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。     

高氧液对家兔心肌缺血再灌注损伤的保护作用

目的 :观察高氧液对家兔心肌缺血再灌注损伤的保护作用。方法 :结扎兔冠状动脉左室支中段 ,40 min后解除结扎行再灌注 ,制成心肌急性缺血再灌注模型。于缺血前 10 min、再灌注前 10 m in,分别静滴平衡盐液、高氧平衡盐液 ,观察在急性缺血及再灌注状态下心电图、血浆肌酸磷酸激酶 （CK）、丙二醛 （MDA）和超氧化物岐化酶 （SOD）的变化。结果 :高氧平衡盐液能使抬高的心电图 S- T段明显下降 ,缺血再灌注心肌 CK活性明显降低 ;并能保护SOD的活性 ,降低脂质过氧化反应代谢产物 MDA的含量。结论 :高氧平衡盐液对家兔在体心肌缺血再灌注损伤具有明显的保护作用。     

蝙蝠葛酚性碱对心肌缺血再灌注损伤内皮功能的影响

目的 :旨在研究中药蝙蝠葛酚性碱对心肌缺血再灌注 ( MIR)损伤时内皮功能的保护作用。方法 :实验兔 2 4只 ,随机分为三组。 1假手术组 ;2心肌缺血再灌 ( myocardial ischem ia reperfusion,MIR)组 ;3MIR 蝙蝠葛酚性碱组。观察缺血前、缺血后 30 m in、再灌注即时、30 min、1h、2 h、3h、4h血液一氧化氮 ( NO)、超氧化物岐化酶 ( SOD)、丙二醛 ( MDA)的含量变化。缺血前 10 min静注蝙蝠葛酚性碱对上述指标的影响。结果 :1与假手术比再灌即时血 NO下降 ,SOD下降 ,MDA上升 ,NO于再灌 1h下降最明显 ( P<0 .0 1) ,SOD于再灌即时下降最明显 ( P<0 .0 1) ,MDA于再灌 2 h上升最明显 ( P<0 .0 1)。2蝙蝠葛酚性碱干预后 NO明显上升 ,在 30 min点最明显 ( P<0 .0 1) ,MDA下降在 2 h点明显 ( P<0 .0 5 ) ,SOD上升在 1h点明显 ( P<0 .0 5 )。结论 :MIR可诱发内皮功能紊乱 ,而蝙蝠葛酚性碱改善 MIR损伤时的内皮功能 ,并增加氧自由基清除能力 ,从而起到对心肌细胞的保护作用     

参附注射液对犬心肌缺血/再灌注损伤的保护作用

目的探讨参附注射液（SFI）预处理对犬心肌缺血／再灌注损伤的保护作用及机制。方法21只犬随机分为3组。假手术组（Sham组）、缺血/再灌注组（I／R组）和参附注射液（SFI）预处理组（SFI纽）。观察血清乳酸脱氢酶（LDH）、肌酸磷酸激酶同工酶（CK-MB）和心肌钙蛋白（cTn-I）含量,测定心肌梗死范围、心肌组织丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性等指标。结果与Sham组比较,I／R组和SFI组LDH、CK-MB和cTn-I值均明显升高,心肌组织SOD活性显著下降,MDA含量显著升高,心肌梗死范围明显增大（P〈0．01）。与I／R组比较,SFI纽能显著降低血清LDH、CK-MB、cTn-I值和心肌组织MDA含量（P〈0．01）,显著缩小心肌梗死范围（P〈0．05）,升高心肌SOD活性（P〈0．05）。结论SFI预处理对心肌缺血／4g灌注损伤心肌有保护作用,机制可能与减轻脂质过氧化反应有关。     

牛磺酸对大鼠心肌缺血再灌注损伤细胞凋亡的影响

目的观察牛磺酸对大鼠心肌缺血再灌注损伤后细胞凋亡的影响。方法实验大鼠40只,随机分为5组：假手术组（8只）,再灌注模型组（8只）,牛磺酸低、中、高剂量（30mg／kg、100mg／kg、300mg／kg）组（各8只）。再灌注后观察各组血清SOD、LDH、MDA含量,TUNEL法检测心肌细胞凋亡。结果①牛磺酸对大鼠心肌缺血再灌注后血清SOD、LDH、MDA含量的影响：与假手术组比较,其余各组大鼠血清SOD活性明显降低,LDH、MDA含量明显增高（P〈0．05,P〈0．01）;与模型组比较,牛磺酸中、高剂量组大鼠血清SOD活性明显升高（P〈0．01）,LDH、MDA含量明显降低（P〈0．05,P〈0．01）。②牛磺酸对大鼠心肌缺血再灌注（I／R）损伤后细胞凋亡的影响：I／R后心肌细胞凋亡指数（AI）为（45．6±4．6）,明显高于假手术组的（8．50±1．13）（P〈0．01）,牛磺酸低、中、高组分别为（37．03±3．52）、（30．32±8．23）和（25．62±6．12）,均明显低于I／R（P〈0．01）。结论牛磺酸可降低再灌注损伤大鼠氧自由基值,抑制心肌细胞凋亡。     

参麦与血塞通合用对心肌缺血再灌注家兔血清TNF-α、IL-8的影响

目的　研究参麦注射液与血塞通注射液合用对心肌缺血再灌注家兔血清肿瘤坏死因子(TNF -α)、白介素 -8(IL -8)的影响。方法　将 3 2只家兔随机分为 4组 ,造成在体心肌缺血再灌注模型 ,分别于再灌注前经静脉注射生理盐水、参麦、血塞通、参麦加血塞通。分别于缺血前 5min、缺血后 2 5min(给药前 )、再灌注 3 0min、再灌注 90min、再灌注 180min检测血清TNF -α、IL -8的浓度 ,并于实验结束后测定心肌组织超氧化物歧化酶(SOD )活性及丙二醛 (MDA)的含量。结果　参麦注射液与血塞通注射液合用能显著降低心肌缺血再灌注后家兔血清TNF -α、IL -8的含量 ,升高心肌组织SOD的活性 ,降低心肌组织MDA的含量。结论　参麦注射液与血塞通注射液合用能够减轻TNF -α、IL -8对缺血再灌注心肌的损伤 ,其效果优于二者单独应用。     

缺血后适应对家兔急性心肌梗死再灌注心电图的影响

目的探讨缺血后适应对家兔急性心梗再灌注后心电图的影响及机制。方法采用夹闭左室支方法制作家兔急性心肌缺血再灌注动物模型,然后分为对照组和后适应组,观察两组家兔于再灌注前至再灌注2h期间的心电变化,并测定缺血前、再灌注前、再灌注结束时血清丙二醛（MDA）、超氧化物岐化酶（SOD）、血清谷胱甘肽过氧化物酶（GSH-PX）水平。结果缺血后适应组兔再灌注2h末Ⅱ、Ⅲ、aVF导联ST段平均抬高值低于对照组,而心肌再灌注的有效率高于对照组（p〈0.05）;再灌注性恶性心律失常的发生率及持续时间、再灌注3h末CK-MB及cTNI水平,均低于对照组（p〈0.05）;再灌注1h血浆MDA水平低于对照组,SOD、GSH-PX活性高于对照组（p〈0.05）;而再灌注3h两组间MDA、SOD、GSH-PX水平无显著差异（p〉0.05）。结论缺血后适应可明显改善心电图ST段、心律失常等心肌损伤指标,对心肌梗死起良好的保护作用,其机制与抑制再灌注早期氧自由基的活化,减轻心肌急性缺血再灌注损伤有关。     

心痛灵滴丸预适应对兔心肌缺血再灌注损伤保护作用的研究

目的：探讨心痛灵滴丸预适应对兔心肌缺血再灌注损伤的保护作用。方法：采用冠状动脉粥样硬化(AS)家兔在体心肌缺血再灌注损伤模型，观察心痛灵滴丸预适应对兔心肌组织形态结构和脂质过氧化的影响。结果：心痛灵滴丸预适应能减轻缺血再灌注时心肌组织及细胞超微结构的形态学损伤，能显著提高兔血清超氧化物歧化酶(SOD)活性，降低血清丙二醛(MDA)含量，而且能加强缺血预适应对兔心肌缺血再灌注损伤的保护作用。结论：心痛灵滴丸预适应能诱导缺血预适应样心脏保护作用，其机制可能与清除氧自由基、抑制脂质过氧化反应有关。     

野菊花注射液玻璃体内注射对兔缺血再灌注损伤视网膜中SOD、MDA水平的影响

目的观察野菊花注射液玻璃体内注射对兔缺血再灌注损伤视网膜中超氧化物歧化酶（SOD）、丙二醛（MDA）水平的影响。方法将54只兔随机分为A组6只及B、C组各24只,A组不处理,B、C组制作兔视网膜缺血再灌注损伤动物模型后,分别于玻璃体内注射平衡盐溶液和野菊花注射液各0．1ml。治疗后1、6、24、72h,检测兔视网膜中的SOD、MDA。结果与A组比较,B组视网膜中MDA升高,随后逐渐下降;SOD活性降低,随后逐渐增强,到72h均恢复至正常范围。C组SOD活性及MDA水平变化趋势同B组,但与B组比较,P均〈0．05。结论野菊花注射液玻璃体内注射后,兔缺血再灌注损伤视网膜中SOD活性增高、MDA表达降低。     

红细胞生成素对大鼠心肌缺血-再灌注后抗氧化酶及NO等的影响

目的：探讨红细胞生成素（erythropoietin，EPO）对大鼠心肌缺血-再灌注损伤心肌组织中超氧化物岐化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-px）、过氧化氢酶（CAT）、一氧化氮（NO）及一氧化氮合酶（NOS）表达的影响。方法：以左冠脉穿线结扎法制备心肌缺血再灌注模型，造模前24h开始给药。在大鼠心肌缺血30min再灌注24h后分别检测心肌组织的MDA，GSHpx，SOD，CAT，NO及NOS。结果：EPO干预组的SOD活力有明显增高，MDA含量明显下降（P均〈0．05），GSHpx及CAT含量均显著提高（P〈0．05）。同时，EPO的预处理也降低了NO和NOS的含量（P〈0．01）。结论：对于大鼠心肌缺血再灌注损伤，EPO干预可以提高多种抗氧化酶活性，同时对NO产生增多有一定的抑制作用。     

肾脏缺血后处理对兔急性缺血再灌注心肌细胞凋亡和Bcl-2、Bax蛋白表达的影响

目的研究肾脏缺血后处理对兔急性缺血再灌注心肌细胞凋亡的影响,并探讨其保护机制。方法24只新西兰大白兔随机分为3组,每组8只。（1）缺血再灌注组（IR组）：结扎左冠状动脉前降支1h,再灌注6h。（2）肾脏缺血后处理组（RI-Post组）：操作同IR组,在再灌注即刻用动脉血管夹反复夹闭左侧肾动脉（阻断30S,再通30S,重复3次）,再灌注6h。（3）药物干预组（MI组）：结扎左冠状动脉前降支1h,再灌注前10min给予蛋白激酶C抑制剂-GF109203X（O．05mg／kg）耳缘静脉注射持续10min,再灌注即刻行RI-Post组操作,最后心肌再灌注直至6h。实验结束,采用Tunel法检测24只兔梗死区的心肌细胞凋亡,用免疫组化法检测Bax和Bcl-2蛋白在心肌细胞中的表达水平。结果肾脏缺血后处理组与对照组和药物干预组比较,心肌细胞凋亡指数明显减少（P〈0．05）,Bcl-2表达明显增多（P〈0．01）,Bax表达明显减少（P〈0．05）;而药物干预组与对照组相比各检测指标无明显差别（P〉0．05）。结论肾脏缺血后处理可减少急性缺血再灌注后心肌细胞凋亡,并影响Bcl-2、Bax蛋白的表达,从而对缺血心肌产生保护作用,其保护机制可能与激活蛋白激酶C有关。     

远距缺血后适应对缺血再灌注心肌的保护作用

目的:探讨远距缺血后适应(RIP)对兔局部短期缺血再灌注心肌的保护作用.方法:将24只新西兰白兔随机平均分成4组:假手术对照组(S组)、缺血再灌注对照组(IR组)、缺血后适应组(Post组)、RIP组.采用TUNEL分析检测各组心肌组织的细胞凋亡情况,Western blot方法检测Bcl-2、Bax蛋白的表达.结果:...     

谷氨酰胺心肌缺血再灌注损伤治疗中的效果与机制分析

目的：探讨谷氨酰胺心肌缺血再灌注损伤治疗中的效果与机制。方法：研究时间为2015年2月到2015年10月,选择清洁级SPF大鼠48只完全随机分为包括假手术组、缺血再灌注组和谷氨酰胺组,每组16只,建立心肌缺血再灌注损伤后,谷氨酰胺组给予腹腔注射谷氨酰胺治疗,观察三组心功能与炎症因子的表达变化情况。结果：缺血再灌注组和谷氨酰胺组都顺利建立心肌缺血再灌注损伤模型,表现为抬高的ST段逐步恢复,MAP逐步恢复,左心室颜色转红。同时心功能无明显变化,提示谷氨酰胺对心脏的无明显毒性。三组心率HR在缺血前无明显差异,但缺血再灌注组再灌注后有下降趋势,而再灌注30min后谷氨酰胺组HR较缺血再灌注组升高(P<0.05)。假手术组给药前后MAP无明显变化,缺血再灌注组与谷氨酰胺组在给药后出现轻度下降,不过对比差异无统计学意义(P>0.05)。谷氨酰胺组再灌30min的TNF-α与IL-6含量均明显低于缺血再灌注组(P<0.05),而与假手术组比较差异均无统计学意义(P>0.05)。结论：谷氨酰胺可以对抗缺血再灌注损伤引起的心肌损伤,发挥心脏保护作用,其机制可能与抑制炎症反应有关。     

Renal ischemia/reperfusion remotely improves myocardial energy metabolism during myocardial ischemia via adenosine receptors in rabbits: effects of “remote preconditioning”

ObjectivesThis study examined the changes in myocardial energy metabolism during myocardial ischemia after “remote preconditioning” and investigated the involvement of adenosine receptors in the mechanisms of this effect.BackgroundRecent studies have indicated that a brief period of ischemia and reperfusion (ischemic preconditioning, PC) in a remote organ reduces myocardial infarct size (IS) protecting against subsequent sustained myocardial ischemia. However, the mechanisms of “remote PC” remain unclear. We assessed myocardial energy metabolism during sustained myocardial ischemia and reperfusion after renal PC (RPC), in comparison with that after myocardial PC (MPC) in open-chest rabbits. It has been established that adenosine receptors are involved in the mechanisms of MPC.MethodsRabbits that had been anesthetized with halothane were divided into six groups. The control (CNT) group underwent 40-min coronary occlusion followed by 120 min reperfusion. Before the procedure, the MPC group underwent an additional protocol of 5 min coronary artery occlusion and 20 min reperfusion, and the RPC group received a 10 min episode of renal artery occlusion and 20 min reperfusion. In additional experimental groups, 8 sulfophenyltheophylline (SPT, 10 mg/kg), an adenosine receptor inhibitor, was intravenously injected before the 40 min myocardial ischemia (SPT, MPC + SPT and RPC + SPT groups, respectively). Myocardial levels of phosphocreatine (PCr), ATP and intracellular pH (pHi) were measured by ³¹P-NMR spectroscopy.ResultsRPC and MPC delayed the decreases in ATP levels, preserved pHi during 40-min myocardial ischemia and resulted in better recovery of ATP and PCr during 120 min reperfusion compared with the controls. SPT abolished the improvement in myocardial energy metabolism and the reduction in myocardial IS caused by MPC or RPC. Myocardial IS in the CNT (n = 8), MPC (n = 9), RPC (n = 9), SPT (n = 6), MPC + SPT (n = 8) and RPC + SPT (n = 8) groups averaged 42.8 ± 3.5%, 18.2 ± 1.8%1, 19.6 ± 1.3%1, 44.9 ± 5.0%, 35.6 ± 2.7% and 34.8 ± 3.6% of the area at risk (1p < 0.05 vs. CNT), respectively.ConclusionsPC in a remote organ, similar to MPC, improved myocardial energy metabolism during ischemia and reperfusion and reduced IS in vivo by an adenosine-dependent mechanism in rabbits.     

Cardioprotective effect of mexiletine in acute myocardial ischemia tudies in the rabbit closed chest ischemia mode.

ATP-sensitive K+ (KATP) channel openers have a cardioprotective effect and so mexiletine (Mex), a class Ib anti-arrhythmic drug, may also be cardioprotective because of its KATP channel-opening effect. The present study examined the effect of Mex on acute myocardial ischemia in a closed-chest acute ischemia and reperfusion model in rabbits. The rabbits were divided into 3 groups: (1) control (n=8); (2) Mex (n=8), continuous infusion of mexiletine (24 mg x kg(-1) h(-1)); and (3) Mex+Gli (n=8), pre-administration of glibenclamide (Gli; 0.5mg/kg) followed by mexiletine infusion. The incidence of arrhythmia, the hemodynamics and left ventricular ejection fraction (LVEF), and the infarct size were evaluated and compared among the 3 groups. The incidence of fatal ventricular fibrillation (VF) was least in the Mex group. The LVEF at 30 min after reperfusion was least in the Mex group, but at 360 min after reperfusion, it was least in the Mex+Gli group. The area of myocardial infarction determined by 2,3-triphenyltetrazolium chloride (TTC) staining was smallest in the Mex group. In this model, Mex reduced infarct size and improved left ventricular function during the late phase after reperfusion, although the effect was totally negated by the addition of glibenclamide.     

兔右冠状动脉缺血预适应对窦房结功能及房室传导有效不应期的影响

探讨兔右冠状动脉 (简称冠脉 )缺血预适应对缺血再灌注 (I/R)损伤时窦房结功能和房室传导有效不应期的影响。随机将 36只健康家兔分为正常对照组、单纯I/R损伤组 (IR组 )和缺血预适应组 (IP组 )。对照组只穿线不阻断血流 ;IR组右冠脉阻闭 6 0min ,继以再灌注 6 0min ;IP组阻闭右冠脉 5min后再灌注 10min ,再重复IR方案。在不同时相分别测定IR和IP组心房快速起搏或程序电刺激后的窦房传导时间 (SACT)、窦房结恢复时间 (SNRT)、最大起搏峰值 (PCLP)以及房室有效不应期 (AVERP) ,并以电镜观察右心超微结构。结果显示 :①IR及IP组的再灌注5min、IR组缺血 5min时的SACT均较正常对照组明显延长 ;②除IP组缺血 10min的SNRT及IP组再灌注 40min的AVERP外 ,两实验组的SNRT及PCLP值均较正常对照组明显延长 (P <0 .0 1) ;③IP组 4项电生理指标的改变程度均较同期的IR组明显减轻 (P <0 .0 5或 0 .0 1) ;④较之IR组 ,IP组的右心房肌超微结构损伤明显减轻。提示在体兔右冠状动脉IP可保护右房肌的超微结构 ,减轻I/R对窦房结功能及AVERP损伤。     

Toll样受体4在大鼠心肌缺血再灌注损伤中表达的实验研究

目的 观察心肌缺血再灌注早期Toll样受体4 mRNA(TLR4 mRNA)及蛋白表达,探讨TLR4在心肌缺血再灌注损伤中的作用.方法 雄性SD大鼠随机分为2组:假手术组(Sham组)、缺血再灌注组(IR组),每组36只,建立大鼠心肌缺血再灌注模型,按照不同的再灌注时间(0、0.5、1、24和8 h)处死动物.光镜和电镜观察心肌组织形态及超微结构改变.免疫组化检测心肌TLR4蛋白表达情况.实时定量逆转录聚合酶链反应定量心肌TLR4 mRNA表达水平.酶联免疫吸附试验测定心肌中肿瘤坏死因子-α(TNF-α)含量.结果 (1)Sham组心肌组织形态及超微结构改变不明显;IR组心肌损伤较重,缺血心肌恢复血液灌注8 h内,其病理学变化未见显著改善.(2)Sham组与IR组TLR4蛋白都有阳性表达,IR组TLR4表达增加,且以再灌注1 h最为明显(19.62±3.84,P＜0.01).(3)与Sham组比较,IR组心肌,TLR4 mRNA表达水平均出现不同程度上调,以再灌注1 h达到峰值[(4.03±0.85)×10-2,P＜0.01],而Sham组各时间点未见明显改变.(4)IR组心肌TNF-α水平高于各对应时间点Sham组(P均＜0.05),且心肌TLR4 mRNA表达与TNF-α呈正相关(r=0.728,P＜0.01).结论 心肌缺血再灌注早期,心肌TLR4表达迅速上调,TLR4的激活可能通过促进TNF-α等炎性因子的产生分泌增多来介导心肌缺血再灌注损伤.     

Human superoxide dismutase failed to limit the size of myocardial infarct after 20-, 30-, or 60-minute ischemia and 72-hour reperfusion in the rabbit

The effect of superoxide dismutase (SOD) on the size of the myocardial infarct resulting from various durations of ischemia and a 72-hour reperfusion was examined in the rabbit. A coronary branch of the circumflex artery was occluded for 20, 30, or 60 min and then reperfused. Seventy-two hours after the coronary occlusion, the infarct size and the size of the area at risk (vascular bed of occluded coronary artery) were determined by histology (hematoxylin-eosin and Mallory's staining) and by fluorescent particles, respectively. Human SOD (45,000 units/kg) was injected intravenously as a bolus in SOD-treated rabbits, while only saline was administered to control rabbits. The percentage of the area at risk which actually infarcted (%I/AAR) was 25.5 +/- 12.9% (mean +/- S.D.) in the 20-min ischemia control group (n = 9), 19.7 +/- 10.2% in the 20-min ischemia SOD group (n = 9), 44.8 +/- 9.0% in the 30-min ischemia control group (n = 9), 41.0 +/- 6.3% in the 30-min ischemia SOD group (n = 9), 74.2 +/- 13.8% in the 60-min ischemia control group (n = 9), and 76.6 +/- 8.2% in the 60-min ischemia SOD group (n = 7). The %I/AAR was not significantly different between the control and SOD groups for any duration of ischemia. Heart rate, blood pressure, and the size of area at risk were comparable in all six groups. These findings suggested that oxygen-free radicals produced during initial moments of reperfusion were unlikely to contribute to myocardial necrosis regardless of the duration of ischemia in the rabbit.     

Evaluation of myocardial viability following ischemic and reperfusion injury using phosphorus 31 nuclear magnetic resonance spectroscopy in vivo

Recovery of myocardial high-energy phosphate (HEP) metabolism after coronary occlusion and reperfusion may vary with ischemic duration and may provide information about the extent of tissue viability. To evaluate the differences between varying durations of ischemia and to attempt to identify metabolic indexes of salvaged viable tissue, intact New Zealand white rabbits underwent either 30 (group 1; n = 8) or 60 (group 2; n = 8) minutes of coronary occlusion followed by reperfusion. HEP metabolism was evaluated with cardiac gated phosphorus 31 (31P) nuclear magnetic resonance (NMR) spectroscopy with a 2.0 T spectrometer. While similar HEP changes were observed during ischemia in both groups, differences in HEP recovery between groups were seen following reperfusion. Group 1 animals demonstrated a gradual decrease in inorganic phosphates (Pi) (p less than 0.05 versus group 2), an immediate recovery of phosphocreatine (PCr) (p = ns versus baseline), and a gradual increase of adenosine triphosphate (ATP) to pre-ischemic levels. Group 2 animals had elevated levels of Pi (p less than 0.05 versus baseline; p less than 0.05 versus group 1), slow recovery of PCr, and continued reduction of ATP (p less than 0.05 versus baseline; p less than 0.05 versus group 1). Group 1 rabbits had a greater extent of viable myocardium than group 2 (77.1 +/- 9.7% of risk area versus 39.4 +/- 9.4%; p less than 0.001). Significant correlations were found between PCr and Pi reperfusion values and myocardial viability (r = 0.59, p less than 0.05; r = 0.73, p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

左旋卡尼汀对兔心肌缺血再灌注损伤的保护

目的探讨左旋卡尼汀在心肌缺血再灌注损伤状态下对心肌的保护作用。方法制备兔缺血再灌注模型,实验分为空白对照组、盐水对照组和左旋卡尼汀组,左旋卡尼汀组心肌缺血30 min后给予左旋卡尼汀。观察各组缺血再灌注过程中心电图的动态改变,以及再灌注结束后动脉血游离脂肪酸、超氧化物歧化酶、丙二醛、肌酸激酶的含量和组织中Na -K -ATP酶和Ca2 -Mg2 -ATP酶活性;用Western blot法检测结扎点以下5 mm处左心室全层心肌热休克蛋白70的含量。结果盐水对照组和左旋卡尼汀组均造成明显的心电图动态改变,与盐水对照组比较,左旋卡尼汀组心电图ST段出现有效改善;左旋卡尼汀组分别与盐水对照组和空白对照组相比,游离脂肪酸和丙二醛含量均显著减少(P<0.05);Na -K -ATP酶、Ca2 -Mg2 -ATP酶活性及超氧化物歧化酶的含量显著增多(P<0.05),肌酸激酶含量有下降趋势(P>0.05);心肌热休克蛋白70含量显著增多(P<0.05)。结论左旋卡尼汀可能诱导产生热休克蛋白70,并对心肌缺血再灌注损伤有保护作用。