七氟醚对大鼠离体心脏全心缺血-再灌注心律失常及电生理的影响

目的观察七氟醚对大鼠离体心脏全心缺血-再灌注心律失常及电生理的影响。方法健康成年雄性SD大鼠,体重280～320g,取成功制备Langendorff心脏灌注模型24个,K-H液灌注15min后,随机分为三组,每组8只。对照组(C组):K-H液继续灌注105min;全心缺血-再灌注组(IR组):K-H液继续灌注15min后,注射Thomas液(4℃,20ml/kg)使心脏停跳60min,在心脏周围用低温(4℃)Thomas液保护,30min时半量复灌Thomas液(4℃,10ml/kg),停灌60min时再灌注K-H液30min;七氟醚组(Sev组):K-H液含饱和1.0MAC的七氟醚,余同IR组。记录再灌注期间心律失常发生情况、心脏复跳时间及心律失常持续时间;记录平衡灌注15min(T_0)、继续灌注15min(T_1)、再灌注15min/继续灌注105min(T_2)、再灌注30min/继续灌注120min(T_3)的HR及左心室前壁外膜层和内膜层心肌单相动作电位;计算单相动作电位复极50%及90%的时程(MAPD_(50)和MAPD_(90))、跨室壁复极离散度(TDR)。结果与T_0时比较,T_2、T_3时IR组HR明显减慢(P0.05);与T_1时比较,T_2、T_3时IR组HR均明显减慢(P0.05);与IR组比较,T_2、T_3时Sev组HR明显增快(P0.05);与IR组比较,T_2、T_3时Sev组MAPD_(90)明显缩短,TDR明显减小(P0.05);与IR组比较,Sev组心脏复跳时间和心律失常持续时间均明显缩短(P0.05)。结论七氟醚可缩短全心缺血-再灌注心脏MAPD_(90)、减小TDR,从而降低再灌注心律失常的发生风险、缩短心脏复跳和心律失常持续时间。     

七氟醚对低温全心缺血-再灌注心脏电传导及Cx43 Ser368磷酸化的影响

目的 观察七氟醚对低温全心缺血-再灌注心室肌电传导及Cx43 Ser368磷酸化的影响。
方法 制备成功的离体灌注工作心脏24只,随机分为三组：对照组（C组）、低温全心缺血-再灌注组（IR组）和1.0 MAC七氟醚处理组（Sev组）,每组8只。C组：37 ℃ K-H液平衡灌注15 min后继续灌注37 ℃ K-H液105 min;IR组：37 ℃ K-H液平衡灌注15 min后继续灌注37 ℃ K-H液15 min,注射Thomas液（4 ℃,20 ml/kg）使心脏停搏60 min,4 ℃ K-H液保护心脏,停搏30 min时半量复灌Thomas液（4 ℃,10 ml/kg）,60 min时使用37 ℃ K-H液再灌注30 min;Sev组：37 ℃ K-H液平衡灌注15 min后继续灌注含饱和1.0 MAC七氟醚的37 ℃ K-H液15 min,注射Thomas液（4 ℃,20 ml/kg）使心脏停搏60 min,4 ℃ K-H液保护心脏,停搏30 min时半量复灌Thomas液（4 ℃,10 ml/kg）,60 min时使用含饱和1.0 MAC七氟醚的37 ℃ K-H液再灌注30 min。于再灌注即刻至灌注结束,记录离体心脏复跳时间（再灌注即刻至心脏首次跳动所需的时间）,室性心律失常（室性早搏、室性心动过速、室性颤动）发生情况和持续时间。采用心脏刺激仪行程控刺激,测定并记录有效不应期（ERP）、传导速度(CV）。采用免疫印迹法检测心室肌组织Cx43和Cx43 Ser368蛋白相对含量。
结果 与C组比较,IR组和Sev组ERP明显延长,CV明显减慢（P＜0.05）;IR组Cx43及Cx43 Ser368蛋白相对含量明显降低（P＜0.05）。与IR组比较,Sev组心脏复跳时间明显缩短,心律失常发生率明显降低,心律失常持续时间明显缩短,ERP明显缩短,CV明显增快,Cx43及Cx43 Ser368蛋白相对含量明显升高（P＜0.05）。
结论 七氟醚可以上调低温全心缺血-再灌注心室肌组织Cx43和Cx43 Ser368的表达,促使心室肌电传导增快、有效不应期缩短,降低再灌注心律失常的发生。     

不同浓度七氟醚对缺血-再灌注心肌单相动作电位影响

目的观察不同浓度七氟醚对大鼠离体心脏缺血-再灌注时心肌单相动作电位(MAP)的影响。方法健康成年雄性SD大鼠32只,体重280～320g,成功制备langendorff离体心脏灌注模型,K-H液平衡灌注15min后,随机分为四组,每组8只:缺血-再灌注组(IR组):K-H液继续灌注15min后停止,注射Thomas液(4℃,20 ml/kg)使心脏停搏60 min,心脏周围用低温(4℃)Thomas液保护,30min时半量复灌Thomas液(4℃,10ml/kg),60min时再灌注K-H液30min;0.5 MAC七氟醚组(Sev0.5组):K-H液为含饱和0.5 MAC七氟醚液体,余同IR组;1.0 MAC七氟醚组(Sev1.0组):K-H液为含饱和1.0 MAC七氟醚液体,余同IR组;2.0 MAC七氟醚组(Sev2.0组):K-H液为含饱和2.0MAC七氟醚液体,余同IR组。记录平衡灌注15min(T_0)、继续灌注15min(T_1)、再灌注15min(T_2)、再灌注30min(T_3)的HR及左心室前壁外膜层、中层和内膜层心肌MAP,计算MAP复极50%及90%的时程(MAPD_(50)、MAPD_(90))。并记录心律失常发生情况。结果与T_0和T_1时比较,T_2、T_3时IR组、Sev1.0组、Sev2.0组HR明显减慢(P0.05);与IR组比较,T_2、T_3时Sev0.5组、Sev1.0组HR明显增快,Sev2.0组HR明显减慢(P0.05)。与IR组比较,T_3时Sev0.5组MAPD_(50),Sev0.5组、Sev1.0组、Sev2.0组MAPD_(90)明显缩短(P0.05)。心脏复跳时IR组有6例,Sev0.5组有1例,Sev1.0组有2例,Sev2.0组有1例发生心律失常,与IR组比较,Sev0.5组、Sev1.0组和Sev2.0组心律失常发生率明显降低(P0.05)。结论不同浓度七氟醚均可缩短缺血-再灌注心肌单相动作电位MAPD_(90),且这一作用在0.5~2.0 MAC的七氟醚浓度范围内无剂量依赖性,这可能是其减少缺血-再灌注心律失常发生风险的机制。     

七氟醚对在体大鼠肺缺血-再灌注损伤的影响

目的研究七氟醚对在体大鼠肺缺血-再灌注(I-R)损伤的影响。方法40只Wistar大鼠建立在体大鼠肺I-R模型,随机分为四组,每组10只:A组,假手术组,开胸后机械通气120 min;B组,I-R组,阻断左肺门60 min,开放再通气60 min;C组,七氟醚加I-R组,缺血前吸入1 MAC七氟醚30 min,开放再通气同时吸入1 MAC七氟醚60 min;D组,七氟醚组,持续吸入1 MAC七氟醚120min。观察各组实验结束时肺组织的湿/干重比(W/D)、肺丙二醛(MDA)、超氧化物歧化酶(SOD)和肺组织病理学的改变。结果B组及C组肺W/D较A组和D组显著升高(P<0.01,P<0.05),SOD含量显著低于A组和D组(P<0.05);B组肺MDA含量较A组和D组显著升高(P<0.01),C组肺MDA含量较B组低(P<0.05);C组肺W/D、肺MDA显著低于B组(P<0.05),SOD高于B组(P<0.05);病理切片见B组、C组部分肺泡结构破坏,肺泡间隔增宽,肺泡腔内水肿并有出血,以B组改变较为严重,炎症积分显著高于C组(P<0.01)。结论七氟醚对在体大鼠肺I-R损伤有一定的保护作用。     

七氟醚对大鼠急性肾缺血-再灌注损伤的保护作用

目的探讨七氟醚对急性肾缺血-再灌注损伤的保护作用及其机制。方法SD大鼠18只,随机均分为缺血-再灌注组(I/R组)、七氟醚组(S组)和对照组(C组)。建立大鼠急性肾缺血-再灌注损伤模型,缺血-再灌注后3h分别检测血清尿素氮(BUN)、肌酐(Cr)、超氧化物歧化酶(SOD)、丙二醛(MDA)及观察肾组织的病理学变化。结果与C组比较,I/R组和S组血清BUN、Cr水平显著增加(P<0.05),但S组BUN、Cr低于I/R组(P<0.05)。与I/R组比较,S组SOD显著升高,MDA显著降低(P<0.05)。S组肾组织病理损伤分级明显低于I/R组(P<0.05)。结论七氟醚对大鼠急性肾缺血-再灌注损伤具有保护作用,抑制氧自由基反应可能是其重要机制。     

七氟醚和安氟醚对离体大鼠缺血再灌注心脏功能的影响

目的：观测七氟醚和安氟醚对大鼠缺血再灌注心脏功能的影响。方法：采用Ｌａｎｇｅｎｄｏｒｆ离体大鼠心脏模型，将３０只ＳＤ大鼠随机分成对照组、七氟醚组和安氟醚组。全心缺血３０ｍｉｎ，再灌注３０ｍｉｎ。结果：１ＭＡＣ的七氟醚或安氟醚可以降低再灌注心律失常的发生率和冠脉阻力，增加再灌注心肌的冠脉流量，促进再灌注损伤后左室功能的恢复。在降低缺血损害和提高再灌注冠脉流量方面，七氟醚比安氟醚更明显。结论：七氟醚和安氟醚对缺血再灌注心脏均有一定的保护作用。     

芬太尼对大鼠全心缺血/再灌注损伤及心律失常的影响

心肌缺血／再灌注损伤及心律失常是围麻醉期的一种病理生理变化。本研究采用Ｌａｎｇｅｎｄｏｒｆｆ心脏离休灌注模型和大鼠在体、离体局部心肌缺血／再灌注心律失常模型，系统观察芬太尼对其的影响。材料与方法再灌注损伤模型　采用Ｌａｎｇｅｎ－ｄｏｒｆｆ心脏离体灌注模型及Ｍａｃｌａｂ记录系统，将３０只ＳＤ大鼠随机分为对照组（Ｃ组）和两芬太尼组（Ｆ１及Ｆ２组）。３％戊巴比妥钠３０ｎｇ·ｍｌ－１、肝素５００Ｕ·ｋｇ－１腹腔麻醉，１０分钟后开胸取心迅速投入（０～４）℃Ｋ－Ｈ液中停搏，经主动脉插管行非循环式Ｌａｎｇｅｎ…     

七氟醚预处理对大鼠肾缺血再灌注损伤的影响

目的 评价七氟醚预处理对大鼠肾缺血再灌注损伤的影响.方法 雄性SD大鼠24只,体重250～300 g,采用随机数字表法,将大鼠随机分为3组(n=8):假手术组(S组)、肾缺血再灌注组(I/R组)和七氟醚预处理组(SP组).I/R组和SP组采用切除右肾然后夹闭左侧肾动脉45 min再开放的方法 制备肾缺血再灌注模型.SP组吸入2.2%七氟醚1 h,停止吸入后10 min时进行肾缺血.于再灌注2 h时采集静脉血样,测定血清肌酐(Cr)、尿素氮(BUN)和胱抑素C(Cys C)的浓度,取肾组织,光镜下及透射电镜下观察病理学结果,并根据肾小管病变程度进行Paller评分.结果 与S组比较,I/R组血清Cr和BUN浓度差异无统计学意义(P＞0.05),血清Cys C浓度和Paller评分明显升高(P＜0.05);与I/R组比较,SP组血清Cys C浓度和Paller评分明显降低(P＜0.05).SP组肾组织损伤程度轻于I/R组.结论 七氟醚预处理可减轻大鼠肾缺血再灌注损伤.

Abstract：

Objective To investigate the effects of sevoflurane preconditioning on renal ischemia-reperfusion(I/R)injury in rats.Methods Twenty-four adult male SD rats weighing 250-300 g were randomly divided into 3 groups(n=8 each):sham operation group (group S);I/R group; sevoflurane preconditioning group (group SP). After the rats underwent right nephrectomy, renal I/R was produced by occlusion of left renal artery for 45 min followed by reperfusion in I/R and SP groups.In group SP, the rats inhaled 2.2% sevoflurane for 1 h, then the inhalation was stopped and renal ischemia was performed 10 min later. Venous blood samples were collected at 2 h of reperfusion to determine the concentrations of serum creatinine(Cr), urea nitrogen (BUN), cystatin C (Cys C) . The renal tissues were obtained for microscopic examination, and Paller's score was recorded. Results Compared with group S, there was no significant difference in the serum Cr and BUN concentrations (P＞0.05), while the serum Cys C concentration and Paller's score for acute renal tubular injury were significantly increased in group I/R(P＜0.05). The serum Cys C concentration and Paller's score were significantly lower in group SP than in group I/R(P＜0.05).I/R-induced renal injury was significantly reduced in group SP compared with group I/R. Conclusion Preconditioning with sevoflurane can provide significant protection against renal I/R injury.     

七氟醚延迟预处理对大鼠缺血再灌注心肌ARC表达的影响

目的 评价七氟醚延迟预处理对大鼠缺血再灌注心肌带有Caspase富集功能域的凋亡抑制蛋白(ARC)表达的影响.方法 成年雄性SD大鼠64只,体重270～350 g,采用随机数字表法,将其随机分为4组(n=16):假手术组(S组)、心肌缺血再灌注组(I/R组)、七氟醚+假手术组(S-S组)和七氟醚延迟预处理+心肌缺血再灌注组(S-VR组).S-S组和S-I/R组分别吸入33%氧气和2.5%七氟醚2 h,停止吸入后24 h行假手术或心肌缺血再灌注;I/R组和S-I/R组采用结扎左冠状动脉前降支30 min,再灌注2 h的方法制备心肌缺血再灌注模型.于再灌注2 h时处死8只大鼠,取左心室组织,测定心肌梗死范围及细胞凋亡情况,计算凋亡指数,于缺血前即刻及再灌注2 h时各处死4只大鼠,取左心室组织,测定ARC及Caspase-8的表达水平.结果 与S组比较,I/R组和S-I/R组心肌梗死范围及细胞凋亡指数升高,缺血前即刻S-S组和S-I/R组ARC表达上调,再灌注2 h时I/R组Caspese-8、表达上调(P＜0.05);与I/R组比较,S-I/R组心肌梗死范围和细胞凋亡指数降低,再灌注2 h时S-S组和S-I/R组ARC表达上调,Caspase-8表达下调(P＜0.05).结论 七氟醚延迟预处理可上调心肌ARC表达,减少细胞凋亡的发生,从而减轻大鼠心肌缺血再灌注损伤.

Abstract：

Objective To investigate the effects of sevoflurane delayed preconditioning on caspase recruitment domain (ARC) expression during myocardial ischemia-reperfusion (I/R) in rats. Methods Sixty-four adult male SD rats weighing 270-350 g were randomly divided into 4 groups ( n = 16 each): sham operation (group S); myocardial I/R group; sevoflurane + sham operation group (group S-S) and sevoflurane delayed preconditioning + myocardial I/R group (group S-I/R) . Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h of reperfusion in groups I/R and S-I/R. Group S-S inhaled 33% oxygen for 2 h, and sham operation was performed 24 h later. Group S-I/R inhaled 2.5% sevoflurane for 2 h, and then myocardial I/R was induced 24 h later. Eight animals were sacrificed at the end of 2 h reperfusion in each group and the hearts removed for determination of myocardial infarct size (IS) as a percentage of area at risk (AAR) by triphenyl tetrazolium chloride staining (IS/AAR) . Myocardial apoptosis was detected using TUNEL and apoptosis index was calculated. Another 4 animals were sacrificed immediately before ischemia and at the end of 2 h reperfusion to determine the expression of ARC and Caspase-8 in myocardium by Western blot. Results Compared with group S, the infarct size and apoptosis index were significantly increased in groups I/R and S-I/R, and ARC expression was up-regulated immediately before ischemia in groups S-S and S-I/R, and Caspase-8 expression was up-regulated at 2 h of reperfusion in group I/R ( P ＜ 0.05) . Compared with group I/R, the infarct size and apoptosis index were significantly decreased in group S-I/R, and ARC expression was up-regulated, while Caspase-8 expression was down-regulated at 2 h of reperfusion in groups S-S and S-I/R ( P ＜ 0.05) . Conclusion Sevoflurane delayed preconditioning can attenuate myocardial I/R injury through up-regulating the ARC expression and decreasing the myocardial apoptosis.     

七氟醚对心肌缺血-再灌注幼兔心肌细胞凋亡及Fas/FasL蛋白表达的影响

目的探讨七氟醚对幼兔缺血-再灌注心肌细胞凋亡及Fas、FasL蛋白表达的影响。方法取30只日本大耳白幼兔随机均分为三组,缺血-再灌注组(IR组):结扎30min,再灌注120min;七氟醚预处理组(S组):缺血前吸入2.5%七氟醚30min,洗脱15min后处理同IR组;假手术组(C组):只穿线不结扎。观察三组兔心肌细胞凋亡和Fas、FasL蛋白表达情况,电镜观察细胞超微结构。结果心肌细胞凋亡率S组(13.71±6.01)%明显低于IR组(31.33±7.04)%(P<0.05),而C组(3.3±0.5)%明显低于IR组和S组(P<0.05)。S、C组Fas、FasL蛋白表达的平均灰度高于IR组(P<0.05)。电镜显示S组细胞损伤程度小于IR组。结论七氟醚能明显降低幼兔缺血-再灌注心肌细胞的凋亡。     

七氟醚预处理联合后处理对大鼠心肌缺血-再灌注损伤的影响

目的 探讨七氟醚预处理联合后处理对大鼠缺血-再灌注损伤心肌的保护作用及其相关机制.方法 清洁级成年雄性SD大鼠40只,体重230～270 g,采用随机数字表法,将其均分为五组:假手术组(S组)、心肌缺血-再灌注组(IR组)、七氟醚预处理组(SP1组)、七氟醚后处理组(SP2组)、七氟醚预处理联合后处理组(SS组).除S组外均采用结扎左冠状动脉前降支30 min,再灌注120 min的方法制备大鼠心肌缺血-再灌注模型,S组只穿线,不结扎;SP1和SP2组分别于缺血前30min、再灌注前10 min吸入2.5％七氟醚15 min,洗脱15 min;SS组于缺血前30 min和再灌注前10min均吸入2.5％七氟醚15 min,洗脱15 min.于缺血前30 min、缺血30 min、再灌注120 min时记录HR和MAP,计算RPP(SBP×HR).于再灌注120 min时取心脏制病理切片,光镜下观察各组心肌病理学变化,测定凋亡指数(AI),检测心肌组织SOD和MDA含量,免疫组化法检测心肌组织TNF-α和caspase-3的表达.结果 与S组比较,其余四组再灌注120 min时MAP和RPP明显降低,AI明显升高,心肌组织SOD含量明显降低,MDA含量明显升高,TNF-α和caspase-3表达明显增高(P＜0.05);与IR组比较,SP1组、SP2组和SS组AI明显降低,心肌组织SOD含量明显升高,MDA含量明显降低,TNF-α和caspase-3表达明显降低(P＜0.05);与SP1组和SP2组比较,SS组AI明显降低,心肌组织SOD含量明显升高,MDA含量明显降低,TNF-α和caspase-3表达明显降低(P＜0.05).结论 与单纯七氟醚预处理或后处理比较,两种方法联合应用可使心肌组织AI降低,SOD含量升高,MDA含量降低,TNF-α和caspase-3的表达降低,从而进一步减轻了大鼠心肌缺血-再灌注损伤.     

七氟醚预处理对局灶性脑缺血再灌注损伤大鼠皮质C/EBP同源蛋白表达的影响

目的 探讨七氟醚预处理对局灶性脑缺血再灌注损伤大鼠皮质C/EBP同源蛋白(CHOP)表达的影响.方法 健康雄性SD大鼠36只,体重250～280 g,采用随机数字表法,将大鼠随机分为3组(n=12):假手术组(S组)、局灶性脑缺血再灌注组(I/R组)和七氟醚预处理组(Sevo-pc 组).采用线栓法阻断右侧大脑中动脉1 h,再灌注24 h,制备局灶性脑缺血再灌注损伤模型.Sevo-pc 组于缺血前1 h吸入2.7%七氟醚.各组于再灌注24 h时行神经功能缺陷评分后断头取脑,TIC染色法测定脑梗死体积,免疫组化法测定缺血侧皮质CHOP表达,TUNEL法计数凋亡神经细胞.结果 与S组比较,I/R组和Sevo-pc组神经功能缺陷评分升高,脑梗死体积比升高,缺血侧皮质CHOP表达上调,凋亡细胞数增加(P＜0.01);与I/R组比较,Sevo-pc组神经功能缺陷评分降低,脑梗死体积比降低,缺血侧皮质CHOP表达下调,凋亡细胞数减少(P＜0.05或0.01).结论 七氟醚预处理可能通过下调皮质CHOP表达减轻大鼠局灶性脑缺血再灌注损伤.

Abstract：

Objective To investigate the effect of sevoflurane preconditioning on CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) expression in the cerebral cortex after focal cerebral ischemiareperfusion (I/R) injury in rats and the mechanism. Methods Thirty-six male SD rats weighing 250-280 g were randomly divided into 3 groups ( n = 12 each) : sham operation group (group S) , focal cerebral I/R group (group I/R) and sevoflurane preconditioning group (group Sevo-pc). The animals were anesthetized with intraperitoneal chloral hydrate 300 mg/kg. In groups I/R and Sevo-pc, focal cerebral ischemia was induced by middle cerebral artery occlusion using a nylon thread with rounded tip inserted into the right internal carotid artery and advanced cranially until resistance was met. The occlusion was maintained for 1 h followed by 24 h reperfusion. Group Sevo-pc inhaled 2.7% sevoflurane for 1 h before ischemia. Neurological deficits were assessed and scored at the end of 24 h reperfusion and then the rats were decapitated. Their brains were immediately removed. The cerebral infarct size was determined by TTC staining. The CHOP expression in the ischemic cerebral cortex was determined by immunohistochemistry. The number of apoptotic neurons was counted using TUNEL. Results The neurological deficit scores were significantly higher, the cerebral infarct size was significantly larger, and the CHOP expression and the number of apoptotic neurons were significantly higher in groups I/R and Sevo-pc than in group S ( P ＜ 0.01) . The neurological deficit scores were significantly lower, the cerebral infarct size was significantly smaller, and the CHOP expression and the number of apoptosis neurons were significantly lower in group Sevo-pc than in group I/R ( P ＜ 0.05 or 0.01) . Conclusion Sevoflurane preconditioning may protect the brain against focal cerebral I/R injury by down-regulating CHOP expression in the cerebral cortex in rats.     

七氟醚预处理对局灶性脑缺血再灌注损伤大鼠海马TREK-1表达的影响

目的 探讨七氟醚预处理对局灶性脑缺血再灌注损伤大鼠海马机械敏感性钾通道TREK-1表达的影响.方法 健康雄性SD大鼠36只,体重240～280 g,随机分为3组(n=12):假手术组(S组)、局灶性脑缺血再灌注组(l/R组)和七氟醚预处理组(Sevo组).结扎右侧颈总动脉、颈外动脉,采用线栓法阻断颈内动脉2 h,再灌注24 h制备大鼠局灶性脑缺血再灌注损伤模型;Sevo组于缺血前1 h经半密闭的吸入箱持续吸入含2.5%七氟醚的02;S组仅分离并结扎右侧颈总动脉、颈外动脉,不置入线栓.各组于再灌注24 h时行神经功能缺陷评分后断头取脑,TIC染色后测定脑梗死体积,采用RT-PCR法测定海马TREK-1 mRNA的表达.结果 与S组相比,I/R组和Sevo组神经功能缺陷评分和脑梗死体积比升高(P<0.01);与I/R组相比,Sevo组神经功能缺陷评分和脑梗死体积比降低,海马TREK-1 mRNA表达上调(P<0.05).结论 七氟醚预处理可通过激活海马TREK-1减轻大鼠局灶性脑缺血再灌注损伤.     

低温人工脑脊液灌流对兔脊髓缺血再灌注时水通道蛋白-4表达的影响

目的 探讨低温人工脑脊液灌流对兔脊髓缺血再灌注时水通道蛋白-4(AQP-4)表达的影响.方法 成年雄性新西兰大白兔54只,采用随机数字表法,将其随机分为3组(n=18):假手术组(S组)、脊髓缺血再灌注组(I/R组)和低温人工脑脊液灌流组(FI 组).I/R组和FI组采用阻断肾下腹主动脉60 min后开放的方法 制备脊髓缺血再灌注模型.FI组阻断腹主动脉时以30 ml/h的速率经L4,5间隙蛛网膜下腔输注25℃人工脑脊液,同时开放L7,8间隙蛛网膜下腔引流脑脊液.腹主动脉开放的同时停止人工脑脊液灌流.每组取6只动物,分别在再灌注4、24、48、72 h时进行神经功能评分;每组分别于再灌注4、24、72 h时取6只动物,取L5～8脊髓节段,计算脊髓组织含水量,并测定AQP-4表达水平.结果 与S组比较,I/R组神经功能评分降低,脊髓组织含水量增加,AQP-4表达下调(P＜0.05).与I/R组比较,FI组神经功能评分升高,脊髓组织含水量降低,AQP-4表达上调(P＜0.05).结论 低温人工脑脊液灌流可上调AQP-4表达,从而减轻兔脊髓缺血再灌注损伤.

Abstract：

Objective To investigate the effect of irrigation with hypothermic artificial cerebral-spinal fluid (aCSF)on expression of aquaporin-4(AQP-4) in the spinal cord following spinal ischemia-reperfusion (I/R) in rabbits.Methods Fifty-four adult male New Zealand white rabbits weighing 2.0-2.5 kg were randomly divided into 3 groups (n=18 each):group sham operation(S group); group I/R and group irrigation with hypothermic aCSF (FI group). Spinal I/R was induced by clamping the abdominal aorta below renal artery for 60 min. Hypothermic aCSF(25 X.)was infused at L4,5 interspace at a rate of 30 ml/h and drained from L7,8 interspace during spinal ischemia.Neurological function was evaluated at 4, 24, 48 and 72 h of reperfusion and scored (0=no hind limb activity, 4=hind limb function completely recovered) in 6 animals in each group. Six animals were sacrificed at 4, 24 and 72 h respectively in each group.The lumbar segment (L5-8) was removed for measurement of water content and AQP-4 protein expression (by immuno-histochemistry).Results Neurological function scores were significantly lower,water content was higher and AQP-4 expression smaller in group I/R than in group S. I/R-induced effects were significantly attenuated by irrigation of hypothermic aCSF. Conclusion Irrigation with hypothermic aCSF can ameliorate the spinal cord I/R injuries by up-regulation of AQP-4 expression.     

右美托咪定复合七氟醚后处理对糖尿病患者心肌缺血-再灌注损伤的影响

目的探讨右美托咪定联合七氟醚后处理对糖尿病患者心肌缺血-再灌注损伤的影响。方法选择2019年6月至2020年12月拟在全麻下行心脏瓣膜置换术的2型糖尿病患者80例,男42例,女38例,年龄41～65岁,BMI 18～25 kg/m~2,ASAⅡ或Ⅲ级,心功能NYHAⅡ或Ⅲ级,肝、肾功能正常。采用随机数字表法分为四组:七氟醚后处理组(S组)、右美托咪定组(D组)、右美托咪定复合七氟醚后处理组(SD组)和对照组(C组),每组20例。S组于主动脉开放时经体外循环机给予2%七氟醚15 min; D组于手术开始时予右美托咪定0.5μg·kg~(-1)·h~(-1)持续泵注直至手术结束;SD组于手术开始时予右美托咪定0.5μg·kg~(-1)·h~(-1)持续泵注直至手术结束,于主动脉开放时经体外循环机给予2%七氟醚15 min; C组泵注等体积生理盐水且不使用任何吸入性麻醉药。分别于主动脉阻断前(T_0)和主动脉开放后6 h(T_1)、24 h(T_2)、48 h(T_3)采集中心静脉血样,检测血浆肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的活性和肌钙蛋白I(TnI)、TNF-α、IL-6、NF-κB、血红素氧合酶-1(HO-1)的浓度,记录术中胰岛素使用、心脏起搏器置入、心脏自动复跳情况。结果与T_0时比较,T_1—T_3时四组血浆CK、CK-MB、LDH活性及cTnI、TNF-α、IL-6、NF-κB、HO-1浓度明显升高(P0.05),SOD活性明显降低(P0.05)。与C组比较,D组和SD组T_1—T_3时血浆CK、CK-MB、LDH活性及cTnI、TNF-α、IL-6、NF-κB浓度明显降低(P0.05),SOD活性、HO-1浓度明升高(P0.05),胰岛素使用率明显降低(P0.05),心脏自动复跳率明显升高(P0.05)。与D组比较,SD组T_1—T_3时血浆CK、CK-MB、LDH活性及cTnI、TNF-α、IL-6、NF-κB浓度明显降低(P0.05),SOD活性、HO-1浓度明升高(P0.05),心脏起搏器置入率明显降低(P0.05),心脏自动复跳率明显升高(P0.05)。C组和S组T_1—T_3时血浆CK、CK-MB、LDH、SOD活性及cTnI、TNF-α、IL-6、NF-κB、HO-1浓度以及胰岛素使用率、心脏起搏器置入率、心脏自动复跳率差异无统计学意义。结论右美托咪定可以减轻糖尿病患者心肌缺血-再灌注损伤,并恢复糖尿病患者的抗炎、抗氧化能力,复合七氧醚后处理可以进一步减轻糖尿病患者心肌缺血-再灌注损伤。