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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, Peoples Republic of China
Address correspondence and reprint requests to Ira S. Kass, PhD, Department of Anesthesiology, Box 6, State University of New York Downstate Medical Center, 450 Clarkson Ave., Brooklyn, NY 11203. Address e-mail to ira.kass{at}downstate.edu.
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 µM) or thiopental (250, 600 µM) 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 µM) or thiopental (250, 600 µM) 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.
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