Surgery under Propofol Anesthesia Induced Behavioral Changes Associated With Increased Cerebral Apoptosis in Rats
|Konstanze Plaschke1*, Julia Schneider1and Jürgen Kopitz2|
|1Department of Anesthesiology, Medical Faculty, University of Heidelberg, Germany|
|2Department of Pathology, Medical Faculty, University of Heidelberg, Germany|
|Corresponding Author :||Konstanze Plaschke
Department of Anesthesiology, Experimental Anesthesiology
Medical Faculty of the University of Heidelberg, Germany
E-mail: [email protected]
|Received October 30, 2013; Accepted November 28, 2013; Published December 06, 2013|
|Citation: Plaschke K, Schneider J, Kopitz J (2013) Surgery under Propofol Anesthesia Induced Behavioral Changes Associated With Increased Cerebral Apoptosis in Rats. J Liver 2:136. doi: 10.4172/2167-0889.1000136|
|Copyright: © 2013 Plaschke K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
It is not known whether prolonged propofol anesthesia and/or surgery are responsible for postoperative cerebral deterioration, including Alzheimer-like histological changes, apoptosis and cognitive dysfunction. Therefore, the aim of the present study was to use partial liver resection as a surgical rat model in middle-aged rats in order to distinguish postoperative cerebral changes brain from those in rats after propofol anesthesia without surgery.
In this randomized, controlled study, behavioral changes were investigated in n=36 rats (12- to 14-month-old) using the hole board test system and Morris water maze. Cerebral glycogen synthase kinase-3ß (GSK-3ß) and tau protein were analyzed using ELISA technique. Cerebral amyloid was determined using congo red staining with subsequent fluorescence analysis. Apoptosis in rat brain was analyzed using TUNEL test and caspase-3 immunhistochemistry.
Alzheimer-like specific histological markers were not markedly increased up to 28 days after propofol anesthesia without partial hepatectomy. In contrast, propofol combined with partial liver resection caused long-term deterioration in spatial cognitive behavior in the rats. These postoperative cognitive dysfunctions were associated with pronounced cerebral apoptosis and increased GSK-3ß.
We conclude that a surgical procedure in the form of partial hepatectomy, but not propofol anesthesia alone, induced persistent cognitive deterioration and increased apoptosis in middle-aged rats. Although apoptotic changes seem to be mediated via GSK-3ß, further studies are now necessary to investigate the underlying mechanisms and other potential pathogenetic factors for postoperative cognitive dysfunction.