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Sevoflurane inhalation attenuates the neuron apoptosis by modulation of Bcl-2/Bax expression after cardiac arrest in rats |
Lu Yuan-zheng, Li Heng-jie, Wei Hong-yan, Yang Yan, Li Bo, Mao Hui, Yin Mei-xian, Hu Chun-lin, Liao xiao-xing |
Department of Emergency, the First Affiliated Hospital of Sun Yat-Sen University, Key Laboratory on Assisted Circulation, Ministry of Health, Guang zhou 510080, China |
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Abstract Objective To investigate the effect of sevoflurane on neuron apoptosis administered after reaching restoration of spontaneous circulation (ROSC) during cardiopulmonary resuscitation (CPR) in rats. Methods The cardiac arrest model was established by ventricular fibrillation. Thirty male Wistar rats were assigned randomly into three groups. Six rats in the sham group were anesthetized and intubated without induction of cardiac arrest. 12 rats in the Sevo group were exposed to 2.4% minimal alveolar concentration(1MAC) of sevoflurane after reaching ROSC for 10 mins. 12 rats in the control group received the standard CPR only. 24 hours after ROSC, neuro-deficit scoring (NDS) was used to assess the neurological outcome. Then, all the rats were sacrificed with deep anesthesia, mitochondrial injury was observed by electron microscopy. TUNEL assay was used to count the apoptosis neurons ratio. Additionally, the level of Bcl-2, Bax, cytochrome C proteins expression were detected by Western blot. Cleaved caspase-3 expression was evaluated by immunohistochemical staining. Results There were no statistical difference in weight, heart beat, mean arterial pressure (MAP) among the three groups at the beginning of the experiment, and the CPR duration, defibrillation times, epinephrine dosage were not statistically significant between Sevo group and control group. NDS was higher in Sevo group than control group. Less alternation of the mitochondrial ultra-structure under sevoflurane treatment was revealed. The apoptosis neurons ration in Sevo group was markedly reduced[(12±6)% vs.(22±8)%, P<0.01]. Furthermore, compared to control group, the ratio of Bcl-2/Bax was higher in sevo group[(54±11)% vs.(28±9)%, P<0.01], while the expression of cytochrome C, active Cleaved Caspase-3 were lower. Conclusion The administration of sevoflurane after ROSC can inhibit neuronal apoptosis, mitigate neurological function injury partly attributed to the modulation of Bcl-2/Bax expression.
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Corresponding Authors:
Liao Xiao-xing, E-mail: liaowens@163.com
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