PMID- 21385986
OWN - NLM
STAT- MEDLINE
DCOM- 20110516
LR  - 20181201
IS  - 1526-7598 (Electronic)
IS  - 0003-2999 (Linking)
VI  - 112
IP  - 4
DP  - 2011 Apr
TI  - Sevoflurane preconditioning induces neuroprotection through reactive oxygen 
      species-mediated up-regulation of antioxidant enzymes in rats.
PG  - 931-7
LID - 10.1213/ANE.0b013e31820bcfa4 [doi]
AB  - BACKGROUND: It has been reported that sevoflurane preconditioning can induce 
      neuroprotection, the mechanisms of which, however, are poorly elucidated. We 
      designed the present study to examine the hypothesis that sevoflurane 
      preconditioning could reduce cerebral ischemia- reperfusion injury through 
      up-regulating antioxidant enzyme activities before ischemic injury by generating 
      reactive oxygen species (ROS). METHODS: In preconditioning groups, adult male 
      Sprague-Dawley rats were pretreated with 1 hour sevoflurane exposure at a dose of 
      1%, 2%, or 4% for 5 consecutive days. At 24 hours after the last exposure, all 
      rats were subjected to focal brain ischemia induced by middle cerebral artery 
      occlusion for 120 minutes followed by 72-hour reperfusion. The role of ROS in 
      ischemic tolerance was assessed by administration of the free radical scavenger 
      dimethylthiourea and antioxidant N-acetylcysteine before each preconditioning. 
      Brain ischemic injury was evaluated by neurologic behavior scores and brain 
      infarct volume calculation. Antioxidant enzyme activities (superoxide dismutase, 
      catalase, and glutathione peroxidase [GSH-px]) of brain tissue and blood serum 
      were tested at 24 hours after the last sevoflurane preconditioning. RESULTS: 
      Sevoflurane preconditioning reduced infarct size and improved neurobehavioral 
      outcome in a dose-dependent manner. The neuroprotective effects of sevoflurane 
      preconditioning were abolished by dimethylthiourea and N-acetylcysteine. The 
      activities of catalase and glutathione peroxidase (GSH-px) in the brain tissue 
      were elevated by sevoflurane preconditioning before ischemic injury. The 
      up-regulated activity of GSH-px in serum negatively correlated with brain infarct 
      volume percentage. CONCLUSION: Sevoflurane preconditioning induces cerebral 
      ischemic tolerance in a dose- response manner through ROS release and consequent 
      up-regulation of antioxidant enzyme activity before ischemic injury in rats. 
      Serum GSH-px activity could be developed as a marker to assess the effectiveness 
      of sevoflurane preconditioning before ischemia.
FAU - Yang, Qianzi
AU  - Yang Q
AD  - Department of Anesthesiology, Xijing Hospital, Fourth Military Medical 
      University, Xi'an 710032, Shaanxi Province, China.
FAU - Dong, Hui
AU  - Dong H
FAU - Deng, Jiao
AU  - Deng J
FAU - Wang, Qiang
AU  - Wang Q
FAU - Ye, Ruidong
AU  - Ye R
FAU - Li, Xuying
AU  - Li X
FAU - Hu, Sheng
AU  - Hu S
FAU - Dong, Hailong
AU  - Dong H
FAU - Xiong, Lize
AU  - Xiong L
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110308
PL  - United States
TA  - Anesth Analg
JT  - Anesthesia and analgesia
JID - 1310650
RN  - 0 (Antioxidants)
RN  - 0 (Methyl Ethers)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Reactive Oxygen Species)
RN  - 38LVP0K73A (Sevoflurane)
SB  - IM
MH  - Animals
MH  - Antioxidants/*metabolism
MH  - Brain Ischemia/*enzymology/prevention & control
MH  - Cerebrovascular Circulation/drug effects/physiology
MH  - Dose-Response Relationship, Drug
MH  - Ischemic Preconditioning/*methods
MH  - Male
MH  - Methyl Ethers/*administration & dosage
MH  - Neuroprotective Agents/*administration & dosage
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species/*metabolism
MH  - Sevoflurane
MH  - Up-Regulation/drug effects/physiology
EDAT- 2011/03/10 06:00
MHDA- 2011/05/17 06:00
CRDT- 2011/03/10 06:00
PHST- 2011/03/10 06:00 [entrez]
PHST- 2011/03/10 06:00 [pubmed]
PHST- 2011/05/17 06:00 [medline]
AID - ANE.0b013e31820bcfa4 [pii]
AID - 10.1213/ANE.0b013e31820bcfa4 [doi]
PST - ppublish
SO  - Anesth Analg. 2011 Apr;112(4):931-7. doi: 10.1213/ANE.0b013e31820bcfa4. Epub 2011 
      Mar 8.