College, Wenzhou, Zhejiang Province, People's Republic of China.
authors.forename: Hong
authors.initials: H
authors.lastname: Cao
authors.forename: Ira S
authors.initials: IS
authors.lastname: Kass
authors.forename: James E
authors.initials: JE
authors.lastname: Cottrell
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Bergold
mesh_terms: D000818:Animals; D016923:Cell Death / Q000187:drug effects*; D015687:Cell Hypoxia; D005947:Glucose / Q000172:deficiency; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D007511:Ischemia / Q000188:drug therapy* / Q000473:pathology; D008012:Lidocaine / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D013874:Thiopental / Q000494:pharmacology*
chemical_list: D018696:Neuroprotective Agents; D008012:Lidocaine; D005947:Glucose; D013874:Thiopental