| ||||||||||||||
|
|
|||||||||||||





From the *Klinik für Anästhesiolgie Klinikum der Johannes Gutenberg-Universität, Mainz, Germany;
University of California Anesthesia/Critical Patient Care Veterinary Medical Teaching Hospital, Davis, California;
Klinik für Anaesthesiologie Technischen Universität München, Klinikum rechts der Isar, and
Institut für Pathologie der GSF, Munich, Germany.
Address correspondence and reprint requests to Monika Pape, MD, Klinik für Anästhesiolgie Klinikum der Johannes Gutenberg-Universität, Langenbeckstraße 1, 55131 Mainz, Germany. Address e-mail to pape{at}uni-mainz.de.
We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by immunostaining. No eosinophilic neurons were detected in sevoflurane-anesthetized rats over time, whereas 9%38% of the hippocampal neurons were eosinophilic (days 128) in control animals. On days 1 and 3, the concentration of Bax was 140%200% larger in fentanyl/N2O-anesthetized animals compared with sevoflurane. Bcl-2 was 100% less in control animals during the first 3 days. Activated caspase-3 was detected in neurons of both groups (0.75%2.2%). These data support a sustained neuroprotective potency of sevoflurane related to reduced eosinophilic injury after cerebral ischemia/reperfusion.
This article has been cited by other articles:
![]() |
Y. Dong, G. Zhang, B. Zhang, R. D. Moir, W. Xia, E. R. Marcantonio, D. J. Culley, G. Crosby, R. E. Tanzi, and Z. Xie The Common Inhalational Anesthetic Sevoflurane Induces Apoptosis and Increases {beta}-Amyloid Protein Levels Arch Neurol, May 1, 2009; 66(5): 620 - 631. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Sigaut, V. Jannier, D. Rouelle, P. Gressens, J. Mantz, and S. Dahmani The Preconditioning Effect of Sevoflurane on the Oxygen Glucose-Deprived Hippocampal Slice: The Role of Tyrosine Kinases and Duration of Ischemia Anesth. Analg., February 1, 2009; 108(2): 601 - 608. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Bedirli, E. Ofluoglu, M. Kerem, G. Utebey, M. Alper, D. Yilmazer, A. Bedirli, O. Ozlu, and H. Pasaoglu Hepatic Energy Metabolism and the Differential Protective Effects of Sevoflurane and Isoflurane Anesthesia in a Rat Hepatic Ischemia-Reperfusion Injury Model Anesth. Analg., March 1, 2008; 106(3): 830 - 837. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Fukuda and D. S. Warner Cerebral protection Br. J. Anaesth., July 1, 2007; 99(1): 10 - 17. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Engelhard, U. Winkelheide, C. Werner, J. Kluge, E. Eberspacher, R. Hollweck, P. Hutzler, J. Winkler, and E. Kochs Sevoflurane Affects Neurogenesis After Forebrain Ischemia in Rats Anesth. Analg., April 1, 2007; 104(4): 898 - 903. [Abstract] [Full Text] [PDF] |
||||
|