灯盏花素对大鼠心肌缺血再灌注损伤心肌细胞凋亡及NF-kB通路信号分子α7nAChR、p65、IkB-α的影响

目的观察灯盏花素对大鼠心肌缺血再灌注损伤心肌细胞凋亡及NF-kB通路信号分子α7nAChR、p65、IkB-α的影响。方法 40只SD大鼠随机均分为假手术组、缺血再灌注组、灯盏花素低剂量组(25 mg/kg·d)和灯盏花素高剂量组(50 mg/kg·d),每组各10只。4组均制备缺血再灌注模型,其中灯盏花素治疗组术前连续1周腹腔注射灯盏花素;假手术组以及缺血再灌注组分别注射等量的生理盐水。随后处死,取出心脏检测心肌组织梗死面积;TUNEL法检测心肌细胞的凋亡指数;蛋白印记法检测α7nAChR、p65、IkB-α蛋白的表达。结果缺血再灌注组较假手术组心肌梗死面积、心肌细胞凋亡指数以及IkB-α蛋白显著增加(P0.01),p65和α7nAChR蛋白显著减少(P0.05);灯盏花素高低剂量组较缺血再灌注组心肌梗死面积、心肌细胞凋亡指数以及IkB-α蛋白显著降低(P0.01),p65和α7nAChR蛋白显著增加(P0.05),并呈现剂量依赖性。结论灯盏花素预处理能有效减少大鼠心肌缺血再灌注损伤以及心肌细胞凋亡,其机制可能为上调α7nAChR,从而通过NF-kB通路抑制心肌细胞的凋亡,发挥心肌保护作用。     

温阳通脉方预处理对心肌缺血再灌注大鼠MDA及SOD的影响

目的 观察温阳通脉方预处理对大鼠心肌缺血再灌注损伤（IR）模型丙二醛（MDA）、超氧化物歧化酶（SOD）含量的影响，探讨温阳通脉方对大鼠再灌注心肌的保护机制。方法 采用结扎大鼠冠状动脉左前降支，缺血30min，再灌注120min的方法建立心肌缺血再灌注损伤模型；缺血5min，再灌注5min，反复3次后缺血30min，再灌注120min建立心肌缺血预适应（IP）模型。检测大鼠灌胃14d后温阳通脉方组、心肌缺血预适应组（IP组）、再灌注损伤纽（IR组）、假性处理组血清MDA、SOD含量。结果 温阳通脉方组、IP组MDA含量低于IR组，SOD高于IR组，差异有统计学意义（P〈0．05）。结论 温阳通脉方预处理后，能降低大鼠心肌缺血再灌注损伤模型MDA含量，升高SOD含量，减轻大鼠急性心肌缺血所致心肌损伤，其机制可能是通过模拟心肌缺血预适应参与心肌保护作用。     

灯盏花素对大鼠缺血再灌注心肌细胞凋亡及STAT表达的影响

目的 观察灯盏花素对大鼠心肌缺血再灌注细胞凋亡和信号转导及转录激活因子(STAT)表达的影响,初步探讨其可能的作用机制.方法 采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注模型.将40只SD大鼠随机分为假手术组、缺血再灌注组,灯盏花素1组[25 mg/(kg,d)],灯盏花素2组[50 mg/(kg·d)].缺血30min、再灌注2h后,原位末端标记法测定组织中心肌细胞凋亡率,免疫组化SP法检测心肌组织中STAT蛋白的表达.结果 与假手术组相比,缺血再灌注组细胞凋亡率明显升高(P＜0.01),SP染色见STAT1蛋白表达显著增强(P＜0.05或＜0.01),但STAT3蛋白表达显著减少(P＜0.05或＜0.01);与缺血再灌注组相比,灯盏花素1、2组细胞凋亡率明显下降(P＜0.01),STAT1蛋白表达显著减少(P＜0.05或＜0.01),但STAT3蛋白表达显著增强(P＜0.05或＜0.01).结论 灯盏花素能够减轻缺血再灌注造成的心肌损伤,其机制可能与灯盏花素干预STAT蛋白表达,从而减少心肌细胞凋亡有关;STAT途径可能是灯盏花素抑制细胞凋亡的途径之一.     

舒芬太尼后处理对大鼠心肌缺血再灌注损伤保护作用的实验研究

目的 观察不同剂量舒芬太尼(SFT)后处理的心肌保护作用.方法 健康SD雄性大鼠24只,体重250 g～300 g,随机分为假手术组、缺血再灌注组、舒芬太尼后处理低剂量组、舒芬太尼后处理高剂量组.采用结扎左冠状动脉前降支30 min再灌注120 min的方法制备心肌缺血再灌注模型.假手术组完成模型仅穿线,不结扎;假手术组穿线后腹腔注射生理盐水1 mL,缺血再灌注组缺血再灌注前2 min腹腔注射生理盐水1 mL,舒芬太尼后处理低、高剂量组分别腹腔注射舒芬太尼稀释液1 mL,2 μg/kg、10μg/kg.于实验结束时制作心肌组织匀浆,检测心肌组织中的超氧化物歧化酶(SOD)、丙二醛(MDA)含量;右心室采血常温离心分离检测血清心肌酶(CK)、血清乳酸脱氢酶(LDH)、血清一氧化氮(NO)含量,取左心室切5块,来用氯化硝基四氮唑蓝(N-BT)染色法区分正常和梗死区,用梗死区重量占左心室重量百分比观测梗死程度.结果 与假手术组比较,缺血再灌注组心肌组织SOD活性下降,MDA增高,血清CK及LDH水平增高,血清NO含量减少;与缺血再灌注模型组比较,舒芬太尼后处理组,心肌组织SOD活性升高,MDA降低,血清CK及LDH释放减少;血清NO含量增加;再灌注心律失常明显减少;心肌梗死程度降低;以舒芬太尼后处理高剂量组更为明显.结论 舒芬太尼后处理能够减轻大鼠心肌缺血再灌注损伤的程度,并且呈剂量依赖性.     

灯盏花素联合预适应对兔缺血再灌注心肌肿瘤坏死因子α、核因子-κB的影响

目的:探讨灯盏花联合预适应对兔缺血再灌注心肌肿瘤坏死因子α(TNF-α)、核因子-κB(NF-κB)的影响.方法:采用新西兰大白兔体内心肌缺血再灌注模型,36只动物随机分为假手术组(Sham组)、缺血再灌注组(IR组)、缺血预适应组(IP组)、灯盏花素联合缺血预适应组(BI组).各组分别进行心肌酶学[肌酸激酶(CK)及乳酸脱氢酶(LDH)]检查,并采用伊文思蓝(EB)/氯化三苯基四氮唑(TTC)测定梗死面积,用免疫组化法检测TNF-α及NF-κB蛋白表达水平.结果:IR、IP及BI组较Sham组均有明显的心肌梗死(P<0.01),IP、BI组较IR组能够明显缩小心肌梗死面积(P<0.01),BI组较IP组疗效显著(P<0.05);IR、IP及BI组心肌酶较Sham组均明显升高(P<0.01),IP、BI组各时间点CK和LDH均较IR组明显降低(P<0.01),且BI组较IP组降低更明显(P<0.05);IR、IP及BI组较Sham组TNF-α及NF-κB蛋白表达均明显增加(P<0.01);IP组、BI组TNF-α及NF-κB蛋白表达均较IR组显著较少(P<0.01),且BI组较IP组更明显(P<0.05).结论:缺血预适应及灯盏花素联合预适应均显著缩小心肌梗死面积,降低心肌酶,减少心肌细胞内TNF-α、NF-κB蛋白的表达.     

鬼针草总黄酮对心肌缺血再灌注大鼠的保护作用

目的研究鬼针草总黄酮(TFB)对缺血再灌注大鼠心肌的保护作用,并探讨其作用机制。方法将雄性Wistar大鼠50只随机分为5组:假手术组(SH组)、心肌缺血再灌注模型组(I/R组)、TFB低、中、高剂量组(TFBL组、TFBM组、TFBH组),每组10只。TFB各组分别给予鬼针草总黄酮灌胃,剂量分别为40、80、160 mg/kg,1次/d,连续给药14 d;除SH组外,其他各组结扎冠状动脉左前降支,使心肌缺血30 min,再灌注120 min。ELISA法测定血清乳酸脱氢酶(LDH)、肌酸激酶(CK)、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-8含量,测定心肌组织丙二醛(MDA)含量和过氧化物酶(SOD)活力,氯化三苯基四氮唑红(TTC)染色法测定心肌梗死面积,透射电镜观察心肌超微结构。结果与I/R组相比,TFB各组均能降低心肌组织MDA含量并提高SOD活力,减小心肌梗死面积,改善心肌超微结构;TFBM、TFBH组能有效降低血清中LDH、CK、TNF-α和IL-8的释放量。结论 TFB预处理可减轻缺血再灌注心肌损伤,可能与其抗炎和抗自由基作用有关。     

葛根素对大鼠心肌缺血再灌注损伤的干预作用

目的 观察葛根素对大鼠心肌缺血再灌注损伤后炎症反应的抑制作用并探讨其作用机制.方法 36只SD大鼠随机分成假手术组、模型组和葛根素处理组;采用左冠状动脉结扎法复制大鼠心肌缺血再灌注损伤模型,于缺血开始及再灌注即刻由尾静脉注射葛根素20 mg/kg,缺血1 h,再灌注6 h后取血检测缺血再灌注后心肌髓过氧化物酶(MPO)、丙二醛(MDA)和血清磷酸肌酸激酶(CK)含量,RT-PCR测定缺血再灌注后心肌胞间黏附分子-1(ICAM-1) mRNA含量.结果 葛根素组血清CK明显低于模型组(P<0.01),MPO和MDA的活性明显低于模型组(P<0.01),ICAM-1 mRNA含量较模型组低(P<0.01).结论 葛根素可减轻大鼠心肌缺血再灌注损伤后炎症反应,这可能是其发挥心肌保护机制之一.     

rh-BNP对缺血再灌注心肌细胞氧化应激的影响

目的探讨新活素对缺血心肌再灌注细胞氧化应激的作用。方法将24只缺血心肌再灌注损伤兔,随机分3组:伪手术组8只;缺血再灌注组8只;新活素组8只;测定超氧化酶(SOD)活性、丙二醛(MDA)、髓过氧化物酶(MPO)、心肌酶学指标(CK-MB)含量。结果与伪手术组相比,缺血再灌注组SOD活性下降,MDA和MPO指标上升,CK-MB指标显著提高(P0.05);与缺血再灌注组相比,新活组SOD活性升高,MDA及MPO指标含量下降。心肌酶学CK-MB指标下降(P0.05)。结论新活素静脉滴注后对心肌缺血再灌注组损伤具有明显保护作用,有效减小心肌梗死面积,可作为急性心肌梗死治疗有效药物。     

蛇床子素注射液在犬原位心脏移植中对供心的保护作用

目的探讨蛇床子素注射液在犬原位心脏移植中对供心的保护作用。方法取健康杂种犬24条,随机分为对照组和试验组;建立犬原位心脏移植模型,先于试验开始前1h经供体犬股静脉内滴注蛇床子素注射液(25mg/kg),再用含有蛇床子素注射液(25mg/kg)的4℃改良ST.Thomas液对供体心脏进行灌注和保存,心脏移植成功后5min从右房采集血液标本,检测实验组及对照组血清超氧化物歧化酶(SOD)、丙二醛(MDA)含量及心肌肌钙蛋白(cTnI)、乳酸脱氢酶(LDH)、心肌肌酸激酶(CK)及其同工酶(CK-MB)漏出率;并于移植成功后10min取移植心脏左室心尖部心肌组织用电镜对心肌超微结构进行形态学观察。结果实验组中MDA含量较对照组明显升高,而SOD含量及cTnI、LDH、CK、CK-MB漏出率较对照组明显降低。试验组心肌超微结构损伤程度较对照组轻。结论在心脏移植过程中应用蛇床子素注射液,可减轻移植心脏的缺血/再灌注损伤,对移植心脏功能具有保护作用,能增加心脏移植的成功率。     

PTEN在心肌缺血预适应和后适应中的调控作用

目的探讨人第10号染色体缺失的磷酸酶及张力蛋白同源的基因(PTEN)/Akt信号通路在心肌缺血预适应和后适应中的作用。方法雄性SD大鼠60只,随机分为4组:假手术组(sham组)、缺血再灌注组(IR组)、缺血预适应组(Ipre组)及缺血后适应组(Ipost组)。建立动物模型,实验结束后,计算心肌梗死面积,测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)活性,检测缺血心肌PTEN m RNA和蛋白含量及p-Akt蛋白表达水平。结果与IR组比较,Ipre组和Ipost组的心肌梗死面积明显缩小,CK、LDH的活性降低,PTEN m RNA和蛋白的含量降低,p-Akt蛋白的水平升高(P0.05)。结论 PTEN/Akt信号通路在心肌缺血再灌注损伤中发挥重要作用,心肌缺血预适应和后适应通过调节PTEN/Akt信号通路的表达在缺血再灌注损伤中发挥保护心肌的作用。     

慢性缺氧促心肌耐受急性缺血再灌注损伤的研究

目的:探讨慢性缺氧对心肌耐受急性缺血再灌注损伤的影响。方法:将SD大鼠随机分为在体实验组、在体对照组、离体实验组、离体对照组。在体及离体实验组大鼠在模拟海拔5000 m的动物低压低氧舱中生活,舱内条件:大气压54 kPa、氧分压11.33 kPa、温度25℃;在体及离体对照组大鼠在正常氧环境中喂养。分别通过结扎左冠状动脉前降支或Langendorff离体心脏灌流系统建立在体及离体心肌缺血再灌注模型,检测4组大鼠再灌注损伤前后心功能指标、心肌梗死面积和心肌酶变化。结果:在体实验可见,在体实验组缺血再灌注前心率(HR)、左室收缩末期容积(LVESV)均明显大于在体对照组,舒张期室间隔厚度(IVSd)、收缩期室间隔厚度(IVSs)、舒张期左室后壁厚度(LVPWd)、收缩期左室后壁厚度(LVPWs)、左室射血分数(LVEF)、左室缩短分数(LVFS)、左室舒张末期容积(LVEDV)、每搏输出量(SV)均明显小于在体对照组(P均<0.05);缺血再灌注后,在体实验组HR、IVSs、LVPWd、LVPWs、LVEF、LVFS均明显大于在体对照组,IVSd、LVEDV、LVESV、SV均明显小于在体对照组(P均<0.05);缺血再灌注可使在体实验组、在体对照组的心功能出现不同程度的损伤,而对在体对照组的损伤更明显;再灌注损伤后,在体实验组心肌梗死面积明显小于在体对照组,肌酸激酶同工酶(CK-MB)活性明显低于在体对照组(P均<0.05),两组乳酸脱氢酶(LDH)活性的差异无统计学意义。离体实验可见,缺血再灌注损伤前离体实验组左室发展压(LVDP)、max(dp/dt)、min(dp/dt)均明显低于离体对照组(P均<0.05),两组左室舒张末期压力(LVEDP)的差异无统计学意义;缺血再灌注损伤后离体实验组LVDP、max(dp/dt)、min(dp/dt)均明显高于离体对照组,LVEDP明显低于离体对照组(P均<0.05);再灌注损伤后离体实验组心肌梗死面积明显小于离体对照组,LDH活性明显高于离体实验组(P均<0.05)。结论:慢性缺氧可提升心肌耐受急性缺血再灌注损伤的能力。     

Effect of remote ischemic preconditioning on hepatic microcirculation and function in a rat model of hepatic ischemia reperfusion injury

Background:

Liver transplantation involves a period of ischemia and reperfusion to the graft which leads to primary non-function and dysfunction of the liver in 5–10% of cases. Remote ischemic preconditioning (RIPC) has been shown to reduce ischemia reperfusion injury (IRI) injury to the liver and increase hepatic blood flow. We hypothesized that RIPC may directly modulate hepatic microcirculation and have investigated this using intravital microscopy.

Methods:

A rat model of liver IRI was used with 45 min of partial hepatic ischemia (70%) followed by 3 h of reperfusion. Four groups of animals (Sham, IRI, RIPC+IRI, RIPC+Sham) were studied (n= 6, each group). Intravital microscopy was used to measure red blood cell (RBC) velocity, sinusoidal perfusion, sinusoidal flow and sinusoidal diameter. Neutrophil adhesion was assessed by rhodamine labeling of neutrophils and cell death using propidium iodide.

Results:

RIPC reduced the effects of IRI by significantly increasing red blood cell velocity, sinusoidal flow and sinusoidal perfusion along with decreased neutrophil adhesion and cell death.

Conclusions:

Using intravital microscopy, this study demonstrates that RIPC modulates hepatic microcirculation to reduce the effects of IRI. HO-1 may have a key role in the modulation of hepatic microcirculation and endothelial function.     

大鼠脑缺血／再灌注损伤热休克蛋白70表达及川芎嗪干预

目的研究大鼠脑缺血／再灌注时热休克蛋白（ＨＳＰ）７０表达及川芎嗪对ＨＳＰ７０表达的影响。方法采用ＳＤ大鼠左侧颈总动脉结扎并滴注生理盐水脑缺血／再灌注模型，以免疫细胞化学法检测２４只缺血／再灌注及川芎嗪干预大鼠脑缺血／再灌注３０ｍｉｎ时脑组织ＨＳＰ７０表达并与病理组织学改变进行对照研究。结果（１）非缺血侧脑组织无ＨＳＰ７０表达，缺血３０ｍｉｎ缺血侧大脑皮层可见ＨＳＰ７０表达；再灌注３０ｍｉｎ组仅１只大鼠（１／６）缺血侧大脑皮层有ＨＳＰ７０表达。（２）与单纯缺血大鼠相比，川芎嗪干预组缺血侧大脑皮层ＨＳＰ７０表达明显增强，计算机辅助图像半定量分析ＨＳＰ７０免疫阳性细胞数，分别为平均４３．５５±１２．５１个／片和８４．９５±１６．７个／片（Ｐ＜０．０１）。（３）缺血侧皮层神经细胞呈现轻度缺血改变，川芎嗪干预大鼠缺血损伤程度似有减轻。结论脑缺血时可诱导缺血脑细胞部分ＨＳＰ７０表达，川芎嗪干预可促使缺血大脑皮层ＨＳＰ７０表达明显增强，皮层神经细胞的缺血损伤有所减轻。     

川芎嗪对再灌注大鼠心肌细胞c-fos基因表达及凋亡的影响

目的 :观察川芎嗪 （TMP）对心肌缺血再灌注 （MIR）大鼠心肌 c- fos基因表达及凋亡细胞的作用。方法 :应用免疫组化法检测 MIR不同时期心肌 FOS蛋白的表达 ,并采用末端标记技术对心肌细胞凋亡数进行检测。结果 :1对照组心肌无 FOS蛋白表达 ,亦未见凋亡细胞出现。 2与 MIR组相比 ,TMP干预组心肌 FOS蛋白的表达明显减弱 （6 0 min分别为 5 7± 44个 /片和 6 .4± 3.2个 /片 ,90 m in分别为 46 7± 45 0个 /片和 171± 16 0个 /片 ,12 0 min分别为 2 46± 16 0个 /片和 130± 12 1个 /片 ,均 P<0 .0 5 ） ,TUNEL阳性细胞数均明显减少 （6 0 m in分别为 36 .3± 8.7个 /片和 2 4.7± 7.2个 /片 ,P<0 .0 5 ;12 0 m in分别为 48.0± 2 3.8个 /片和 10 .0± 8.1个 /片 ,P<0 .0 1）。结论 :MIR可诱导终末分化的心肌细胞高表达 FOS蛋白及发生细胞凋亡 ;应用 TMP可使缺血心肌细胞 c- fos基因表达减弱及凋亡减轻     

Redox signaling triggers protection during the reperfusion rather than the ischemic phase of preconditioning

In ischemic preconditioning (IPC) brief ischemia/reperfusion renders the heart resistant to infarction from any subsequent ischemic insult. Protection results from binding of surface receptors by ligands released during the preconditioning ischemia. The downstream pathway involves redox signaling as IPC will not protect in the presence of a free radical scavenger. To determine when in the IPC protocol the redox signaling occurs, seven groups of isolated rabbit hearts were studied. All hearts underwent 30 min of coronary branch occlusion and 2 h of reperfusion. IPC groups were subjected to 5 min of regional ischemia followed by 10 min of reperfusion prior to the 30-min coronary occlusion. The Control group had only the 30-min occlusion and 2-h reperfusion. In the second group IPC preceded the index coronary occlusion. The third group was also preconditioned, but the free radical scavenger N-2-mercaptopropionyl glycine (MPG 300 microM) was infused during the 10-min reperfusion and therefore was present in the myocardium in the distribution of the snared coronary artery during the entire reperfusion phase and also during the subsequent 30-min ischemia. In another preconditioned group MPG was added to the perfusate before the preconditioning ischemia and therefore was present in the tissue only during the preconditioning ischemia and then was washed out during reperfusion. In the fifth group MPG was added to the perfusate for only the last 5 min of the preconditioning reperfusion and therefore was present in the tissue during the last minutes of the reperfusion phase and the 30 min of ischemia. In an additional group of IPC hearts MPG was infused for only the initial 5 min of the preconditioning reperfusion and then allowed to wash out so that the scavenger was present for only the first half of the reperfusion phase. Infarct and risk zone sizes were measured by triphenyltetrazolium staining and fluorescent microspheres, resp. IPC reduced infarct size from 31.3 +/- 2.7% of the ischemic zone in control hearts to only 8.4 +/- 1.9%. MPG completely blocked IPC's protection in the third (39.4 +/- 2.8%) and sixth (36.1 +/- 7.7%) groups but did not affect its protection in groups 4 (8.1 +/- 1.5%) or 5 (7.8 +/- 1.1%). When deoxygenated buffer was used during IPC's reperfusion phase in the seventh group of hearts, protection was lost and infarct size was increased over that seen in control hearts (74.5 +/- 9.0%). Hence redox signaling occurs during the reperfusion phase of IPC, and the critical component in that reperfusion phase appears to be molecular oxygen.     

缺血预处理对肠缺血再灌注损伤的保护作用

目的观察肠缺血预处理（IPC）对缺血再灌注（I／R）损伤的保护作用．探讨IPC在肠I／R损伤中的作用机制。方法对大鼠肠系膜上动脉进行4次循环的5min夹闭／Smin开放（即IPC），24h后实施缺血30min再灌注24h，制作I／R损伤模型。检测IPC后肠组织一氧化氮（NO）含量（以NO2^-／NO3^-代表）、超氧化物歧化酶（SOD）、丙二醛（MDA）的含量及观察肠肌间神经丛一氧化氮合成酶（NOS）阳性神经元的变化，检测血清NO及血浆二氨氧化酶（DAO）．采用Chiu评分法观察肠组织损伤情况。结果IPC后肠组织NO、SOD含量下降．而MDA含量明显升高，肠肌间丛NOS阳性神经元数明显降低，DAO水平明显降低，肠组织损伤程度明显减轻。结论IPC对I／R损伤有明显保护作用，其机理与灭活了氧自由基，降低NO含量有关。     

贝前列素钠预处理对兔心肌缺血/再灌注损伤的早期拮抗作用

目的:探讨贝前列素钠（beraprost sodium,BPS）预处理对兔心肌缺血/再灌注(I/R)损伤的早期拮抗作用。方法: 将36只日本大耳白兔随机分为3组,即A组（假手术组）、B组（I/R组:缺血40 min后,再灌注90 min）和C组（BPS预处理组:以15 μg/kg,2次/d,［1］连续喂养4周,最后1次喂养后3 h内进行I/R）。以上3组均开胸暴露心脏,A组在左冠状动脉左室支处穿线不结扎,观察130 min结束实验;B组及C组开胸后结扎左冠状动脉左室支40 min,心电图若出现Ⅱ导联ST段升高及结扎周围心肌的颜色变紫或变深显示已形成心肌梗死(MI)模型。然后进行以下检测:①再灌注90 min后,随机选取6只日本大耳白兔,立即取结扎点下损伤的心肌组织,用100 g/L福尔马林固定后,部分进行HE染色在光镜下观察心肌形态学改变;部分用免疫组化染色法检测心肌细胞中Bax、Bcl-2的表达。②再灌注4 h后,取右心房（或股静脉）血应用电化学发光免疫法检测血浆中心肌中肌酸激酶(CK-MB)的变化。结果: ①HE染色显示,A组的心肌结构正常,B组的心肌损伤较严重,C组的心肌损伤较轻。②免疫组化染色法检测显示,A组Bcl-2的表达呈阳性,Bax的表达呈阴性;B组Bax的表达呈强阳性,Bcl-2的表达呈弱阳性;C组Bax的表达呈弱阳性,Bcl-2的表达介于A组与B组之间。③用电化学发光免疫法检测心肌酶学结果,CK-MB升高者3个组依次为B组>C组>A组,B组CK-MB的水平均明显高于C组与A组（P<0.01）。结论: BPS预处理对兔心肌I/R损伤早期具有拮抗作用。     

脑缺血预处理和缺血耐受机制

脑缺血预处理系指机体对短暂缺血的适应性反应,能增强神经元对再次缺血的耐受性,其内源性保护机制涉及多个分子,如腺苷受体、热休克蛋白、阿片受体、低氧诱导因子、N-甲基-D-天冬氨酸受体、环氧合酶和抗氧化酶等.由于这种内源性保护具有临床应用价值,对脑保护机制研究和药物开发具有重要意义,因此受到牛命科学界广泛关注.     

Effects of ischemic postconditioning on reperfusion injury in rat liver grafts after orthotopic liver transplantation

Aim: The effects of ischemic postconditioning (IPostC) on ischemia reperfusion (IR) injury of liver grafts was examined in rats after orthotopic liver transplantation (OLT). Methods: Male Wistar rats were used as donors and recipients to establish a liver transplantation model. The animals were randomly divided into four groups: sham‐operated (SO, n = 6), IR (n = 6), IPostC1 (n = 6) and IPostC2 (n = 6). IPostC was achieved by several intermittent interruptions of blood flow in the early phase of reperfusion. Several parameters of hepatic damage, oxidative stress, neutrophil infiltration and the expression of TNF‐α and MIP‐2 were detected as well as microscopic examination. Nitric oxide release and liver NO synthases (endothelial NO synthase and inducible NO synthase) expression were also measured. Results: We observed that a significant reduction in alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase values in two IPostC groups when compared with IR group. The increases in hepatic malondialdehyde, and decreases in superoxide dismutase and reduced glutathione levels after orthotopic liver transplantation were significantly inhibited by IPostC. IR induced increase in hepatic myeloperoxidase content, TNF‐α and MIP‐2 expression were also lowered by IPostC. The increases in NO content and NOS protein expression were much more prominent in IPostC treated groups. Animals treated with IPostC presented minimal hemorrhage and reduced signs of liver injury. There was no significant difference between two IPostC treated groups. Conclusions: IPostC provided significant protection against IR injury to liver grafts. The protective effect of IPostC is closely related to the NO production following the increase in endothelial and inducible NO synthases expression and the suppression of tumor necrosis factor‐α and macrophage inflammatory protein‐2 overproduction.