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 inju-ry 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 af-ter 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 pro-tein ( 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
hip-pocampal
neurons.