
J Neuropsychiatry Clin Neurosci 19:331-334, August 2007
doi: 10.1176/appi.neuropsych.19.3.331
© 2007 American Neuropsychiatric Association
Clinical and Research Reports |
Buprenorphine Does Not Aggrevate Ischemic Neuronal Injury in Experimental Focal Cerebral Ischemia
Burak Yulug, M.D.,
Ertugrul Cam, M.D.,
Aysegul Yildiz, M.D. and
Ertugrul Kilic, M.D.
Received May 5, 2006; revised September 20, 2006; accepted September 26, 2006. Dr. Yulug is affiliated with the Department of Neurology, University of Uludag, Bursa, Turkey. Dr. Cam is affiliated with the Department of Anatomy, University of Zurich, Switzerland. Dr. Yildiz is affiliated with the Department of Psychiatry, University of Dokuz Eylul, Izmir, Turkey. Dr. Kilic is affiliated with the Department of Neurology, University of Zurich, Switzerland. Address correspondence to Dr. Yulug, University of Uludag Faculty of Medicine, Department of Neurology, Bursa 16059, Turkey; yulug{at}gmx.de (e-mail).
ABSTRACT
Buprenorphine has been increasingly used as maintenance therapy in opioid dependence as an alternative to methadone and other pharmacological therapies. However, available data suggest increased risk of cerebrovascular events in opioid-dependent patients. Therefore, an opioid that provides safety with regard to neurological function should be considered by opioid-dependent patients. The evidence for the in vitro neurotoxic effects of buprenorphine is rapidly increasing. In order to clarify whether buprenorphine is also neurotoxic under the condition of cerebral ischemia in vivo, we applied an acute dose of buprenorphine in a transient model of focal cerebral ischemia in rats. Our study provides preclinical evidence for the usage of buprenorphine during the postoperative period following ischemic events as well as for the maintenance therapy of opioid-dependent patients wherein the risk of cerebrovascular events is increased.
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