Effect of sevoflurane postconditioning on oxidative stress responses during focal cerebral ischemia-reperfusion in rats

Abstract

Objective To investigate the effect of sevoflurane postconditioning on oxidative stress responses during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Twenty-four male Wistar rats,weighing 240-280 g,were randomly assigned into 3 groups:sham operation group (group S),focal cerebral I/R group (group I/R) and sevoflurane postconditioning group (group SP).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 350 mg/kg.Focal cerebral I/R was produced by middle cerebral artery occlusion.In group SP,3.9％ sevoflurane (1.5 MAC) was inhaled starting from 20 min before reperfusion until 10 min after reperfusion.While 100％ O2 and air were given instead of sevoflurane in groups I/R and S,respectively.Six rats chosen from each group at 24 h of reperfusion were sacrificed and brains were removed for determination of malondialdehyde (MDA),glutathione (GSH),superoxide dismutase (SOD),catalase (CAT),glutathione peroxidase (GSH-Px) and glutathione reductase (GR) levels and for microscopic examination.The cerebral infarct size was measured by TTC staining.Results Compared with group S,MDA level and cerebral infarct size were significantly increased in groups I/R and SP,and GSH,SOD,CAT,GSH-Px and GR levels were decreased in group I/R,and GSH-Px level was decreased in group SP (P ＜ 0.05).Compared with group I/R,cerebral infarct size and MDA level were decreased,and GSH,SOD,CAT,GSH-Px and GR levels were decreased in group SP (P ＜ 0.05).The pathological changes were significantly attenuated in group SP compared with group I/R.Conclusion The mechanism by which sevoflurane postconditioning mitigates focal cerebral I/R injury in rats is related to enhanced antioxidase activity and inhibition of oxidative stress responses. Key words: Anesthetics, inhalation ; Oxidative stress ; Reperfusion injury ; Brain