缺血预处理,心肌

摘要： 目的 研究瘦素预处理对心肌缺血再灌注损伤(myocardial ischemia reperfusion injury,MIRI)模型SD大鼠心肌细胞自噬的影响.方法 将18只成年雄性SD大鼠随机分为假手术组、模型组和预处理组,每组6只.假手术组仅开胸不结扎血管;模型组和预处理组大鼠用绳栓法建立MIRI模型;预处理组建模前行瘦素预处理;用TTC染色检测心肌梗死面积,苏木精-伊红染色检测心肌损伤程度,采用Western blot法检测大鼠心肌P62和自噬微管相关蛋白轻链3 (LC3B)蛋白表达.结果 与假手术组比较,模型组和预处理组大鼠心肌梗死面积增大,心肌损伤评分升高(P＜0.05),模型组大鼠P62蛋白表达显著升高,LC3B蛋白表达显著降低;预处理组大鼠心肌组织P62蛋白和LC3B蛋白表达均升高.与模型组比较,预处理组大鼠心肌梗死面积缩小[(17.83±1.86)％ vs (32.33±2.29)％],心肌损伤评分程度明显减轻[(0.67±0.41)％vs (1.67±0.75)％],P62蛋白表达显著降低(0.21±0.02 vs 0.34±0.04)、LC3B蛋白表达显著升高(0.34±0.04 vs 0.24±0.04,P＜0.05).结论 瘦素预处理可促进LC3B蛋白生成,降低P62蛋白表达,通过诱导心肌细胞自噬减轻MIRI.

摘要： 目的 观察右美托咪定预处理联合后处理对心肌缺血再灌注损伤的保护作用.方法 选取天津医科大学总医院120例心脏瓣膜置换术患者.随机分为3组,右美托咪定预处理组(preD组)、右美托咪定后处理组(posD组)及右美托咪定预处理联合后处理组(pre-posD组),每组40例.preD组和pre-posD组于阻断主动脉前30 min静脉输注右美托咪定1μg/kg,posD组输注等容量生理盐水;posD组和pre-posD组于开放主动脉前30 min灌注液中加入右美托咪定0.2～1.0μg/kg进行心脏灌注,preD组灌注液中加入等容量生理盐水.观察麻醉诱导前5 min(T0)、开放主动脉后15 min(T1)、体外心肺转流(CPB)结束时(T2)、术后4 h(T3)、术后16 h(T4)、术后36 h(T5)、术后72 h(T6)的心率(HR)、平均动脉压(MAP)及术中脑电双频指数(BIS)的变化,记录心脏复跳时间和心脏复跳情况,记录3组前并行循环时间(Tpre)、主动脉阻断时间(Tab)及后并行循环时间(Tpos).检测各时间点血浆肿瘤坏死因子 α(TNF-α)、白细胞介素-6(IL-6)、血清心肌肌钙蛋白(cTn I)浓度及肌酸激酶同工酶(CK-MB)活性.结果 不同时间点3组HR、MAP值差异无统计学意义(P>0.05).T1～T6时pre-posD组血浆TNF-α 浓度低于preD和posD组(P<0.05).T2～T6时pre-posD组血浆IL-6浓度低于preD组和posD组(P<0.05).T1～T6时pre-posD组血浆CK-MB活性弱于preD组和posD组(P<0.05).结论 右美托咪定预处理联合后处理较单纯的预处理或单纯的后处理能更有效地抑制炎症因子的产生和释放,具有更好的心肌保护功能.

摘要： Methods Primary cardiomyocytes of Sprague-Dawley rats were isolated by trypsin and divided into 5 groups(n=6 each):control group, hypoxia injury group, hypoxia preconditioning group, paclitaxel group,and paclitaxel + hypoxia preconditioning group. The structure of microtubules and the expression of hypoxia-inducible factor-1α(HIF-1α) were analyzed by immunofluorescence staining. The Langendorff isolated heart perfusion model was applied in 4 groups: hypoxia reperfusion injury group, hypoxia preconditioning group, paclitaxel group, and paclitaxel+hypoxia preconditioning group. Each group was further divided into elderly subgroup and adult subgroup (n=6 each). Left ventricular developed pressure and maximum rate of rise in left ventricular pressure were analyzed. Results (1) Primary cardiomyocyte experiments showed that the myocardial tubular microtubule structure in control group was intact and evenly stained; most of the microtubules in the hypoxia-injured group were absent and the tubular tissue was broken; the hypoxia-induced damage on microtubule structure was smaller in the hypoxic preconditioning group compared with the hypoxic injury group (microtubule staining was not uniform, and the lattice structure was broken, but not that obvious as in the hypoxia group);the tubular structure of the microtubules of the paclitaxel group was basically complete, and the staining was basically uniform.The integrity of tubular structure was maintained to some extent, similar to a normal microtubule structure in paclitaxel+hypoxia preconditioning group. The expression of HIF-1αin the cytoplasm and nucleus was very low in the control group, which was evidenced in both cytoplasm and nucleus in the hypoxic injury group. The expression was further increased in hypoxic preconditioning group, significant nuclear HIF-1 expression was found in the paclitaxel group, the expression was aggregated in the nucleus in the Paclitaxel+ hypoxia preconditioning group. (2)In Langendorff isolated heart perfusion model, left ventricular developed pressure was similar between the elderly subgroup and the adult subgroup at the end of the infusion,after precondition, 5 minutes of reperfusion, 30 minutes of reperfusion, and 60 minutes of reperfusion in the hypoxic injury group (all P>0.05).In the hypoxic injury group, both the elderly subgroup and the adult subgroup had lower left ventricular developed pressure at 30 minutes of reperfusion when compared with the end of the infusion((15.63 ± 4.88) mmHg (1 mmHg=0.133 kPa) vs. (95.63 ± 22.14)mmHg and (17.31 ± 2.75)mmHg vs. (91.00 ± 9.58)mmHg, respectively,all P0.05);在缺氧损伤组中,老年亚组和成年亚组的再灌注30 min左心室发展压均低于平衡灌注末[分别为(15.63±4.88)mmHg(1 mmHg=0.133 kPa)比(95.63±22.14)mmHg和(17.31±2.75)mmHg比(91.00±9.58)mmHg,P均<0.05].在缺氧预处理组中,成年亚组再灌注5和30 min的左心室发展压均高于老年亚组[分别为(7.13±1.02)mmHg比(3.75±1.06)mmHg和(43.94±3.21)mmHg比(16.31±1.54)mmHg,P均<0.01].在紫杉醇组中,成年亚组再灌注30和60 min的左心室发展压均高于老年亚组[分别为(44.31±7.59)mmHg比(5.44±1.21)mmHg和(51.56±6.03)mmHg比(22.19±5.14)mmHg,P均<0.01].在紫杉醇联合缺氧预处理组中,老年亚组和成年亚组再灌注30 min左心室发展压均低于平衡灌注末[分别为(18.63±4.30)mmHg比(99.94±8.23)mmHg,P<0.01;(49.69±5.34)mmHg比(95.31±5.26)mmHg,P<0.05];成年亚组再灌注30 min的左心室发展压高于老年亚组[(49.69±5.34)mmHg比(18.63±4.33)mmHg,P<0.01].缺氧预处理组、紫杉醇组和紫杉醇联合缺氧预处理组的成年亚组再灌注60 min左心室内压最大上升速率变化比率均高于老年亚组[分别为(62.83±3.92)％比(33.33±3.20)％,(44.17±2.32)％比(36.67±2.88)％,(72.50±2.66)％比(53.17±2.56)％,P均<0.01].结论 紫杉醇能够增强老年大鼠心肌组织缺血预处理的心肌保护作用,其机制是通过稳定微管结构而促进HIF-1α核转位.

摘要： 目的 探讨经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)术前抗栓预处理对急性ST段抬高型心肌梗死(ST elevation myocardial infarction,STEMI)自发再灌注及短期预后的影响.方法 回顾分析2014年1月1日—2016年7月31日解放军白求恩国际和平医院心血管内科诊治的急性STEMI并行PCI的206例临床资料.研究方法:①据术前抗血小板预处理情况分为氯吡格雷组105例和替格瑞洛组101例,比较两组自发再灌注情况;②在负荷剂量抗血小板预处理基础上,据术前抗栓预处理情况分为对照组(未处理)84例、肝素组(普通肝素70～100 U/kg)26例、替罗非班组(替罗非班10μg/kg)96例,比较各组自发再灌注情况;③据冠状动脉造影结果,分为自发再灌注组56例,未自发再灌注组150例,分析自发再灌注对预后的影响.结果 ①替格瑞洛组自发再灌注率明显高于氯吡格雷组(P=0.040);②肝素组、替罗非班组自发再灌注率明显高于对照组(P=0.004、P=0.006);③自发再灌注组院内心脏不良事件发生率明显低于未自发再灌注组(P=0.030),出院后3个月自发再灌注组左室射血分数、左室舒张末期内径均优于未自发再灌注组(P=0.000).结论 急性STEMI患者PCI术前选择替格瑞洛抗血小板预处理、确诊后即刻予肝素或术前予替罗非班均有助于自发再灌注的发生,可减少住院期间心脏不良事件发生.%Objective To investigate the effect of antithrombotic pretreatment before percutaneous coronary interven-tion ( PCI) on spontaneous reperfusion and acute short-term prognosis of acute ST-elevation myocardial infarction ( STEMI) . Methods Retrospective analysis of January 1, 2014 to July 31, 2016, clinical data of 206 patients with acute STEMI com-bined with emergency PCI diagnosed by Cardiology of Bethune International Peace Hospital. Respectively:① According to preoperative antiplatelet pretreatment,the cases were divided into 105 cases of clopidogrel group and 101 cases of ticagrelor group,then the spontaneous reperfusion rates in both groups were compared;②On the basis of load antiplatelet pretreatment, all were divided into three groups,control group ( untreated) 84 cases, heparin group ( general heparin 70-100 U/kg) 26 ca-ses, tirofiban group ( tirofiban 10 μg/kg) 96 cases, according to preoperative antithrombotic pretreatment, then compared the spontaneous reperfusion rates of each group;③ According to the results of coronary angiography, 56 cases were divided into spontaneous reperfusion group, 150 cases were not spontaneous reperfusion group, and the effect of spontaneous reperfusion on prognosis was analyzed. Results ①The spontaneous reperfusion rate of ticagrelor group was significantly higher than clopi-dogrel group (P=0. 040);② The spontaneous reperfusion rate of heparin group and tirofiban group spontaneous reperfusion rate were significantly higher than control group (P=0. 004, P=0. 006);③ The incidence of adverse cardiac events in the spontaneous reperfusion group was significantly lower than that in the spontaneous reperfusion group (P=0. 030). The LVEF and LVID were significantly superior to those of the spontaneous reperfusion group after three months of discharge ( P =0. 000). Conclusion In patients with acute STEMI, the selection of ticagrelor antiplatelet pretreatment, once diagnosed im-mediately given heparin or preoperative application of tirofiban, all contribute to spontaneous reperfusion and can reduce the incidence of cardiac adverse events during hospitalization.

摘要： 目的 观察地奥心血康胶囊对大鼠急性缺血心肌连接蛋白43(Cx43)的影响,进一步探讨其抗心律失常的可能机制.方法 采用随机数字表方法将30只大鼠分成假手术组(SM组,n=10)、缺血组(IM组,n=10)、地奥心血康胶囊组(DA组,n=10).术前地奥心血康胶囊组给予胶囊粉(250 mg/kg),假手术组及缺血组均给予等量0.9％氯化钠注射液,连续干预4周.末次灌胃后,利用在体结扎冠状动脉前降支法建立急性心肌梗死模型,假手术组只穿线不结扎.观察2h各组心律失常的发生情况;造模2h后处死动物,应用免疫组化SP法检测Cx43在各组急性缺血心肌中的表达;应用黄嘌呤氧化酶法和硫代巴比妥酸法测各组动物血清中丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活力.结果 与SM组比较,IM组心律失常评分[(3.8±0.7)分比(0.7±0.2)分,t=13.466,P<0.01]和血清MDA含量[(8.3±0.8)nmol/mL比4.2±0.7)nmol/mL,t=12.197,P<0.01]显著增高,SOD活力[(68.2±5.5)U/mL比(144.1±7.9)U/mL,t=24.932,P<0.01]降低,心室肌Cx43含量[(0.39±0.06)比(0.92±0.05),t=21.459,P<0.01]显著降低、分布紊乱;与IM组相比,DA组心律失常评分[(2.6±0.8)分比(3.8±0.7)分,t=3.570,P<0.01]降低,Cx43含量[(0.60±0.08)比(0.39±0.06),t=6.641,P<0.01]增高、分布规律.结论 地奥心血康胶囊能有效抑制大鼠急性心肌缺血心室肌Cx43降解,减少心律失常的发生,其机制可能与抗氧化有关.%Objective To observe the effects of Di ao Xin xue Kang on connexin 43 ( Cx43 ) , in order to make clear the protective mechanism against ischemia -induced arrhythmias .Methods The rats were randomly divided into 3 groups according to the digital table:SM operation group(group SM,n=10),ischemia group(group IM,n=10),Di ao Xin xue Kang group(group DA,n=10).Myocardial infarction was induced by legation the left anterior descending coronary artery for 120 min.The expression of Cx43 of the ischemic myocardium was studied by immunohistochemistry technique .The ventricular arrhythmia was observed , and MDA, SOD levels were measured . Results Compared with the SM group ,the arrhythmia score[(3.8 ±0.7)points vs.(0.7 ±0.2)points,t=13.466, P<0.01]and serum MDA level[(8.3 ±0.8)nmol/mL vs.(4.2 ±0.7)nmol/mL,t=12.197,P<0.01]in the IM group were significantly increased,SOD activity in the IM group[(68.2 ±5.5)U/mL vs.(144.1 ±7.9)U/mL,t=24.932,P<0.01]decreased,and serum Cx43 content[(0.39 ±0.06) vs.(0.92 ±0.05),t=21.459,P<0.01] significantly decreased.Compared with IM group,the arrhythmia score of the DA group [(2.6 ±0.8) vs.(3.8 ± 0.7),t=3.570,P<0.01]decreased,and serum Cx43 content[(0.60 ±0.08) vs.(0.39 ±0.06),t=6.641,P<0.01]increased and distributed regularly.Conclusion Di ao Xin xue Kang can effectively alleviate Cx43 degrading induced by acute myocardial infarction ,the mechanism of this effect is associated with resisting oxidative stress .

摘要： 目的 探讨埋线预处理对ZDF大鼠缺血再灌注损伤后心肌相关凋亡蛋白Bcl-2、Bax及Caspase-3表达的影响.方法 2015年1月-2016年5月,选取SPF级雄性ZDF大鼠24只,随机分为4组,每组6只.空白组常规饲养,不做任何处理.缺血再灌注组饲养7d后缺血30 min,再灌注60 min.缺血预处理组饲养7d后缺血5 min,再灌注5 min,反复3次后,缺血30 min,再灌注60 min.埋线预处理组第1天对内关、膻中、心俞穴进行埋线,7d后缺血30 min,再灌注60 min.酶联免疫吸附法检测血清过氧化氢酶(CAT)、一氧化氮(NO)水平,Westernblotting法检测心肌组织Bcl-2、Bax及Caspase-3表达,电镜观察心肌组织超微结构.结果 缺血再灌注组血清CAT、NO水平低于空白组,缺血预处理组、埋线预处理组血清CAT、NO水平高于空白组、缺血再灌注组(P＜0.05).缺血再灌注组、缺血预处理组、埋线预处理组Bcl-2、Bax及Caspase-3相对表达量均高于空白组,缺血预处理组、埋线预处理组Bc1-2、Caspase-3相对表达量高于缺血再灌注组,Bax相对表达量低于缺血再灌注组(P＜0.05).电镜下,缺血再灌注组心肌组织可见大量线粒体肿胀且密度降低,呈囊泡状;缺血预处理组及埋线预处理组仅见少量线粒体肿胀.结论 埋线预处理可能通过上调心肌组织Bcl-2及Caspase-3表达,下调Bax表达,抑制细胞凋亡和促进自噬,对ZDF大鼠缺血再灌注损伤后心肌发挥保护作用.

摘要： 目的 研究吗啡受体在心肌腺苷预处理心肌保护中的作用.方法 以离体大白鼠工作心脏模型,比较经腺苷预处理和纳洛酮+腺苷预处理,在心肌缺血再灌前后,左室压(LVP)、左室舒张末期压(LVDEP)、左心室内压上升及下降最大速率(±dp/dtmax) 、主动脉压(AP)、冠脉流量(CF)、主动脉流量(AF)和测定冠脉流出液乳酸脱氢酶(LDH),心肌三磷酸腺苷(ATP)含量、超氧化物岐化酶(SOD)活性、脂质过氧化物(LPO)含量及自灌注停搏液至完全停搏的时间(AT).结果 复跳30 min后,除LVDEP 外,Control组和Nal+APT组各项心功能指标均低于ATP组,均差异有统计学意义(P<0.05).复灌工作心30 min后,各组LPO、LDH均有提高,但APT组明显低于于Nal+APT组和Control组;各组ATP、SOD均有所下降.结论 腺苷预处理的心肌保护作用需要阿片样受体介导,腺苷受体的心肌保护作用与阿片样受体可能存在交互作用.%Objective To investigate the role of opioid receptor on myocardial preservation with adenosine pretreatment in isolated rat hearts which suffer from ischemia/reperfusion injury.Method The model of Langendorff perfused isolated rat heart was used to study the effects of APT and Nal+APT on left ventricular pressure(LVP)、left ventricular end-diastolic pressure(LVDEP)、the maximal rate of rise and fall in left ventricular pressure (±dp/dt max)、aortic pressure(AP)、coronary flow(CF)、aortic flow(AF),activities of lactate dehydrogenase (LDH),superoxide dismutase(SOD) a lipid peroxidation(LPO) ,concentrations of ATP level pre-and post-ischemia/reperfusion.Result Nal+APT Compared with ischemia/reperfusion group and APT,Naloxone restrained the the recovery of cardiac hemodynamics and promoted the recovery of contractile function,decreased ATP level and SOD activity ,and increased leakage of intracellular lactic dehydrogenase.Conclusion Adenosine pretreatment cardioprotection requires the activation of opioid receptors and relies on these receptors functionally interacting with adenosine receptors.

摘要： 目的:观察丹参酮ⅡA(T anⅡA)预处理对心肌缺血再灌注损伤后线粒体通透性的影响.方法:使用SD大鼠,在T anⅡA预处理5 d后进行心肌缺血/再灌注损伤造模并检测心肌梗死面积、肌钙蛋白表达,使用酶联免疫吸附法观察线粒体通透性转换孔(M PT P)开放性以及细胞色素C释放情况.结果:TanⅡA预处理能够减轻心肌梗死面积、减少肌钙蛋白表达;抑制MPTP开放以及细胞色素C释放.结论:TanⅡA预处理能够通过抑制MPTP、减少心肌细胞凋亡发挥心肌保护作用.

摘要： 目的 探讨穴位埋线对缺血再灌注损伤高脂血症合并2型糖尿病(ZDF)大鼠心肌保护作用的机制,为临床治疗提供理论依据.方法 2015年1月-2016年5月选取ZDF大鼠24只,随机分为对照组、缺血再灌注组、缺血预处理组和穴位埋线组,每组6只.适应性饲养1周后第7天,对照组直接开胸取材,其余3组均结扎冠状动脉左前降支,建立缺血再灌注损伤模型.缺血再灌注组缺血30 min,再灌注60 min;缺血预处理组缺血5 min、再灌注5 min,重复3次,之后操作同缺血再灌注组;穴位埋线组在适应性饲养1周后第1天,“内关”“膻中”“心俞”穴进行穴位埋线,之后操作同缺血再灌注组.采用透射电镜观察各组ZDF大鼠心肌组织超微结构及自噬水平,Westernblotting法检测心肌内质网应激相关蛋白葡萄糖调节蛋白78 (GRP78)、自噬相关蛋白Beclin-1水平,酶联免疫吸附实验(ELISA)法检测髓过氧化物酶(MPO)、丙二醛(MDA)水平.结果 透射电镜下对照组线粒体和心肌细胞形态结构正常,未见明显自噬体;缺血再灌注组线粒体和心肌细胞肿胀明显,细胞膜破裂、内容物泄漏,仅见空泡或空腔及少量自噬泡;缺血预处理组、穴位埋线组与缺血再灌注组相比,心肌细胞超微结构损伤较轻,且自噬泡数量明显增多;缺血再灌注组心肌细胞超微结构破坏最为严重,且未见明显自噬泡.缺血再灌注组、缺血预处理组、穴位埋线组GRP78、Beclin-1、MPO、MDA水平高于对照组(P＜0.05);缺血预处理组、穴位埋线组GRP78、Beclin-1水平高于缺血再灌注组,但MPO、MDA水平低于缺血再灌注组(P＜0.05).结论 穴位埋线可能通过促进GRP78、Beclin-1水平升高,进而起到对再灌注损伤心肌的保护作用.%Objective To explore the mechanism of catgut implantation at acupoints for the protection of myocardium from ischemia-reperfusion injury in hyperlipidemia zucker diabetic fatty (ZDF) rats,models of type 2 diabetes mellitus,in order to provide a theoretical basis for clinical treatment.Methods This study was conducted during January 2015 to May 2016.Twenty-four ZDF rats were selected and randomly divided into control group,ischemia reperfusion (IR) group,ischemic pretreatment (IP) group and catgut implantation (CI) group,with 6 in each.On the 7th day after one week of adaptive feeding,myocardial tissues of the control group were taken out via thoracotomy,the other three groups were used for establishing IR models after ligation of the left anterior descending coronary artery.IR group first received myocardial ischemia treatment for 30 min,then received reperfusion for 60 min.IP group received 3 rounds of 5-min myocardial ischemia treatment and 5-min reperfusion,then received 30-min myocardial ischemia treatment and 60-min reperfusion.CI group received the same treatment given to IR group except on the first day after one week of adaptive feeding,they received catgut implantation at Neiguan,Danzhong,and Xinshu acupoints.The ultrastructure and level of autophagy of myocardium of ZDF rats were observed by transmission electron microscope.Western blotting was used to detect the levels of myocardial endoplasmic reticulum stress-related protein glucose-regulated protein 78 (GRP78) and autophagy-related protein Beclin-1.The levels of myeloperoxidase (MPO) and malondialdehyde (MDA) were measured by enzyme-linked immunosorbent assay (ELISA).Results Transmission electron microscope observation showed that,the control group demonstrated normal mitochondria and cardiomyocytes without many autophagysomes;IR group presented significantly swollen mitochondria and cardiomyocytes with ruptured cell membrane and leaked contents,leaving vacuoles or cavities and a small amount of autophagic vacuoles.Compared with IR group,the myocardial cell ultrastructural damage in IP and CI groups was lighter and the number of autophagic vacuoles was significantly increased.The myocardial cell ultrastructural damage in IR group was the most serious,even there were no many autophagic vacuoles.The levels of GRP78,Beclin-1,MPO and MDA were significantly lower in the control group than in the other three groups (P ＜0.05).IR group had lower levels of GRP78 and Beclin-1 but higher levels of MPO and MDA compared with IP and CI groups (P ＜ 0.05).Conclusion Catgut implantation at Neiguan,Danzhong,and Xinshu acupoints may play a role in the protection of myocardium from ischemia-reperfusion injury by increasing the levels of GRP78 and Beclin-1.

摘要： 目的：观察术前舒芬太尼延迟性预处理对体外循环下冠状动脉旁路移植术（CABG ）围术期认知功能和心肌的保护作用。方法：选择择期在体外循环下行CABG的患者60例，随机均分为舒芬太尼预处理组（舒芬太尼组）和常规治疗对照组（对照组），分别在术前、主动脉开放1h、6h、12h、24h、48h采集血标本，测定心肌肌钙蛋白I （cTnI）水平，并在术前，术后7d接受神经心理（POCD）评价。结果：舒芬太尼组血清cTnI水平在主动脉开放后1h到术后48h均明显低于对照组[1h ：（14.96±2.13） ng／ml比（23.66±3.15） ng／ml]， P均＜0.05；两组在进入ICU后12h、24h、48h的正性肌力药物使用得分舒芬太尼组明显低于对照组[12h ：（6.4±0.6）分比（8.4±0.6 ）分]， P均＜0.05；舒芬太尼组术后认知功能障碍（POCD ）发生率明显低于对照组（13.3％比30.0％， P＝0.041）。结论：舒芬太尼的延迟预处理对体外循环下冠状动脉旁路移植术患者有心肌保护效应，同时可降低认知功能障碍的发生率，具有一定的脑保护作用。%Objective:To observe influence of preoperative sufentanil delayed preconditioning (SPC) on perioperative cogni‐tive function and myocardial protection effect in patients undergoing on -pump coronary artery bypass grafting (OP‐CABG) .Methods:A total of 60 patients undergoing selective OPCABG were randomly and equally divided into sufentanil group (SPC group) and routine treatment control group (control group) ,blood sample was collected before operation ,1h , 6h ,12h ,24h and 48h after aorta declamping to measure level of cardiac troponin I (cTnT );and all patients received neu‐ropsychological assessment before and 7d after operation .Results:Compared with control group ,there was significant re‐ductions in serum cTnI levels [1h:(23.66 ± 3.15) ng/ml vs .(14.96 ± 2.13) ng/ml] in sufentanil group from 1h after aor‐ta declamping to 48h after CABG ,P<0.05 all .The inotropic agent usage score on 12h ,24h and 48h after entering ICU of sufentanil group was significantly lower than that of control group [12h:(6.4 ± 0.6) scores vs .(8.4 ± 0.6) scores] , P<0.05 all .Incidence rate of postoperative cognitive dysfunction (POCD) in sufentanil group was significantly lower than that of control group (13.3% vs .30.0% ,P=0.041) .Conclusion:Preoperative sufentanil delayed preconditioning posses‐ses myocardial protection effect , and reduce incidence rate of cognitive dysfunction so also possesses certain brain protection in patients undergoing on-pump coronary artery bypass grafting .

摘要： 预处理组件包括有分离装置、回收容器以及裙板部。分离装置为筒状的容器，具有上方开口的内部空间，在该内部空间内设有使试样通过而使试样中的特定成分从试样中分离的分离层，并且，在下端部设有用于提取已通过分离层的试样的提取口。回收容器能够相对于分离装置装卸，具有回收自分离装置的提取口被提取的试样的内部空间，回收容器以该内部空间收容有分离装置的下端部的状态嵌入于构成过滤口的凹部，该过滤口用于进行试样的提取处理。裙板部与分离装置构成一体，设为以与分离装置的外周面之间形成有上方封闭且下方开口的空间的方式与外周面之间空开间隙地包围外周面，设置为在将收容有分离装置的下端部的状态下的回收容器嵌入于凹部时，使该下端部与凹部的开口的周围的面紧密接触。

摘要： 本发明公开了一种缺血预处理模型的制备方法，所述制备方法包括如下步骤：将用于制备所述模型的小动物放置并固定在鼠笼中，所述小动物的身体垂直于小动物离心机的主轴，并使其头部朝向轴心；打开电机，使所述电机按照预定的速度旋转5分钟；所述电机停止5分钟；每24小时重复上述步骤3次，72小时后可得到缺血预处理模型。相应的，本发明还提供一种用于上述制备方法的小动物离心机。采用本发明提供的小动物离心机可以在不损伤小动物的前提下，简单有效地得到研究用的缺血预处理模型。

摘要： 预处理组件包括有分离装置、回收容器以及裙板部。分离装置为筒状的容器，具有上方开口的内部空间，在该内部空间内设有使试样通过而使试样中的特定成分从试样中分离的分离层，并且，在下端部设有用于提取已通过分离层的试样的提取口。回收容器能够相对于分离装置装卸，具有回收自分离装置的提取口被提取的试样的内部空间，回收容器以该内部空间收容有分离装置的下端部的状态嵌入于构成过滤口的凹部，该过滤口用于进行试样的提取处理。裙板部与分离装置构成一体，设为以与分离装置的外周面之间形成有上方封闭且下方开口的空间的方式与外周面之间空开间隙地包围外周面，设置为在将收容有分离装置的下端部的状态下的回收容器嵌入于凹部时，使该下端部与凹部的开口的周围的面紧密接触。

摘要： 本发明公开了一种在衰老心肌缺血后处理缺血再灌注损伤治疗用miRNA标志物及其应用，属于分子生物学和基因工程技术领域，测血液样本中miR‑30a表达水平的试剂在制备治疗在衰老心肌缺血后处理缺血再灌注损伤产品中的应用，用于检测人血液样本的和用于检测小鼠或大鼠心肌样本中的所述miR‑30a的序列如SEQ：ID：NO：1所示。本发明首次提供一种用于IPostC预防或治疗I/R损伤的稳定性很好的药物组合物，为研制抗I/R损伤所致的心肌梗死的新药开辟新的途径。

摘要： 本发明公开了一种缺血预处理模型的制备方法，所述制备方法包括如下步骤：将用于制备所述模型的小动物放置并固定在鼠笼中，所述小动物的身体垂直于小动物离心机的主轴，并使其头部朝向轴心；打开电机，使所述电机按照预定的速度旋转5分钟；所述电机停止5分钟；每24小时重复上述步骤3次，72小时后可得到缺血预处理模型。相应的，本发明还提供一种用于上述制备方法的小动物离心机。采用本发明提供的小动物离心机可以在不损伤小动物的前提下，简单有效地得到研究用的缺血预处理模型。

摘要： 本发明提供了一种预处理植物粉末、植物秸秆预处理方法和植物秸秆预处理系统，属于环境治理技术领域。本发明将植物秸秆进行破碎处理，得到植物粉末，将所述植物粉末在磁性沸石‑锰氧化物催化材料与弱酸水溶液存在条件下进行预热处理，之后继续在弱碱水溶液存在条件下进行热水解处理，最终得到预处理植物粉末。采用本发明方法能够高效破坏植物中的木质素结构，将其转化为容易被生物酶解的物质，且尽可能不破坏纤维素以及半纤维素结构，提高植物的生物利用性，所得预处理植物粉末经酶解处理后，可用于污水处理厂反消化碳源；且本发明方法工艺简单，生产成本低，适合规模化连续生产和应用。

摘要： 顶点削减装置(10)具有：顶点削减部(131)，其作为判定作为判定对象的坐标是否存在于内外判定用多边形的内外的判定处理的预处理，取得内外判定用多边形的各顶点的坐标信息，削减内外判定用多边形的顶点；以及通信部(11)，其将顶点削减部(131)削减顶点之后的多边形的各顶点的坐标信息输出至进行判定处理的装置。

摘要： 旋转装置(210)具有：旋转部(2131)，其作为判定作为判定对象的坐标是否存在于内外判定用多边形的内外的判定处理的预处理，取得内外判定用的多边形的各顶点的坐标信息和内外判定用的多边形的各顶点的坐标信息，使作为判定对象的坐标和内外判定用的多边形旋转；以及通信部(211)，其输出旋转后的内外判定用的多边形的各顶点的坐标信息和作为旋转后的判定对象的坐标，作为旋转后坐标信息。

摘要： 一种肢体缺血预处理自动充气装置，包括主机，主机内设有充放气装置，充放气装置与气囊压迫带连接、并通过控制器控制气囊压迫带定时、定压充放气；所述充放气装置包括充气管、放气管及主管，充气管、放气管及主管构成Y型结构；其中，充气管上设有气泵、进气电磁阀，放气管上设有出气电磁阀、喷气筒。本实用新型提供的一种肢体缺血预处理自动充气装置，通过机电控制气囊压迫带自动完成肢体远端缺血数分钟后恢复血流数分钟，达到肢体缺血预处理的效果，方便临床应用。

摘要： 本实用新型公开了一种具有自动局部缺血预处理功能按键的电子医疗器材。其特性具有局部缺血预处理(Ischemic Preconditioning)的功能按键，以利心血管急症患者，在病发急救或送往医院的过程中，透过“远距局部缺血预处理”程序的急救，可减少组织坏死以及心肌梗塞的机率，提升存活率。