Inhibition of sevoflurane postconditioning against cerebral ischemia reperfusion-induced oxidative injury in rats.
The volatile anesthetic sevoflurane is capable of inducing preconditioning and postconditioning effects in the brain. In this study, we investigated the effects of sevoflurane postconditioning on antioxidant and immunity indexes in cerebral ischemia reperfusion (CIR) rats. Rats were randomly assigned to five separate experimental groups I-V. In the sham group (I), rats were subjected to the same surgery procedures except for occlusion of the middle cerebral artery and exposed to 1.0 MAC sevoflurane 90 min after surgery for 30 min. IR control rats (group II) were subjected to middle cerebral artery occlusion (MCAO) for 90 min and exposed to O₂ for 30 min at the beginning of reperfusion. Sevoflurane 0.5, 1.0 and 1.5 groups (III, IV, V) were all subjected to MCAO for 90 min, but at the beginning of reperfusion exposed to 0.5 MAC, 1.0 MAC or 1.5 MAC sevoflurane for 30 min, respectively. Results showed that sevoflurane postconditioning can decrease serum tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), nitric oxide (NO), nitric oxide synthase (NOS) and increase serum interleukin-10 (IL-10) levels in cerebral ischemia reperfusion rats. In addition, sevoflurane postconditioning can still decrease blood lipid, malondialdehyde (MDA) levels, infarct volume and increase antioxidant enzymes activities, normal pyramidal neurons density in cerebral ischemia reperfusion rats. It can be concluded that sevoflurane postconditioning may decrease blood and brain oxidative injury and enhance immunity indexes in cerebral ischemia reperfusion rats.
Department of Anesthesiology, Tianjin Huanhu Hospital, Tianjin 300060, China.
Yan
Y
Zhang
Fu-Geng
FG
Zhang
Chun
C
Meng
Shou-Yuan
SY
Tian
Ya-Xin
YX
Wang
Wei
W
Zhao
Jun
J
Chen
Xiu-Shan
XS
Zhang
Yu
Y
Liang
Shi-Dong
SD
Zhang
Yan-Jie
YJ
Xing
D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000097:blood; D020244:Infarction, Middle Cerebral Artery / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D018836:Inflammation Mediators / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D057775:Ischemic Postconditioning; D008055:Lipids / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008738:Methyl Ethers / Q000494:pharmacology / Q000627:therapeutic use*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000097:blood; D018384:Oxidative Stress; D010088:Oxidoreductases / Q000097:blood; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D000077149:Sevoflurane; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D018836:Inflammation Mediators; D053583:Interleukin-1beta; D008055:Lipids; D008738:Methyl Ethers; D018696:Neuroprotective Agents; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009569:Nitric Oxide; D000077149:Sevoflurane; D008315:Malondialdehyde; D010088:Oxidoreductases; D005978:Glutathione