Effect of sevoflurane preconditioning on brain injury induced by cardiopulmonary bypass in rats

Abstract

Objective To evaluate the effect of sevoflurane preconditioning on brain injury induced by cardiopulmonary bypass(CPB)in rats. Methods Forty adult male Sprague-Dawley rats, aged 6-8 months, weighing 350-450 g, were randomly divided into 5 groups(n=8 each)using a random number table: sham operation group(S group), CPB group, and preconditioning with different concentrations of sevoflurane groups(SP1, SP2 and SP3 groups). In SP1, SP2 and SP3 groups, sevoflurane with the final concentrations of 1.2%, 2.4% and 3.6%, respectively, was inhaled for 1 h, and then CPB was started.After sevoflurane preconditioning and before CPB(T0), at 30 min of CPB(T1), at the end of CPB(T2), and at 1, 2 and 3 h after termination of CPB(T3-5), venous blood samples were collected from the right internal jugular vein for determination of serum S100-β protein concentrations by enzyme-linked immunosorbent assay.Rats were sacrificed at T5, and hippocampi were isolated for determination of neuronal apoptosis(by TUNEL)and NF-κB p65 expression(by immunohistochemistry). Results Compared with group S, the concentration of serum S100-β protein was significantly increased at T1-5, the number of apoptotic neurons was significantly increased, and the expression of NF-κB p65 was significantly up-regulated in CPB, SP1, SP2 and SP3 groups(P<0.05). Compared with group CPB, the serum S100-β protein concentration was significantly decreased at T1-5, the number of apoptotic neurons was significantly decreased, and the expression of NF-κB p65 was significantly down-regulated in SP1, SP2 and SP3 groups(P<0.05). Compared with group SP1, the serum S100-β protein concentration was significantly decreased at T1-5, the number of apoptotic neurons was significantly decreased, and the expression of NF-κB p65 was significantly down-regulated in SP2 and SP3 groups(P<0.05). Compared with group SP2, the serum S100-β protein concentration was significantly decreased at T1-5, the number of apoptotic neurons was significantly decreased, and the expression of NF-κB p65 was significantly down-regulated in group SP3(P<0.05). Conclusion Sevoflurane preconditioning can attenuate CPB-induced brain injury probably by inhibiting activation of NF-κB in hippocampal neurons of rats. Key words: Anesthetics, inhalation; Ischemic preconditioning; Cardiopulmonary bypass; Brain injuries