Objective To determine the dose-response relationship of sufentanil blunting responses to double-lumen endotracheal intubation when combined with propofol given by target-controlled infusion (TCI) in patients with pulmonary tuberculosis.Methods One hundred patients of both sexes with pulmonary tuberculosis,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,aged 24-58 yr,with body mass index ＜30 kg/m2,with Mallampati grade Ⅰ or Ⅱ,undergoing thoracic surgery under general anesthesia,were divided into Ⅰ-Ⅴ groups (n =20 each) using a random number table.Anesthesia was induced with iv sufentanil 0.35 μg/kg (group Ⅰ),0.40 μg/kg (group Ⅱ),0.45 μg/kg (group Ⅲ),0.50 μg/kg (group Ⅳ) and 0.55 μg/kg (group Ⅴ),and propofol TCI (target plasma concentration 3.5 μg/ml) and iv vecuronium 0.15 mg/kg.The patients were endotracheally intubated and mechanically ventilated.The response to double-lumen endotracheal intubation was defined as positive when mean arterial pressure increased by＞ 20％ of the baseline value and/or heart rate ＞ 90 bpm within 5 min after intubation.The median effective dose (ED50),ED95 and 95％ confidence interval (95％ CI) of sufentanil blunting the responses to double-lumen endotracheal intubation were calculated by Probit analysis.Results The ED50 (95％ CI) and ED95 (95％ CI) of sufentanil blunting the responses to intubation were 0.411 (0.370-0.441) μg/kg and 0.635 (0.556-0.888) μg/kg,respectively,when combined with propofol given by TCI.Conclusion When combined with propofol given by TCI (target plasma concentration 3.5 μg/ml),the ED50 and ED95 of sufentanil blunting the responses to double-lumen endotracheal intubation are 0.411 and 0.635 μg/kg,respectively,in patients with pulmonary tuberculosis.

Objective To evaluate the effect of mild hypothermia on the expression of phosphorylated eukaryotic translation initiation factor 2α (p-eIf2αt) in the hippocampus in a mouse model of cerebral ischemia-reperfusion (I/R).Methods Sixty pathogen-free healthy male C57BL6 mice,aged 8-12 weeks,weighing 20-30 g,were divided into 3 groups (n =20 each) using a random number table:sham operation group (group S),group I/R and mild hypothermia group (group H).Cerebral I/R was induced by 15-min occlusion of bilateral common carotid arteries followed by reperfusion in chloral hydrate-anesthetized mice.Surface cooling was started immediately after reperfusion to maintain the rectal temperature at 32-34 ℃ for 3 h in group H.The neurologic deficit score was evaluated at 24 h of reperfusion.The mice were then sacrificed,brains were immediately removed,and hippocampi were isolated for examination of pathologic changes of hippocampal CA1 region and for determination of neuroapoptosis (by TUNEL) and expression of peIf2α (by Western blot).The apoptosis rate was calculated.Results Compared with group S,the neurologic deficit scores at 24 h of reperfusion and apoptosis rate of hippocampal neurons were significantly increased,and the expression of p-eIf2α was up-regulated in I/R and H groups (P＜0.05).Compared with group I/R,the neurologic deficit scores at 24 h of reperfusion and apoptosis rate of hippocampal neurons were significantly decreased,and the expression of p-eIf2α was down-regulated in group H (P＜ 0.05).Conclusion Mild hypothermia reduces endoplasmic reticulum stress and inhibits neuroapoptosis through inhibiting the expression of p-eIf2α in the hippocampus in a mouse model of cerebral I/R.