异丙酚对小肠缺血再灌注大鼠肺损伤的影响

目的 探讨不同临床剂量异丙酚对小肠缺血再灌注(I-R)大鼠肺损伤的影响。方法雄性SD大鼠40只,随机分为5组,假手术对照组(Ⅰ组)、小肠I-R组(Ⅱ组)及分别用微量泵连续静脉输注异丙酚4 mg·kg-1·h-1、8 mg·kg-1·h-1、10 mg·kg-1h-1(Ⅲ、Ⅳ、Ⅴ)组,每组8只;制作小肠I-R模型。测定肺组织血管内皮细胞上细胞间粘附分子-1基因表达、髓过氧化物酶活性及肺湿干重。结果 异丙酚可明显抑制小肠I-R后血管内皮细胞上细胞间粘附分子-l基因表达和肺组织髓过氧化酶活性升高(P<0.01),并可改善肺组织损伤;肺组织细胞间粘附分子-1基因的表达量与肺组织湿干重比和髓过氧化酶活性均呈高度正相关(r=0.975、r=0.996,P<0.05)。结论 小肠I-R后肺血管内皮细胞细胞间粘附分子-1表达增高是引起肺组织内中性粒细胞粘附的重要机制,在小肠I-R后肺损伤过程中起重要作用;临床剂量异丙酚可以不同程度地抑制其表达,减轻肺组织损伤。     

异丙酚对大鼠油酸性急性肺损伤的保护作用

目的观察异丙酚对大鼠油酸性急性肺损伤(ALI)的保护作用及其机制。方法 40只成年雄性 SD 大鼠,体重：250～290g,随机分成5组：正常对照组(Ⅰ组)、ALI 组(Ⅱ组)、4mg·kg~(-1)·h~(-1) 异丙酚治疗组(Ⅲ组)、8mg·kg~(-1)·h~(-1)异丙酚治疗组(Ⅳ组)、16mg·kg~(-1)·h~(-1)异丙酚治疗组(Ⅴ组)；Ⅱ～Ⅴ组静脉注射油酸250μl·kg~(-1)制备大鼠 ALI 模型,然后Ⅲ～Ⅴ组持续静脉输注异丙酚4h 时处死大鼠。测定肺组织 MDA 含量及 MPO、SOD 活性；透射电镜观察肺组织超微结构变化；免疫组化及流式细胞术测定肺组织白介素(IL)-18、IL-10水平；电泳迁移率变动分析技术测定肺组织 NF-(?)B 的表达。结果电镜显示Ⅱ组肺泡Ⅱ型上皮细胞线粒体、粗面内质网及嗜锇性板层小体损伤；Ⅲ～Ⅴ组肺泡Ⅱ型上皮细胞细胞器损伤均有不同程度改善,尤以Ⅳ组效果明显。与Ⅰ组比较,Ⅱ组肺组织 MDA、IL-10、 IL-18、NF-(?)B 水平升高,MPO、SOD 活性降低(P＜0.05)；静脉输注异丙酚使 ALI 大鼠肺组织 MPO、SOD 活性升高,MDA、IL-18、NF-(?)B 水平降低,IL-10水平升高(P＜0.05)。结论 4～16mg·kg~(-1)·h~(-1)异丙酚均可抑制油酸性 ALI 时的氧化应激反应,阻断 NF-(?)B 的活化,减轻肺部炎性反应,对油酸性 ALI 起到一定的保护作用,8mg·kg~(-1)·h~(-1)剂量效果较好。     

异丙酚、氯胺酮对哮喘大鼠气道痉挛及气道渗出的作用

目的 观察异丙酚、氯胺酮对抗原诱发哮喘大鼠气道痉挛及气道渗出的影响。方法哮喘大鼠30只随机分为5组:I组,静注生理盐水;Ⅱ组,静注异丙酚50 mg·kg·-1·h-1;Ⅲ组,静注异丙酚100 mg·kg-1·h-1;Ⅳ组,静注氯胺酮50 mg·kg-1·h-1;V组,静注氯胺酮100 mg·kg-1·h-1。30 min后静注伊文氏蓝;5 min后静注卵蛋白激发哮喘发作,并维持30 min。观察气道压、肺系数、肺湿干重比、肺含水量、肺组织伊文氏蓝含量变化。结果异丙酚和氯胺酮能显著缓解卵蛋白激发引起的气道痉挛反应(P<0.05),相同剂量异丙酚和氯胺酮对气道压的影响无显著性差异。异丙酚和氯胺酮均可明显降低大鼠肺系数、肺湿干重比和肺含水量(P<0.05)。静注异丙酚或氯胺酮后,肺组织伊文氏蓝渗出明显减少,与I组比较差异有显著性(P<0.05)。结论 异丙酚和氯胺酮均能缓解抗原诱发哮喘大鼠的气道痉挛,且能明显抑制哮喘大鼠的气道渗出。     

异丙酚对肝脏缺血/再灌注损伤的保护作用

目的 研究异丙酚对肝脏缺血/再灌注损伤的影响。方法60只家兔分三组,C组（n=20）生理盐水2ml·kg-1·h-1。P组（n=20）异丙酚20mg·kg-1·h-1。E组（n=20）依托咪酯0.1mg·kg-1·h-1。再灌注前后测AST、ALT及SOD,测肝组织MDA;肝组织行电镜检查。结果（1）再灌注后ALT、AST、MDA均升高,以P组为轻,与C组比较差异非常显著（P<0.0 1）,与E组比较亦有显著性差异（P<0.05）。再灌注后SOD均下降,以P组为轻,与C组比较有非常显著性差异（P<0.01）,与E组比较亦有显著性差异（P<0.05）;（2）肝组织超微结构示C组与E组线粒体肿胀,嵴消失或紊乱,核蛋白体脱落,内质网呈空泡状。P组线粒体肿胀轻微,嵴排列尚整齐,内质网排列整齐。结论 异丙酚对肝脏缺血/再灌注损伤有保护作用。     

瑞芬太尼后处理及其联合异丙酚后处理对大鼠肝脏缺血再灌注损伤的影响

目的 评价瑞芬太尼后处理及其联合异丙酚后处理对大鼠肝脏缺血再灌注损伤的影响.方法 健康雄性SD大鼠30只,体重220 ～ 280 g,采用随机数字表法,将其随机分为5组(n=6):假手术组(Ⅰ组)、缺血再灌注组(Ⅱ组)、异丙酚后处理组(Ⅲ组)、瑞芬太尼后处理组(Ⅳ组)和异丙酚联合瑞芬太尼后处理组(Ⅴ组).Ⅱ组～Ⅴ组采用夹闭门静脉和肝动脉30 min的方法制备肝脏缺血再灌注损伤模型,Ⅰ组仅开腹.Ⅲ组、Ⅳ组和Ⅴ组再灌注即刻分别静脉输注异丙酚30 mg· kg-1·h-1、瑞芬太尼1μg·kg -1·min -1和异丙酚30 ng·kg-1·h-1+瑞芬太尼1μg·kg-1·min-1 1 h,Ⅱ组给予等容量生理盐水.于再灌注1h时采集静脉血样,测定血清AST、ALT活性、IL-8、IL-10的浓度,然后处死大鼠,取肝组织,测定肝细胞c-fos和c-jun表达,电镜下观察肝组织病理学结果.结果 与Ⅰ组比较,Ⅱ组～Ⅴ组血清AST、ALT活性及IL-8、IL-10的浓度升高,肝细胞c-fos和c-jun表达上调(P＜0.05或0.01);与Ⅱ组比较,Ⅲ组～Ⅴ组血清AST、ALT活性及IL-8浓度降低,IL-10浓度升高,肝细胞c-fos和c-jun表达下调(P ＜0.05或0.01);与Ⅲ组及Ⅳ组比较,Ⅴ组上述指标差异无统计学意义(P＞0.05).Ⅲ组～Ⅴ组肝组织病理学损伤程度明显轻于Ⅱ组.结论 瑞芬太尼后处理可减轻大鼠肝脏缺血再灌注损伤,联合异丙酚后处理时其效应与单独一种方法的效应相似,其机制与抑制炎性反应和肝细胞凋亡有关.     

丙泊酚对大鼠小肠缺血-再灌注后肺损伤氧自由基变化的影响

目的 探讨不同临床剂量丙泊酚对大鼠小肠缺血-再灌注后肺损伤氧自由基变化的影响及其保护作用。方法 雄性SD大鼠40只,随机分为假手术对照组(C组)、小肠缺血-再灌注组(R组)及分别给予丙泊酚4mg·kg~(-1)·h~(-1)、8mg·kg~(-1)·h~(-1)、10mg·kg~(-1)·h~(-1)(P4、P8、P10)五组;制作小肠缺血-再灌注模型。实验结束即刻留取血样和肺组织,待测脂质过氧化物和肺组织形态学变化。结果 R、P4组血中脂质过氧化物明显升高,与C、P8、P10组相比均有非常显著差异(P<0.01),P8、P10组与C组相比无统计学差异;肺组织脂质过氧化物各实验组与对照组相比差异非常显著(P<0.01),以R组改变最为明显;各用药组指标均得以改善,与R组相比有显著差异(P<0.01),P4与P8、P10组相比亦差异显著(P<0.01)。假手术组肺组织结构正常,R组可见肺泡压闭实变,腔内有大量渗出,炎性细胞浸润,毛细血管扩张,支气管壁增厚,各用药组肺部改变较R组明显减轻,P8、P10两组除了有少量改变外,肺组织结构基本接近正常。结论 氧自由基在大鼠小肠缺血-再灌注后肺损伤中有重要作用,临床剂量丙泊酚不同程度地抑制脂质过氧化反应,对小肠缺血-再灌注后氧自由基介导的肺损伤产生保护作用。     

异丙酚后处理联合缺血后处理对大鼠肝脏缺血再灌注损伤的影响

目的 探讨异丙酚后处理联合缺血后处理对大鼠肝脏缺血再灌注损伤的影响.方法 健康雄性sD大鼠30只,体重200～250 g,随机分为5组(n=6),假手术组(Ⅰ组)仅开腹;缺血再灌注组(11组)肝脏缺血1 h再灌注4 h;缺血后处理组(Ⅲ组)肝脏缺血1 h后,再灌注10 8,缺血10 8,重复6次进行缺血后处理;异丙酚后处理组(Ⅳ组)肝脏缺血1 h后经尾静脉注射异丙酚10 mg/kg,随后静脉输注异丙酚40 mg·kg~(-1)·h~(-1) h;异丙酚后处理+缺血后处理组(V组)肝脏缺血1 h后进行异丙酚后处理及缺血后处理.于再灌注4 h时测定血清ALT活性、肝组织MDA含量、SOD活性、Bcl-2及Bax的蛋白表达水平,电镜下观察肝细胞超微结构.结果 与Ⅰ组比较,Ⅱ组～Ⅴ组血清ALT活性及肝组织MDA含量升高,肝组织Bcl-2蛋白表达上调,Ⅲ组-Ⅴ组肝组织SOD活性升高,Ⅱ组、Ⅲ组及Ⅴ组肝组织Bax蛋白表达上调(P<0.05或0.01);与Ⅱ组比较,Ⅲ组-Ⅴ组血清ALT活性及肝组织MDA含量降低,肝组织SOD活性升高,Bcl-2蛋白表达上调,Bax蛋白表达下调(P<0.05或0.01);与Ⅲ组比较,Ⅳ组血清ALT活性及肝组织MDA含量降低(P<0.05或0.01).Ⅲ组-Ⅴ组肝组织病理学损伤较Ⅱ组明显减轻.结论 异丙酚后处理联合缺血后处理可减轻大鼠肝脏缺血再灌注损伤,与异丙酚后处理单独应用时效果相同,其机制可能与抑制肝组织脂质过氧化反应及细胞凋亡有关.     

异丙酚对大鼠肠缺血再灌注后肺损伤的影响

目的探讨异丙酚对大鼠肠缺血再灌注后肺损伤的影响。方法32只成年SD大鼠,随机分为4组（n=8）,缺血再灌注组（I/R组）缺血1 h,再灌注2 h;异丙酚1组（P1组）在缺血前10 min、异丙酚2组（P2组）在再灌注前10min静脉注射异丙酚10mg,kg,然后以10mg·kg^-1·h^-1持续输注,余处理同I/R组;假手术组（C组）不行缺血再灌注及异丙酚输注。所有大鼠在再灌注120 min时处死。光镜下观察肺组织形态学及细胞凋亡;测定肺组织超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量及含水量。结果I/R组光镜下可见大量肺泡塌陷、实变,肺实质水肿及中性粒细胞浸润聚集。与C组比较,I/R组及P2组肺组织细胞凋亡计数增加,I/R组肺组织SOD活性降低,MDA含量升高,含水量升高（P＜0．05或0．01）;与I/R组比较,P1组SOD活性升高,MDA含量降低（P＜0．01）。结论细胞凋亡参与了大鼠肠缺血再灌注后肺损伤的发生,肠缺血前给予异丙酚可明显减轻肠缺血再灌注后肺损伤。     

大鼠肝缺血/再灌注后肝细胞凋亡的评价及异丙酚对细胞凋亡的影响

目的 观察大鼠肝脏缺血再灌注后肝窦内皮细胞凋亡及异丙酚对肝脏细胞凋亡的影响。方法 选用健康SD雄性大鼠24只,随机分为三组(n=8):A组,肝脏缺血30 min再灌注6 h,再灌注即刻从股静脉输入生理盐水10ml·kg-1·h-1 60 min;B组,再灌注即刻静脉注射异丙酚20 mg/kg,继之输入5％异丙酚50 mg·kg-1·h-1 h;C组,给予假手术处理,未予缺血,余处理同A组。再灌注6 h后取肝组织标本行病理组织学观察,同时测定血浆ALT活性和肝组织MDA含量的变化。采用DNA琼脂糖凝胶电泳、TUNEL染色观察细胞凋亡的情况。结果与C组相比,A组凋亡的肝细胞和肝窦内皮细胞明显增加,且凋亡的细胞主要是肝窦内皮细胞,肝细胞凋亡和坏死则较少。与A组相比,再灌注6 h B组TUNEL阳性肝细胞和肝窦内皮细胞数明显减少(p<0.01),肝组织DNA片段形成也明显减少。同时,B组肝组织坏死程度、血浆ALT活性和肝组织MDA含量均明显低于A组(JD<0.01)。电镜显示B组肝细胞和肝窦内皮细胞损伤也明显轻于A组。结论 细胞凋亡是再灌注早期肝脏细胞死亡的重要机制,肝窦内皮细胞凋亡是再灌注早期肝脏细胞死亡的主要特征。异丙酚可以减少再灌注后的肝脏细胞凋亡和坏死,其抗氧化作用是其减少再灌注后的肝脏细胞凋亡的机制。     

异丙酚对成年大鼠血脑屏障通透性的影响

目的　观察静脉输注不同剂量异丙酚对大鼠血脑屏障 (BBB)通透性的影响。方法　 30只成年大鼠随机分为三组 :对照组 (C组 ,不用全麻药 ,n =6 ) ,异丙酚 70mg·kg-1·h-1组 (P1组 ,静脉注射异丙酚 2 0mg/kg继以静脉输注 5 0mg·kg-1·h-11小时 ,n =12 ) ,异丙酚 12 0mg·kg-1·h-1组 (P2组 ,静脉输注异丙酚 12 0mg·kg-1·h-11小时 ,n =12 )。取脑做EB染色观察、镧醛灌注后电镜观察及HE染色光镜观察。结果　P1、P2组EB染色、HE染色及电镜观察结果与C组相比均无明显差别。结论　本实验结果提示 ,静脉输注产生脑电图爆发抑制剂量的异丙酚 (70mg·kg-1·h-1)及更大剂量(12 0mg·kg-1·h-1) 1小时 ,虽然后者产生明显的循环抑制 ,但两者均未增加大鼠BBB对大分子 (EB 白蛋白 )和小分子 (镧离子 )的通透性 ,对中枢神经系统形态也无明显影响。     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

目的 评价缺血预处理.后处理对大鼠肠缺血再灌注损伤的影响.方法 清洁级成年雄性SD大鼠40只.体重225～275 g,随机分为5组(n=8):假手术组(S组)仅分离肠系膜上动脉(SMA),不夹闭;肠缺血再灌注组(IIR组)采用夹闭SMA 60 min,再灌注60 min的方法制备肠缺血再灌注损伤模型;缺血预处理组(IPr组)夹闭SMA 10 min,再灌注10 min,余同IIR组;缺血后处理组(IPo 组)夹闭SMA 60 min后,再灌注30 s,缺血30 s,反复3次,再灌注60 min;缺血预处理.后处理组(IPr-IPo组)先行缺血预处理,再行缺血后处理,操作过程同IPr组和IPo组.于再灌注60 min时各组取肠粘膜组织,观察肠粘膜形态并行Chiu评分,检测丙二醛(MDA)含量,超氧化物歧化酶(SOD)及髓过氧化物酶(MPO)活性,同时采集动脉血样检测血浆肿瘤坏死因子α(TNF-α)及白细胞介素6(IL-6)浓度.结果 与S组比较,其余各组Chiu评分、MDA含量、MPO活性、血浆TNF-α与IL-6浓度升高,SOD活性降低(P<0.05).与IIR组比较,IPr组、IPo组及IPr-IPo组Chiu评分、MDA含量、MPO活性、血浆TNF-α和IL-6浓度降低.SOD活性升高(P<0.01).与IPr组和IPo组比较,IPr-IPo组Chiu评分和MDA含量降低,SOD活性升高(P<0.05).IPr组与IPo组各指标比较差异无统计学意义(P>0.05).结论 缺血预处理-后处理可减轻大鼠肠缺血再灌注损伤,较单独应用时效果好.     

异丙酚对心肌缺血再灌注兔胃粘膜pH值的影响

目的 观察兔心肌缺血再灌注后胃粘膜pH值(pHi)的变化,并探讨异丙酚对心肌缺血再灌注后兔内脏器官微循环灌注的影响。方法20只健康家兔,麻醉后随机分为生理盐水对照组(A组)及异丙酚组(B组,术中5mg·kg-1·h-1)。于基础状态(T0),心肌缺血60min(T1),再灌注后60min(T2)、90min(T3)和180min(T4)分别记录收缩压(SBP)、舒张压(DBP)、心率(HR)和pHi值。结果 两组动物5个不同时点的HR、SBP、DBP无显著差异(P>0.05)。两组动物缺血及再灌注后HR、SBP、DBP均有显著性下降(P<0.01)。pHi变化:与A组相比,B组动物T3点pHi值较低(P<0.05);组内,两组动物缺血及再灌注后pHi值均有显著性下降(P<0.01)。两组动物收缩压(SBP)及HR与pHi的变化均具有显著意义的相关性。结论 兔心肌缺血再灌注后,pHi持续显著降低,且pHi与血流动力学变化趋势一致,具有显著意义相关性。兔缺血再灌注期间,5mg·km-1·h-1异丙酚持续静注并不能改善胃肠道微循环灌注,甚至有可能加重胃肠道的低灌注及氧合障碍。     

异丙酚对大鼠肺一氧化氮合酶活性的影响

目的 了解异丙酚对大鼠肺一氧化氮合酶(NOS)活性的影响,探讨异丙酚对肺血管、支气管扩张作用的机理。方法40只SD大鼠,随机分为异丙酚组(n=20)、对照组(n=20),分别腹腔注射等容积异丙酚(1ml·kg-1,即100mg·kg-1)和生理盐水(10ml·kg-1)。异丙酚组待鼠翻正反射消失后,经尾缘静脉泵以异丙酚10mg·kg-1·h-1,20min后处死,对照组鼠腹腔注射20min后处死。检测支气管肺泡灌洗液NO水平、肺组织匀浆中NOS酶活性、NO水平及内皮型NOS(eNOS)、神经型NOS(nNOS)在肺内的表达与分布(免疫组化法)。结果 异丙酚组支气管灌洗液和肺组织匀浆中NO水平均明显高于对照组(P<0.01),肺组织匀浆中NOS酶活性也明显大于对照组(P<0.01)。异丙酚组肺血管内皮细胞nNOS和eNOS、支气管粘膜上皮细胞nNOS染色表达强阳性。结论 异丙酚可以刺激肺中NOS活性,升高肺内内源性NO水平,在异丙酚的扩张肺血管、支气管中发挥一定的作用。     

Prevention of pain on injection of propofol: a comparison of remifentanil with alfentanil in children

AIM: Propofol has a high incidence of pain on injection, particularly when a vein on the back of hand is used. Administration of lidocaine, either before or mixed with propofol remains the most widely used method to attenuate this pain. The use of opioids such as alfentanil and fentanyl has been found to decrease pain induced by propofol injection. The purpose of this study was to evaluate the effects of different doses of remifentanil and alfentanil in minimizing the pain caused by propofol. METHODS: In this randomized, double-blind, placebo-controlled study, healthy premedicated children between the age group of 5-12 years admitted for adenotonsillectomy were randomly allocated to one of 6 treatment groups. Group I: remifentanil 0.25 microg kg(-1); Group II: remifentanil 0.50 microg kg(-1); Group III: alfentanil 15 microg kg(-1); Group IV: alfentanil 20 microg kg(-1) 60 s prior to propofol mixed with 1 mL of 0.9% normal saline; Group V: lidocaine 1 mL of 1% (10 mg) added to 100 mg of propofol and Group VI: normal saline. During the injection of propofol (3 mg kg(-1)) pain perception was assessed with a four-point behavioural scale: none, mild, moderate, or severe. RESULTS: There were 52 subjects in Group I, 51 in Group II, 49 in Group III, 52 in Group IV, 52 in Group V and 52 in Group VI; 63.46% of patients in Group I, 39.21% in Group II, 38.77% in Group III, 36.53% in Group IV, 38.46% in Group V and 84.61% in Group VI experienced pain. Statistically, Groups II, III, IV and V were significantly better than placebo in the reduction of propofol pain (P<0.0001). Groups II, III and IV significantly reduced the pain in comparison with Group I (P<0.001). CONCLUSION: Pretreatment with intravenous remifentanil 0.5 microg kg(-1), alfentanil 15 microg kg(-1) and 20 microg kg(-1) were equally effective in reducing pain associated with propofol injection in children between the age group of 5-12 years.     

大鼠肠缺血再灌注时肺组织β-防御素-2 mRNA表达的变化

目的 观察大鼠肠缺血再灌注时肺组织β-防御素-2(BD-2)mRNA表达的变化.方法 72只雄性SD大鼠随机分为2组(n=36):假手术组(S组)和肠缺血再灌注组(II/R组).采用夹闭肠系膜上动脉(SMA)的方法制备肠缺血再灌注模型.II/R组阻断SMA 1 h后再灌注,S组仅分离SMA.分别于再灌注即刻(T0),再灌注15(T1)、30(T2)、60 min(T3)、3 h(T4)和6 h(T5)时处死6只大鼠,取肺组织,光镜下观察肺组织病理学结果,计算肺通透性指数(PPI),检测肺组织肿瘤坏死因子-α(TNF-α)含量和BD-2 mRNA表达水平.结果 S组肺组织结构未见异常,II/R组出现肺水肿和中性粒细胞浸润.与S组比较,II/R组再灌注各时点PPI升高,BD-2 mRNA表达上调,T0-3时TNF-a含量升高(P＜0.05或0.01).II/R组BD-2 mRNA表达水平与TNF-a含量及PPI的相关系数分别为0.823和-0.615(P＜0.01).结论 大鼠肠缺血再灌注时肺组织BD-2基因表达上调.     

Experimental studies on the effects of superoxide dismutase on warm ischemic-reperfusion injury of the lung]

Transient impairment of the transplanted lung in early postoperative period is one of difficult problems in lung transplantation. It is likely that reperfusion injury of the warm ischemic lung is contributory. The purpose of this study is to evaluate the effects of superoxide dismutase (SOD) on reperfusion injury of warm ischemic lung. Thirty mongrel dogs were divided into four groups. In group I (n = 6), the left lung with complete hilar stripping was placed in warm ischemic state under deflation for 1 hour. In group II (n = 9), the left lung with complete hilar stripping was kept in warm ischemic condition under inflation. Group III (n = 6) animals with same manipulation as group I received superoxide dismutase (SOD 20 mg/kg) before reperfusion. Group IV (n = 9) animals underwent same manipulation as group II and received SOD (20 mg/kg) before reperfusion. Before warm ischemia, immediately after reperfusion, and 1 and 2 hours, blood gases, left pulmonary vascular resistance were measured under the occlusion of right pulmonary artery. Extra vascular lung water content (EVLW) was measured at autopsy and lung was processed for histology. In group II, III and IV, blood gases and EVLW showed significantly better values than group I. In group I and III, left pulmonary vascular resistance increased prominently after reperfusion, however did not change in group II and IV. From these results, we concluded that inflated lung reduced the extent of pulmonary edema after reperfusion and SOD was effective in preventing warm ischemic damage even in deflated lung.     

丙泊酚预处理对大鼠心肌缺血-再灌注损伤心肌细胞膜ATP酶活性的影响

目的 研究丙泊酚预处理对大鼠心肌缺血-再灌注损伤心肌细胞膜ATP酶活性及心肌组织形态学的影响.方法 40只雄性SD大鼠随机分成五组,每组8只:对照组(C组),缺血-再灌注组(IR组),丙泊酚1组(P1组),丙泊酚2组(P2组),丙泊酚3组(P3组).各组于再灌注60 min后立即取左室心尖部心肌,检测心肌匀浆中心肌细胞膜Na+-K+-ATP、Ca2+-Mg2+-ATP酶活性;光镜下观察心肌组织形态学变化.结果 IR时心肌细胞膜Na+-K+-ATP、Ca2+-Mg2+-ATP酶活性与C组相比明显下降(P<0.01);O1、P2、P3组心肌细胞膜Na+-K+-ATP、Ca2+-Mg2+-ATP酶活性与IR组相比明显升高,但仍低于C组(P<0.05).结论 丙泊酚可以减轻大鼠心肌缺血-再灌注损伤,其机制可能与恢复心肌细胞膜Na+-K+-ATP、Ca2+-Mg2+-ATP酶活性有关.     

Ex vivo transfection of transforming growth factor-beta1 gene to pulmonary artery segments in lung grafts

OBJECTIVE: Proximal pulmonary artery segment transfection may provide beneficial downstream effects on the whole-lung graft. In this study, transforming growth factor-beta1 was transfected to proximal pulmonary artery segments, and the efficacy of transforming growth factor-beta1 transfection was examined in ischemia-reperfusion injury and acute rejection models of rat lung transplantation. METHODS: In the ischemia-reperfusion injury model, orthotopic left lung transplantation was performed in F344 rats. In group I, the PPAS was isolated and injected with saline solution. In 2 other groups, lipid67:DOPE:sense (group II) or antisense transforming growth factor-beta1pDNA construct (group III) was injected instead of saline solution. After cold preservation at 4 degrees C for 18 hours, lung grafts were implanted. Graft function was assessed 24 hours later. In the acute rejection model, donor lung grafts were harvested. Proximal pulmonary artery segments were injected with saline solution (group I) or sense (group II) or antisense lipid gene construct (group III) and then implanted. Graft function was assessed on postoperative day 5. RESULTS: In the ischemia-reperfusion injury study, there were no significant differences in oxygenation, wet-to-dry weight ratios, graft myeloperoxidase activity, or transforming growth factor-beta1 levels in platelet-poor serum or proximal pulmonary artery segment homogenates. In the acute rejection study, oxygenation was significantly improved in group II receiving transforming growth factor-beta1 (group II vs I and III, 136.0 +/- 32.5 vs 54.0 +/- 9.6 mm Hg and 53.8 +/- 14.8 mm Hg; P =.016 and.016). There were no significant pathologic differences. Transforming growth factor-beta1 concentrations from proximal pulmonary artery segment homogenates in group II were significantly higher compared with controls. CONCLUSIONS: Ex vivo transfection of transforming growth factor-beta1 to proximal pulmonary artery segments did not affect reperfusion injury of lung isografts. In acute rejection, however, ex vivo transfection of transforming growth factor-beta 1 to proximal pulmonary artery segments improved allograft function. This suggests that transfection to proximal pulmonary artery segments exerts beneficial downstream effects on the whole-lung allograft.     

Lazaroid U74389G ameliorates ischemia-reperfusion injury in the rat lung transplant model.

We investigated the effect of Lazaroid U74389G on ischemia-reperfusion injury in the rat orthotopic left lung transplantation model. Five groups of reperfused lungs were studied. In group I, donor lungs were transplanted after 12 hours of preservation in University of Wisconsin (UW) solution at 4C. In groups II, III, and IV, Lazaroid was intravenously administrated at a dose of 1 mg/kg, 8 mg/kg, and 15 mg/kg, respectively, to the donors 30 minutes before preservation and also to the recipients 30 minutes before reperfusion after 12 hours of storage in UW solution at 4C. In group V, Lazaroid was added to the UW solution (80 micromol/l), and also was administered intravenously (6 mg/kg) 30 minutes before reperfusion. After 1 hour of reperfusion, gas exchange function and tissue lipid peroxide levels were significantly improved in Lazaroid-treated groups III, and V compared with no treatment group I. Histologic damage was less severe in groups III, IV, and V than in group I. These findings suggest that Lazaroid U74389G ameliorates ischemia-reperfusion injury in the rat lung transplants by inhibiting lipid peroxidation, regardless of whether it is administrated intravenously or given as an additive to the preservation solution.     

A comparison of enflurane and propofol in thoracic surgery

Comparisons between propofol and inhalational anesthetics for maintenance of anesthesia are limited. The purpose of our prospective study was to examine differences between enflurane and propofol during pulmonary resections with one-lung ventilation (1LV). METHOD. 28 patients, ASA risk group II-III, gave written informed consent for inclusion in this institutionally approved study. The patients were randomly allocated to one of the following groups: A: propofol 10 mg kg-1 h-1, B: 1 MAC enflurane, for maintenance of anesthesia. In both groups analgesia was achieved by fentanyl and muscle relaxation, by pancuronium. Ventilation via a double-lumen tube was controlled (FiO2 = 1.0, PaCO2 35-40 mmHg). Measurements, including hemodynamics and arterial and mixed venous blood gases, were obtained before induction (I), during two-lung ventilation (2LV) 15 min after induction in the supine position (II) and 20 min after surgical opening of the chest in the lateral decubitus position (III), 20 min after starting 1LV (IV), and after extubation (V). RESULTS. No significant differences between the two groups were found before induction (I), during 2LV (II, III), or after extubation (V). The only significant differences between the two groups were observed during 1LV (IV): the shunt fraction was 33.9 +/- 2.5% in A and 38.5 +/- 2.6% in B (P less than or equal to 0.05). Hypoxic pulmonary vasoconstriction was not inhibited in A, but was inhibited by 21.5% in group B during 1LV. Since no case of hypoxemia occurred in group A during 1LV (range of PaO2: 75.2-417.0 mmHg), but four patients developed hypoxemia in group B (Range of PaO2: 46.6-431.0 mmHg), regimen A might be of value in high-risk patients during thoracic surgery when 1LV is planned.