Objective To investigate the effects of remifentanil postconditioning on apoptosis in hippocampal neruons in a rat model of cerebral ischemia-reperfusion(I/R)and the mechanism involved.Methods Twentyfour male SD rats weighing 250-300 g were randomly divided into 4 groups(n = 6 each): sham operation group (group S);global cerebral I/R group(group I/R);remifentanil 0.6μg·kg- 1·min-1+global cerebral I/R group (group R1)and remifentanil 1.8μg·kg-1·min-1 + global cerebral I/R group(group R2).Global cerebral ischemia was induced by 10 min occlusion of bilateral common carotid combined with hypotension.In group R1 and R2,remifentanil at 0.6 and 1.8μg·kg-1·min-1 were infused for 5 min before ischemia respectively.The cognitive function was tested with Morris water maze and step-down tests from the day 3 to day 8 after reperfusion.When Morris water maze test was finished,rat brains were removed for HE staining and determination of the expression of caspase-3 in hippocampal CA1 region by immuno-histochemistry.Apoptosis in neurons in hippocampal CA1 region was detected by TUNEL assay.Results Compared with group S,the cognitive function was significantly decreased and the number of apopotic neurons in hippocampus CA1 region increased in group I/R,R1 and R2,and the expression of caspase-3 was up-regulated in group I/R(P＜0.05).Compared with group I/R,the cognitive function was significantly increased,the expression of caspase-3 was down-regulated,and the number of apopotic neurons in hippocampus CA1 region was significantly decreased in group R1 and R2(P＜0.05).Conclusion Remifentanil postconditioning can improve the cognitive function through down-regulating caspase-3 expression and inhibiting the apoptosis in hippocampal neruons in a rat model of cerebral I/R.

Objective To compare the effects of different doses of dexmedetomidine in inhibition of cardiovascular response to endotracheal intubation. Methods One hundred and twenty ASA Ⅰ or Ⅱ patients, aged 18-60 yr, weighing 45-80 kg, scheduled for upper abdominal surgery, were randomly assigned to one of 4 groups (n = 30 each): control group (group C); low, median and high doses of dexmedetomidine groups (group M1-3) .In group M1-3, 15 min before anesthesia induction, dexmedetomidine 0.25, 0.5 and 1.0 μg/kg were infused over 15 min respectively, while normal saline 15 ml was given instead of dexmedetomidine in group C. After anesthesia induction, tracheal intubation was performed when the BIS value ≤ 60 and it was maintained for 5 s. The patients were mechanically ventilated. BP and HR were recorded before infusion of dexmedetomidine (T0), before intubation (T1), immediately after intubation (T2) and at 1, 3, 5 and 10 min after intubation (T3-6). Venous blood samples were also taken at the same time to measure the plasma concentrations of epinephrine (E) and norepinephrine (NE). Results Compared with T0, HR was significantly decreased at T1 in group M1-3, BP was significantly increased at T1 in group M3, and the plasma concentrations of E and NE were significantly increased at T4-6 in group C and M1(P ＜0.05). BP and HR were significantly lower at T2, while higher at T3-5 in group C and M1than at T1 (P ＜ 0.05). BP at T1-6 was significantly higher in group M3 than in group M2 (P ＜ 0.05). Conclusion When the dose of dexmedetomidine reaches 0.5 μg/kg, it may effectively inhibit the stress reaction to noxious stimulation.