Effect of sevoflurane anesthesia on cognitive impairment in rats with traumatic brain injury

Abstract

Objective To evaluate the effect of sevoflurane anesthesia on cognitive impairment in rats with traumatic brain injury. Methods One hundred and and twenty healthy male Wistar rats, aged 2-3 months, weighing 190-220 g, were assigned into 4 groups (n=30 each) using a random number table method: control group (group C), traumatic brain injury group (group T), sevoflurane anesthesia group (group S), and traumatic brain injury plus sevoflurane anesthesia group (group T+ S). A 40 g hammer was freely dropped onto the left parietal bone window from a height of 20 cm to establish the traumatic brain injury model in T and T+ S groups.Twelve days later, S and T+ S groups inhaled 3% sevoflurane for 3 h, and C and T groups inhaled pure oxygen for 3 h. On 1 day before anesthesia and 3 and 7 days after anesthesia, 10 rats in each group were randomly selected for performing Morris water maze test.Rats were sacrificed after the end of Morris water maze test, and the hippocampal tissues were obtained for determination of the apoptosis rate of hippocampal neurons, cytoplasmic calcium concentration [Ca2+ ]i (by flow cytometry), expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) (by immunohistochemistry), and expression of caspase-3 and caspase-12 (by Western blot). Results Compared with group C, the escape latency was significantly prolonged, the number of crossing platform was decreased, the apoptosis rate of hippocampal neurons and [Ca2+ ]i were increased, and the expression of caspase-3, caspase-12, GRP78 and CHOP in hippocampal tissues was up-regulated in S, T and T+ S groups (P<0.05). Compared with T and S groups, the escape latency was significantly prolonged, the number of crossing platform was decreased, the apoptosis rate of hippocampal neurons and [Ca2+ ]i were increased, and the expression of caspase-3, caspase-12, GRP78 and CHOP in hippocampal tissues was up-regulated in group T+ S (P<0.05). Conclusion Sevoflurane anesthesia can accentuate cognitive impairment in rats with traumatic brain injury, and the mechanism may be related to aggravating the degree of endoplasmic reticulum stress-induced calcium overload and increasing the apoptosis rate of hippocampal neurons. Key words: Anesthetics, inhalation; Brain injuries, traumatic; Cognition disorders