非控制性出血性休克低压复苏治疗效果的研究

目的　应用大鼠脾损伤非控制性出血性休克模型探讨低压及低压扩容复苏治疗非控制性出血性休克的可行性。方法　雄性Wistar大鼠 5 0只 ,在大鼠脾损伤模型复制成功后随机等分为 5组 ,组 1 :假手术组 ;组 2 :休克未处理组 ;组 3:常压复苏组 (急救期控制MAP在 80mmHg以上 ) ;组 4 :低压复苏组 (急救期控制MAP在 6 0mmHg±5mmHg) ;组 5 :低压扩容复苏组 (急救期输入硝普钠 5 μg·kg- 1 ·min- 1 ,同时输液控制MAP在 6 0mmHg± 5mmHg)。结果　 1～ 5组平均存活时间 (min)分别为 1 80、73.5 0± 8.0 4、1 1 4 .30± 31 .33、1 4 6 .70± 2 8.0 7和 1 71 .6 0± 1 5 .74 ,除组1、组 5外 (P =0 .0 6 71 ) ,其余各组间比较均有统计学意义 (P <0 .0 5 ) ;2～ 5组的急救期出血量 (ml·kg- 1 )分别为 :3.79± 1 .39、1 7.4 1± 8.88、8.6 7± 4 .5 9、1 0 .33± 4 .31 ,其中组 3出血量明显高于其他各组 (P <0 .0 1 ) ;组 4、组 5与组 2比较出血量明显增多 (P <0 .0 5 )。结论　在非控制性出血性休克治疗中 ,低压及低压复合适量硝普钠扩容复苏方法可改善组织代谢 ,提高生存时间 ,是更为理想的复苏方法     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

内皮祖细胞在急性肺损伤中应用的研究进展*

急性肺损伤是由各种肺内外因素导致的进行性呼吸困难和难治性低氧血症,其病理特征包括炎 症反应及肺泡-毛细血管屏障功能破坏,微循环血管内皮损伤是主要标志。内皮祖细胞可以从骨髓动员迁移 到损伤部位,分化为成熟内皮细胞发挥直接修复作用,并通过间接免疫调节作用改善微环境。此外内皮祖细 胞还可以分泌细胞因子以自分泌或旁分泌方式促进新生血管生成从而减少器官功能障碍。文章旨在综述内皮 祖细胞在急性肺损伤中的应用,从而为治疗急性肺损伤提供新思路。     

异丙酚或异氟烷复合麻醉对肺癌根治术病人细胞免疫功能的影响

目的观察异丙酚或异氟烷复合麻醉对肺叶切除术肺癌病人细胞免疫功能的影响。方法择期行肺叶切除术肺癌病人30例,ASAⅠ或Ⅱ级,年龄42～70岁,男女不限。随机分为2组(n= 15)：异丙酚(Ⅳ)组和异氟烷(IH)组,麻醉诱导后气管插管,Ⅳ组静脉输注异丙酚5～12 mg·kg~(-1)·h~(-1),IH组吸入异氟烷,呼气末浓度维持1．3～1．5 MAC,两组分别在血压、心率高于基础值20％以上时,追加0．05～0．1 mg芬太尼。于麻醉诱导前即刻(T_0)、麻醉诱导后10 min(T_1)、切皮后1h(T_2)、麻醉停药即刻(T_1)、术后1h(T_4)及24 h(T_5)采集静脉血,用流式细胞仪测定血浆CD4~+ CD28~+、CD8~+ CD28~+表达率,用ELISA法测血清IFN-γ、IL-12、IL-4浓度,用放射免疫法测定皮质醇浓度。结果与T_0比较,Ⅳ组T_4,时CD4~+ CD28~+、CD8~+ CD28~+升高,T_5时IL-12浓度升高,L_(4,5)时IFN-γ浓度升高,Ⅳ、IH组T(1-5)时皮质醇浓度均升高(P＜0．05或0．01),IH组的变化较Ⅳ组更明显；与T_4比较,Ⅳ组T_5时IFN-γ浓度升高(P＜0．05)。结论与异氟烷复合麻醉比较,异丙酚复合麻醉可增强肺叶切除术肺癌病人细胞免疫功能。     

SLIPA喉罩用于腹腔镜胆囊切除术患者气道管理的效果

SLIPA喉罩是一种新型的声门上通气装置,根据咽部结构由特殊材料吹制塑形而成,虽然没有充气罩,但仍可获得良好的气道密封效果,可用于正压通气和自主呼吸[1].本研究拟评价SLIPA喉罩用于腹腔镜胆囊切除术患者气道管理的效果.     

预设麻醉亚专业课题方向的研究生培养模式的探讨

麻醉学专业研究生生源多样化,致使研究生培养的水平参差不齐。目前,大多数医院把重点集中在研究生临床工作能力的培养,不注重提高学生的科研能力,致使大多数研究生在毕业后不具有独立开展临床实验研究的能力。因此,如何制定专业型麻醉学研究生的培养模式,既培养了其临床工作能力,又锻炼其科研能力,使其适应当前社会对麻醉学人才的需要,这一直是麻醉学研究生教育领域里的难点。通过预先设立亚麻醉专科的课题方向,专业学位的研究生不仅能提高临床操作技能,还能开阔科研思维,提高创新能力,成为从事临床麻醉的高水平人才。在此基础上就预设麻醉亚专业课题方向的研究生培养模式的方法和意义进行了探讨。     

右美托咪啶对超声引导下臂丛神经阻滞镇痛的影响

目的 探讨右美托咪啶对超声引导下臂丛神经阻滞术中及术后镇痛效果的影响.方法 选取60例择期行单侧手或前臂手术的患者,均接受超声引导下臂丛神经阻滞.将患者按随机数字表法分为研究组和对照组,每组30例.研究组患者使用0.5％罗哌卡因100 mg和0.75μg/kg右美托咪啶合剂,对照组患者使用0.5％罗哌卡因100 mg.记录入手术室时、臂丛神经阻滞后、切皮时、手术结束患者心率、平均动脉压（MAP）、脉搏血氧饱和度（SpO2）.臂丛神经阻滞成功后,记录切皮时、手术1h及术后1,2,6,12,24和48 h视觉模拟评分（VAS）.当VAS超过4分时给予吗啡治疗,并记录术后首次使用吗啡时间及术后48 h吗啡用量.记录不良反应.结果 两组入手术室时和臂丛神经阻滞后心率、MAP比较差异无统计学意义（P＞0.05）,研究组切皮时和手术结束心率、MAP明显低于入手术室时和同期对照组,差异有统计学意义（P＜0.05）.两组各时间点SpO2比较差异无统计学意义（P＞0.05）.研究组术后6,12,24和48 h VAS均低于对照组[（3.0±0.9）分比（4.9±0.5）分、（3.0±0.7）分比（5.6±1.2）分、（2.2±0.9）分比（4.8±1.8）分、（1.7±0.5）分比（3.2±1.0）分],差异有统计学意义（P＜0.05）.研究组术后首次使用吗啡时间明显长于对照组[（450±37） min比（368±42）min],术后48 h吗啡用量明显少于对照组[（8.3±2.8）mg比（15.5±4.5） mg],差异有统计学意义（P＜0.05）.两组患者均未发生明显不良反应.结论 超声引导下臂丛神经阻滞时罗哌卡因复合应用0.75μg/kg右美托咪啶可显著延长镇痛时间,减少术后48 h吗啡用量,而且未发生显著的不良反应.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.