BACKGROUND: The aim of this study was to determine whether a combination of sevoflurane postconditioning and albumin provides additive neuroprotective effects after transient global cerebral ischemia in rats. METHODS: Forty-three rats were assigned to 4 groups: the control group (group C; n=13; 3 died) received no treatment. The albumin group (group A; n=10) received 2 g/kg of albumin for 5 minutes after ischemia. The sevoflurane postconditioning group (group P; n=10) underwent 2 sevoflurane inhalations after ischemia. Each inhalation consisted of 5 minutes of 2.5% sevoflurane and a subsequent washout time of 5 minutes. The sevoflurane postconditioning plus albumin group (group PA; n=10) received additional albumin during sevoflurane postconditioning after ischemia. In all groups, ischemia was induced by a bilateral common carotid artery occlusion along with hemorrhagic hypotension and was maintained for 10 minutes. Histologic and neurobehavioral outcomes were measured 7 days after ischemia in CA1 pyramidal cells of the rat hippocampus. RESULTS: Groups A, P, and PA showed an improved neurological outcome and contained more viable cells in the hippocampal CA1 area compared with group C (P<0.05). The number of apoptotic cells was significantly reduced in group PA compared with group C (P<0.01). There was a significant difference in the Bcl-2, an antiapoptotic protein, expression between group C and other groups (P<0.01) and between group A or P and group PA (P<0.05). CONCLUSIONS: A combination of sevoflurane postconditioning and albumin increased the level of Bcl-2 expression compared with sevoflurane postconditioning or albumin alone, suggesting their combination might provide additional neuroprotection by decreasing apoptosis.
BACKGROUND: The aim of this study was to determine whether a combination of sevoflurane postconditioning and albumin provides additive neuroprotective effects after transient global cerebral ischemia in rats. METHODS: Forty-three rats were assigned to 4 groups: the control group (group C; n=13; 3 died) received no treatment. The albumin group (group A; n=10) received 2 g/kg of albumin for 5 minutes after ischemia. The sevoflurane postconditioning group (group P; n=10) underwent 2 sevoflurane inhalations after ischemia. Each inhalation consisted of 5 minutes of 2.5% sevoflurane and a subsequent washout time of 5 minutes. The sevoflurane postconditioning plus albumin group (group PA; n=10) received additional albumin during sevoflurane postconditioning after ischemia. In all groups, ischemia was induced by a bilateral common carotid artery occlusion along with hemorrhagic hypotension and was maintained for 10 minutes. Histologic and neurobehavioral outcomes were measured 7 days after ischemia in CA1 pyramidal cells of the rat hippocampus. RESULTS: Groups A, P, and PA showed an improved neurological outcome and contained more viable cells in the hippocampal CA1 area compared with group C (P<0.05). The number of apoptotic cells was significantly reduced in group PA compared with group C (P<0.01). There was a significant difference in the Bcl-2, an antiapoptotic protein, expression between group C and other groups (P<0.01) and between group A or P and group PA (P<0.05). CONCLUSIONS: A combination of sevoflurane postconditioning and albumin increased the level of Bcl-2 expression compared with sevoflurane postconditioning or albumin alone, suggesting their combination might provide additional neuroprotection by decreasing apoptosis.