J Anesth Perioper Med. 2016;3(4):149-159. https://doi.org/10.24015/ebcmed.japm.2016.0020
From Department of Anesthesioloy, Affiliated Xiangya Hospital of Central South University, Changsha, China.
Correspondence to Dr. Qu-lian Guo at qulianguo@ hotmail.com.
EBCMED ID: ebcmed.japm.2016.0020 DOI: 10.24015/ebcmed.japm.2016.0020
Background
Sevoflurane, as a novel volatile anesthetic with minimal pungency, low solubility, and less toxicity, is widely used in anesthetic practice. The purpose of this study was to investigate the effect of sevoflurane postconditioning on endogenous antioxidant status and spatial learning and memory ability after cardiac arrest (CA) and the potential underlying mechanisms.
Methods
A rat model of CA was established by delivering an alternating current between the esophagus and chest wall to induce ventricular fibrillation. Animals were randomly divided into three groups: sham group (no CA), CA group, and CA+sevoflurane postconditioning (CA+SE) group. Sevoflurane postconditioning was achieved by administration of 2.5% sevoflurane for 60 min after resuscitation. The spatial learning and memory ability of rats was measured by the Morris water maze. The antioxidant enzymes activities were assessed at 4 hours, 1 day and 8 days after resuscitation. Moreover, the expressions of hippocampal proteins which could serve as memory enhancement biomarkers including growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD-95) and the transcription factor c-jun/activator protein-1 (AP-1), were detected at 8 days after resuscitation.
Results
We found that CA significantly decreased the ability of spatial learning and memory in contrast to the sham controls. However, sevoflurane postconditioning significantly increased survival rate and antioxidant enzyme activities as well as ameliorated the spatial learning and memory deficits induced by CA. Furthermore, sevoflurane postconditioning regulated hippocampal memory enhancement proteins.
Conclusions
Postconditioning with sevoflurane improved learning and memory deficits in a CA model possibly due to the reduction of oxidative stress and up-regulation of the memory enhancement biomarkers in hippocampus.
Article Type
Original Article
Declaration of Interests
All authors have no other financial support and potential conflicts of interest for this work.
Acknowledgements
This work was supported by the National Natural Science Foundation of China (grant 81201018).
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