瑞芬太尼用于小儿气管异物镜检术麻醉的临床研究

目的研究瑞芬太尼用于小儿支气管异物镜检术麻醉对应激反应的影响。方法气管异物患儿30例,随机分为两组,A组泵注-γOH 100 mg.kg-1,B组泵注-γOH 50 mg.kg-1复合瑞芬太尼0.05μg.kg-1.min-1,检测注药前(T0)、注药后(T1)、下镜时(T2)、下镜后30 min(T3)时的BIS值、HR、RR、SaO2、PEtCO2、皮质醇及血糖浓度。结果A、B组患儿注药后HR、BIS、RR明显下降(P<0.05),但下镜时A组患儿HR明显上升(P<0.05),两组患儿下镜副皮质醇及血糖浓度都升高(P<0.05),以A组明显(P<0.05)。结论瑞芬太尼可抑制小儿气管异物镜检所致的应激反应,且无明显呼吸循环抑制。     

不同局麻药的颈丛阻滞效果及对Q-T间期和Q-T离散度的影响

目的:研究不同局麻药用于颈丛神经阻滞的效果及其对Q-T间期和Q-T离散度(Q-Td)的影响. 方法:60例ASA Ⅰ或Ⅱ级拟在颈丛阻滞下行甲状腺肿物切除患者,随机分为4组(每组15例):罗哌卡因组(Ⅰ组),布比卡因组(Ⅱ组),罗哌/利多卡因组(Ⅲ组),布比/利多卡因组(Ⅳ组),各组分别用3.75 g/L罗哌卡因、3.75 g/L布比卡因、3.75 g/L罗哌卡因/10.0 g/L利多卡因及3.75 g/L布比卡因/10.0 g/L利多卡因20 mL行颈丛神经阻滞,观察麻醉效果及并发症发生情况,记录麻醉前(T0),麻醉即刻(T1),麻醉后10 min(T2),30 min(T3),1 h(T4)及手术结束即刻(T5)的HR,MAP,SpO2,RR,PetCO2,同时记录各时间点的Q-T, Q-Td及校正后的Q-Td(Q-Tcd). 结果:Ⅰ,Ⅱ组;Ⅲ,Ⅳ组麻醉效果相似(P＞0.05),均能满足手术要求;各组对抬头肌力的影响: Ⅱ组强于Ⅰ组(P＜0.05), Ⅳ组与Ⅲ组差异无统计学意义(P＞0.05). 各组患者HR,MAP在麻醉后均有不同程度升高,均在临床安全范围;SpO2,RR,PetCO2差异无统计学意义(P＞0.05). Q-T间期、Q-Td, Q-Tcd麻醉后均延长,其中以Ⅱ组延长最为明显(P＜0.01). 结论:不同局麻药及其配伍用于颈丛神经阻滞均能满足临床麻醉需要,罗哌卡因、罗哌/利多卡因对Q-T间期、Q-Td影响小,临床应用更为安全.     

内质网应激预处理对肝毒性药物导致原代大鼠肝细胞损伤的保护作用研究简

目的探讨大鼠肝细胞的内质网应激预处理对临床相关肝毒性药物肝细胞损伤的保护作用。方法（1）将培养的原代大鼠肝细胞分为8组,分别予以不同浓度的衣霉素和毒胡萝卜素进行干预,尔后检测葡萄糖调节蛋白78GRP78、葡萄糖调节蛋白94GRP78。（2）衣霉素和毒胡萝卜素干预作用24h后,可造成50％～75％的细胞死亡。对肝细胞进行预处理后,再使用顺铂、百草枯和利福平对细胞进行干预,检测细胞生存率。结果内质网应激诱导剂（毒胡萝卜素、衣霉素）对于GRP78和GRP94的表达表现出剂量相关的诱导作用．随着浓度的增加其表达量也逐渐增加,其变化具有明显的统计学意义（P〈0．05）。而临床相关的毒性药物（顺铂、利福平、百草枯）对细胞的损伤可明显地因毒胡萝卜素和衣霉素的内质网应激预处理而减轻,其结果具有统计学意义。结论内质网应激预处理对临床相关肝毒性药物导致原代大鼠肝细胞损伤具有保护作用。这些结果提示在药物导致的肝损伤中内质网应激或许起到了一定作用。     

氯胺酮麻醉对大鼠局灶性脑缺血模型病理结局的影响

目的:研究氯胺酮麻醉对大鼠局灶性脑缺血模型病理结局的影响. 方法: 雄性SD大鼠30只在戊巴比妥或氯胺酮麻醉下制作永久性大脑中动脉阻塞模型,每组15只. 术后4 h行神经病学评分、24 h测量梗塞体积、3 d进行甲苯胺蓝染色检测半暗带内的神经元. 结果:神经病学评分(1.5±1.0 vs 1.4±0.7)和死亡率(42% vs 33%)在戊巴比妥组和氯胺酮组间无显著性差异(P＞0.05),但氯胺酮组的脑梗塞体积小于戊巴比妥组[(28.1±4.1)% vs (37.8±5.0)%, P＜0.05],且半暗带内的神经元密度高于戊巴比妥组[(836±15)个/mm2 vs (740±24)个/mm2, P＜0.05]. 结论:在制作大鼠局灶性脑缺血模型时,氯胺酮麻醉下产生的脑损伤较轻. 在氯胺酮麻醉下的大鼠局灶性脑缺血模型中评价一些药物或方法的神经保护作用时,应考虑到氯胺酮的神经保护作用.     

氯诺昔康复合芬太尼用于全膝关节置换术后病人自控静脉镇痛

目的观察氯诺昔康复合不同剂量芬太尼在全膝关节置换术后患者自控静脉镇痛（PCIA）的效果。方法 45例全膝关节置换术患者,均采用静吸复合全麻,术后根据镇痛方式不同分为3组,每组15例：A组给予芬太尼0.3μg/（kg.h）;B组给予氯诺昔康15μg/（kg.h）＋芬太尼0.25μg/（kg.h）;C组给予氯诺昔康15μg/（kg.h）＋芬太尼0.2μg/（kg.h）。各组均加0.9%氯化钠溶液稀释至100ml,PCIA背景输注速率2ml/h,自控流量0.5ml/15min。观察患者术后4h,8h,24h,48h视觉模拟评分（VAS）,记录平均动脉压（MAP）、心率（HR）、呼吸频率（RR）、脉搏氧饱和度（SpO2）及不良反应。结果 A、B两组术后4h,8h,24h的VAS评分低于C组（P〈0.05）,三组患者术后各时点MAP、HR、RR、SpO2差异无统计学意义（P〉0.05）,A组恶心、嗜睡的发生率较其他两组有增加趋势。三组患者均未出现头晕、呼吸抑制及消化道出血等不良反应。结论氯诺昔康复合芬太尼用于全膝关节置换术后患者PCIA效果确切,并可以减少芬太尼的用量及其不良反应的发生率。     

The Experimental Study on Treatment of Glucocorticoid-Induced Ischemic Necrosis of Femoral Head by Gu Fu Sheng Capsule

Objective:To observe the effects of Gu Fu Sheng Capsule(骨复生胶囊 GFSC)on nitric oxide(NO)leveland fibrinolytic activity in rabbits with glucocorticoid-induced ischemic necrosis of femoral head(GINFH)so as to explain the therapeutic mechanism of GFSC.Methods:48 rabbits were randomly divided into 4groups:GFSC group A,Ma Shi Gu Pian(马氏骨片 MSGP)group B,model group C,and control group D.The models of GINFH were produced by injection of glucocorticoid hormone for 8 weeks.From the 9thweek,GFSC decoction was given to the rabbits of the group A(45g·kg~(-1)·d~(-1))and MSGP extract was givento the group B(0.17 g kg~(-1)·d~(-1))and the same volume of normal saline to group C and D by intragastricinfusion.The content of plasma nitric oxide(NO),and activities of tissue-type plasminogen activator(t-PA),and plasminogen activator inhibitor(PAI)were detected after the hormone was injected for 4 and 8weeks and after the drugs were given for 4 weeks.Results:Compared with the group D,the contents ofNO and t-PA activity in the group C decreased significantly(P<0.01),but the activity of PAI increasedsignificantly(P<0.01).Compared with the group C,the contents of NO and t-PA activity in the group Aand B increased significantly(P<0.05),but the activity of PAI decreased significantly(P<0.05),with nosignificant difference between the two treatment groups(P>0.05).Conclusion:GFSC could increase thelevel of NO,protect endotheolial cells and improve fibrinolytic activity,which might be the mechanism ofGFSC in curing GINFH.     

芬太尼对结肠癌细胞株SW480增殖及侵袭的影响

目的：探讨不同浓度的芬太尼对结肠癌细胞株 SW480增殖和侵袭的影响。方法：选用不同浓度的芬太尼（0．5、5、50ng／ml）干预结肠癌细胞株 SW480,采用四甲基偶氮唑蓝（MMT）法检测细胞增殖,Transwell法测定细胞侵袭。结果：各组芬太尼孵育 SW480细胞48h 及72h 后,均能显著抑制细胞的增殖（P ＜0．05）,且呈浓度和时间依赖性。芬太尼孵育 SW480细胞48h,与对照组相比,各浓度组均浓度依赖性抑制凋亡（P＜0．05）。结论：芬太尼可抑制结肠癌细胞株 SW480的增殖及侵袭。     

硬膜外麻醉期间镇静方法的比较

硬膜外麻醉目前仍因具有不可替代的优点而被广泛应用,但同时也有无法消除患者的紧张、焦虑、术中知晓及不良记忆等缺点.以往临床麻醉医师大多辅助以镇静镇痛药,但其效果难以确定.随着监测设备和给药方法的进步,产生了新的镇静方法,我们采用脑电双频指数（BIS）监测,对不同的镇静方法进行了临床研究.     

转bcl-2基因大鼠全脑缺血再灌注后海马CA1区P-P38的表达

目的 观察转bcl-2基因大鼠全脑缺血组再灌注后P-P38蛋白在海马回CA1区的表达. 方法 90只健康雄性SD大鼠,随机分为三组:假手术组(SO组,n=30),暴露血管而不夹闭;缺血再灌注组(IR组,n=30),采用4-VO法建立全脑缺血再灌注模型,5 min缺血后给予再灌注;转bcl-2基因组(bcl-2组,n=30):大鼠经转基因处理后再缺血再灌注.各组动物于再灌注后2,6,12,24,48,72 h处死,将脑组织切片进行HE染色,免疫组化染色及TUNEL染色,观察海马回神经元形态改变,凋亡细胞数量及P-P38在CA1区表达. 结果 HE染色显示:IR组全脑缺血再灌注后48 h CA1区神经元数目减少,排列紊乱,核膜界限不清,结构模糊;bcl-2组变化不明显.免疫组化染色显示:P-P38在SO组基本呈阴性着色;IR组CA1区2h出现,48 h达高峰,72 h略有下降;bcl-2组P-P38表达趋势同IR组,但各时间点表达强度弱于IR组.TUNEL染色显示:SO组可见到少量凋亡细胞;IR组全脑缺血再灌注后48 h凋亡细胞数达高峰;bcl-2组再灌注后12-72 h凋亡细胞数量较IR组均明显减少. 结论 全脑缺血再灌注后海马CA1区P-P38表达增加,bcl-2可通过抑制P-P38表达抑制脑缺血再灌注后的细胞凋亡.     

The Experimental Study on Treatment of Glucocorticoid-Induced Ischemic Necrosis of Femoral Head by Gu Fu Sheng Capsule

Objective: To observe the effects of Gu Fu Sheng Capsule (骨复生胶囊 GFSC) on nitric oxide (NO) level and fibrinolytic activity in rabbits with glucocorticoid-induced ischemic necrosis of femoral head (GINFH)so as to explain the therapeutic mechanism of GFSC Methods: 48 rabbits were randomly divided into 4 The models of GINFH were produced by injection of glucocorticoid hormone for 8 weeks. From the 9th week, GFSC decoction was given to the rabbits of the group A (45g. kg-1 d-1) and MSGP extract was given to the group B (0.17 g kg-1 d-1) and the same volume of normal saline to group C and D by intragastric infusion. The content of plasma nitric oxide (NO), and activities of tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor (PAI) were detected after the hormone was injected for 4 and 8 weeks and after the drugs were given for 4 weeks. Results: Compared with the group D, the contents of NO and t-PA activity in the group C decreased significantly (P＜0.01), but the activity of PAI increased significantly (P＜0.01). Compared with the group C, the contents of NO and t-PA activity in the group A and B increased significantly (P＜0.05), but the activity of PAI decreased significantly (P＜0.05), with no significant difference between the two treatment groups (P＞0.05). Conclusion: GFSC could increase the level of NO, protect endotheolial cells and improve fibrinolytic activity, which might be the mechanism of GFSC in curing GINFH.