葛根素对在体兔房室结缺血再灌注损伤的影响

目的探讨葛根素对兔房室结缺血再灌注损伤的影响。方法采用健康雄性兔50只,随机分为5组：A组（假手术组）10只;B组（缺血30min,再灌注30min）10只;C组（缺血30min,再灌注240min）10只;D组（葛根素预处理后,缺血30min,再灌注30min）10只;E组（葛根素预处理后,缺血30min,再灌注240min）10只。检测血清天冬酸氨基转移酶（AST）、乳酸脱氢酶（LDH）、肌酸肌酶（CK）变化,免疫组化检测房室结BCL-2基因蛋白表达,电镜观察其超微结构变化。结果A组AST、LDH、CK未升高,免疫组化检测房室结BCL-2基因蛋白未见表达,超微结构无变化。B、C组变化明显。D、E组较B、C组轻。结论用葛根素干预后,缺血再灌注损伤减轻。     

改良法创建兔心房室结缺血再灌注损伤模型

目的　利用对左冠状动脉缺血再灌注损伤模型的改进建立房室结缺血再灌注损伤模型。简化操作 ,不需人工辅助呼吸 ,更接近生理状态具有明显优越性。方法　健康兔 30只 ,雌雄不拘 ,随机分为两组 ,单纯缺血再灌注组(n =15 ,缺血 30min ,再灌注 2 4 0min)正常对照组 (n =15 ,丝线于右冠状动脉下穿过 ,但不结扎 )。结果　 (1)单纯缺血再灌注组血清天冬酸氨基转移酶 (AST)、乳酸脱氢酶 (LDH)、肌酸肌酶 (CK)明显升高 ,氯化 2 ,3,5 三苯基四氮唑(TTC)法测定心肌梗死范围明显 ,免疫组化检测房室结BCL 2基因蛋白高表达。 (2 )假手术组AST、LDH、CK未升高 ,TTC法心肌梗死范围不明显 ,免疫组化检测房室结BCL 2基因蛋白未见表达。结论　本改良法从操作、理论上都证明方法简化和符合病理生理情况 ,房室结缺血再灌注损伤模型是成功的。     

缺血-再灌注诱导家兔房室结细胞凋亡的研究

为探讨缺血 再灌注对在体家兔房室结细胞凋亡的作用 ,以及凋亡相关调控基因蛋白 (Fas、bcl 2、bax)的表达 ,以家兔为实验对象 ,麻醉后开胸暴露心脏 ,结扎右冠状动脉 ,建立房室结缺血 再灌注模型。于预定时间处死动物 ,快速取出房室交界区组织 (3mm× 2mm× 1mm) ,10 %福尔马林磷酸盐缓冲液固定。采用TUNEL法检测房室结细胞凋亡 ;免疫组化法检测Fas、bcl 2、bax基因蛋白表达。结果 :①对照组及单纯缺血 10 ,30min组均未检测到细胞凋亡 ,缺血 6 0min组可见少量散在的凋亡细胞 ,缺血 12 0min房室结可见大量的细胞凋亡 ;②缺血 再灌注组 :不同缺血时间组均出现细胞凋亡 ,凋亡细胞数随缺血时间的延长而增加 (P <0 .0 5 ) ;③随缺血时间的延长 ,Fas、bax的表达明显增加 (P <0 .0 1) ,而bcl 2的表达则无明显增加 (P >0 .0 5 ) ;④缺血 再灌注组较相应时间单纯缺血组细胞凋亡数、Fas、bax表达均明显增加 (P <0 .0 1)。结论 :单纯缺血及缺血 再灌注均可诱导房室结细胞发生凋亡 ,这可能与该条件下Fas、bax基因蛋白的过量表达有关。     

缺血预处理对在体家兔房室结细胞形态结构的影响

目的观察缺血预处理在家兔急性心肌梗死模型中,对在体房室结细胞形态结构的影响.方法健康家兔30只,雌雄不拘,随机分为假手术组,缺血再灌注(IR)A组、B组,缺血预处理(IP)A组、B组,通过结扎右冠状动脉建立家兔房室结缺血再灌注模型,观察经过缺血预处理后,以不同的再灌注时间30 min(A组)、180 min(B组)为实验终点,检测心脏血心肌酶变化,HE染色和透视电镜观察房室结细胞的形态学变化.结果IP组较IR组心肌酶检测值显著降低,光镜下细胞空泡变性及细胞坏死IP组较IR组明显减轻.电镜下房室结细胞的线粒体、肌丝等超微结构在IP组损伤也明显减轻.结论缺血预处理对房室结细胞有保护作用.     

磷酸肌酸对大鼠缺血再灌注后心肌损伤的影响

目的 观察磷酸肌酸对大鼠缺血再灌注后心肌损伤的影响.方法 60只雄性SD大鼠随机分为假手术组、模型组、磷酸肌酸组.结扎大鼠左前降支冠状动脉使心肌缺血,30 min后恢复血流并持续120 min,复制缺血再灌注损伤模型.磷酸肌酸组分别于缺血再灌注前30 min经右颈内静脉注射磷酸肌酸3 mg/kg,模型组及假手术组给予等量的生理盐水.测定血清乳酸脱氢酶(LDH)、磷酸肌酸激酶(CK)及心肌组织丙二醛(MDA)和超氧化物歧化酶(SOD)的含量并观察心肌超微结构的变化.结果 磷酸肌酸组与模型组比较,血清LDH、CK值降低,心肌组织MDA值减小,SOD值升高.光镜及电镜下心肌细胞变性坏死程度及心肌细胞超微结构形态改变显著减轻.结论 磷酸肌酸对大鼠心肌缺血再灌注损伤均有保护作用.     

内皮细胞功能紊乱在肝缺血—再灌注损伤中的作用及葛根素的干预

目的探讨内皮细胞功能紊乱在肝缺血—再灌注损伤中的作用及葛根素对其的影响。方法实验兔和肝癌手术患者均随机分为肝缺血—再灌注组(n=10和n=12)和肝缺血—再灌注 葛根素治疗组(n=10和n=12);分别取缺血前、缺血45min(兔)或25min(患者)和再灌注45min(兔)或25min(患者)共3个时相     

曲美他嗪后处理与缺血后处理对大鼠再灌注心肌保护作用的对比

目的 对比观察曲美他嗪(TMZ)后处理与缺血后处理(IPOC)对大鼠心肌缺血再灌注损伤(MIRI)的保护作用.方法40只Wistar 大鼠随机分为4组(n=10):假手术组、模型组、曲美他嗪组(TMZ组)、缺血后处理组(IPOC组).结扎左冠状动脉前降支,建立大鼠心肌缺血/再灌注损伤模型,记录各组心肌梗死面积,光镜HE染色观察心肌组织细胞形态,透射电镜观察心肌细胞微观结构,测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷草转氨酶(AST)活性变化.结果 TMZ组、IPOC组与模型组比较:①心肌梗死面积减少(P＜0.05);②心肌细胞损伤程度相当,较模型组有明显改善;③心肌细胞超微结构损伤程度相当,较模型组有明显改善;④心肌酶CK、LDH、AST活性较模型组均有明显降低(P＜0.05).结论 TMZ后处理与IPOD对MIRI心肌均有明显的保护作用,二者作用差异不明显.     

苦参总碱对大鼠心肌缺血再灌注损伤的保护作用

目的利用心肌缺血再灌注损伤致大鼠心肌细胞凋亡模型研究苦参总碱(TASF)对心肌细胞的保护作用。方法 80只雄性大鼠随机分组,连续给药7 d,末次给药1 h后除空白组动物外,其余动物结扎左冠脉前降支30 min,再灌注6 h,通过血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、天门天冬氨酸氨基转移酶(AST),心肌病理学、电镜、TUNEL染色及Bcl-2、Bax蛋白表达的检测对TASF保护心肌的作用进行评估。结果与模型组相比,80 mg/kg TASF能够有效降低血清中CK、LDH、AST的含量(P<0.05),40 mg/kg TASF能够有效降低血清中LDH、AST的含量(P<0.05);80 mg/kg和40 mg/kg TASF能够减少缺血再灌注导致的心肌细胞结构的破坏;80 mg/kg TASF可以减少缺血再灌注导致的心肌细胞凋亡(P<0.05),其机制可能与增加Bcl-2蛋白的表达,降低Bax蛋白表达有关。结论 TASF对心肌缺血再灌注引起的心肌细胞损伤具有保护作用,其机制可能为调控Bcl-2、Bax基因表达抑制心肌细胞凋亡。     

含抑肽酶灌注液减轻缺血再灌注心肌的损伤

目的　观察抑肽酶等药物对缺血再灌注离体兔心的影响。方法　 2 4只家兔随机分为两组 :对照组 (B组 )将离体心脏置于 L angendorfl装置 ,经主动脉逆行灌注克氏液 ,灌注 30 min后 ,用 Thomas灌注停跳 40 min,最后再恢复灌注 30 min。用药组 (A组 )克氏液中加入抑肽酶及山莨菪碱。缺血前及再灌注期记录左心室功能及冠状动脉血管阻力 ,并行心肌超微结构观察。结果　再灌注后 30 min,A组左心室功能明显高于 B组 (P<0 .0 5 ) ;收集的灌注液中肌酸磷酸激酶 (CK)及乳酸脱氢酶 (L DH)较 B组明显减少 ;超微结构改善也优于 B组。结论　抑肽酶对缺血再灌注心肌功能有明显保护作用     

兔右冠脉缺血预适应与右心缺血再灌注损伤

目的 :探讨兔右冠脉缺血预适应 (IP)与缺血再灌注损伤 (IR)的相关性。方法 :以单纯缺血 6 0 min 再灌注 6 0 min(IR)为对照 ,观察经 IP(缺血 5min 再灌注 10 min)后 IR心肌缺血型 S- T段、超微结构改变及再灌注心律失常发生率。结果 :较之 IR组 ,IP组的 ST段明显下移 ,电镜下见右室和右房心肌超微结构改变明显减轻 ,缓慢型再灌注心律失常的发生率明显减少。结论 :清醒兔右冠脉 IP可减少 IR引起的右心缺血性超微结构损伤及再灌注心律失常发生率     

磷酸肌酸后适应联合缺血后适应减轻大鼠心肌缺血再灌注损伤

目的探讨磷酸肌酸后适应联合缺血后适应对大鼠心肌缺血再灌注损伤的影响。方法取健康雄性Wistar大鼠40只,随机分成假手术组(Sham组)、缺血再灌注组(I/R组)、缺血后适应组(IPost组)、磷酸肌酸后适应+缺血后适应组(Pcr+IPost组)各10只,均给予心肌缺血30 min,再灌注120 min处理。再灌注2 h后用比色法测量各组血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、髓过氧化物酶(MPO),ELISA方法检测核因子κB(NF-κB),TTC染色测定心肌梗死面积。结果 IPost组血清CK、LDH、MPO活性和NF-κB以及心肌梗死面积显著低于I/R组,Pcr+IPost组较IPost组各项指标进一步降低(P均<0.05)。结论磷酸肌酸后适应联合缺血后适应可以明显减轻大鼠心肌缺血再灌注损伤,其机制之一可能与抑制NF-κB参与的炎症反应有关。     

再灌注损伤抢救激酶对小鼠缺血后适应心肌再灌注损伤中的减轻作用

目的 研究缺血后适应(IPC)对离体小鼠心肌缺血再灌注(I/R)损伤的作用及其影响因素,探讨再灌注损伤抢救激酶在IPC心肌保护中的作用.方法 建立Langendofff小鼠心肌I/R模型,全心缺血30 min后分为6组[(1)对照组,(2)3次IPC组(采取缺血10 s及再灌注10 s的3次IPC周期),(3)6次IPC组(采取缺血10 s及再灌注10 s的6次IPC周期),(4)延迟IPC组(恢复再灌注1 min后进行IPC),(5)IPC+PD98059组,(6)I/R+PD98059组],随后再灌注2 h;观察IPC对心脏血流动力学、心肌酶的释放、心肌超氧化物歧化酶活性和丙二醛的含量、梗死心肌范围的影响以及与细胞外信号调节激酶(ERK1/2)、磷脂酰肌醇3激酶-蛋白激酶B表达水平的关系.结果 与对照组比较,3次IPC组和6次IPC组小鼠心脏血流动力学显著改善,心肌酶释放减少,心肌丙二醛减少、超氧化物歧化酶活性增加,心肌梗死范围减小.6次与3次IPC周期的保护作用相似.而IPC作用在恢复再灌注1 min后消失.3次IPC组和6次iPC组心肌的ERK1/2磷酸化水平显著增高,蛋白激酶B磷酸化水平无明显变化.PD98059显著抑制IPC所致的ERK1/2的磷酸化,并能消除IPC对心肌的保护作用.结论 IPC能有效地减轻离体小鼠心肌缺血再灌注损伤,增加IPC的周期数并没有扩大保护作用,延迟IPC没有产生类似的保护作用.ERK1/2细胞信号途径参与介导IPC对离体心脏缺血再灌注心肌的保护作用.     

The effects of a bradykinin B2 receptor antagonist in extended liver resection with ischemia in dogs

BACKGROUND/AIMS: In liver surgery, total clamping of the portal triad (Pringle's procedure) is commonly used, and sometimes causes liver failure. This study evaluated the effects of a bradykinin B2 receptor antagonist, FR173657 (FR), on ischemia-reperfusion injury during liver resection in dogs. METHODOLOGY: Experimental animals were divided into two groups. In the FR group (n=6), FR (100 nmol/kg/hr) was administered continuously via the portal vein from 30 min before the onset of ischemia until 2 hr after reperfusion. In the control group (n=6), vehicle was injected in the same manner. The right portal pedicle was clamped for 60 min, while the left portal branch was left patent to avoid portal congestion. Following reperfusion, the non-ischemic lobes were resected, and remnant liver function was evaluated. RESULTS: AST and ALT were significantly (p<0.05) lower in the FR group than in the control group. Hepatic tissue blood flow 30 min after reperfusion was significantly (p<0.05) higher in the FR group than in the control group. Histological tissue damage was mild, and polymorphonuclear neutrophil infiltration was significantly (p<0.05) reduced in the FR group compared with the control group. CONCLUSIONS: A bradykinin B2 receptor antagonist ameliorated the ischemia-reperfusion injury caused by Pringle's procedure during extended liver resection.     

芪参益气滴丸减轻心肌缺血再灌注损伤的作用

目的 探究芪参益气滴丸减轻巴马猪急性心肌缺血再灌注损伤的作用以及其对心肌蛋白激酶B(AKT)和磷酸化蛋白激酶B(p-AKT)蛋白表达的影响.方法 将20只健康广西巴马猪(巴马猪)随机分为:模型组和芪参益气滴丸组,每组10只(n=10).两组巴马猪正常喂食外,模型组予100 ml纯净水灌胃,芪参益气滴丸组予芪参益气滴丸+...     

Alanyl-glutamine dipeptide inhibits hepatic ischemia-reperfusion injury in rats

AIM: To investigate the protective effect and mechanism of alanyl-glutamine dipeptide (Ala-Gln) against hepatic ischemia-reperfusion injury in rats. METHODS: Rats were divided into group C as normal control Group (n=16) and group G as alanyl-glutamine pretreatment (n=16). Rats were intravenously infused with 0.9% saline solution in group C and Ala-Gln -enriched (2% glutamine) 0.9% saline solution in group G via central venous catheter for three days. Then all rats underwent hepatic warm ischemia for 30 min followed by different periods of reperfusion. Changes in biochemical parameters, the content of glutathione (GSH) and the activity of superoxide dismutase (SOD) in liver tissue, Bcl-2 and Bax protein expression and morphological changes of liver tissue were compared between both groups. RESULTS: One hour after reperfusion, the levels of liver enzymes in group G were significantly lower than those in group C (P<0.05). Twenty-four hours after reperfusion, the levels of liver enzymes in both groups were markedly recovered and the levels of liver enzyme in group G were also significantly lower than those in group C (P<0.01). One and 24 h after reperfusion, GSH content in group G was significantly higher than that in group C (P <0.05). There was no statistical difference in activities of SOD between the two groups. One and 24 h after reperfusion, the positive expression rate of Bcl-2 protein was higher in group G than in group C (p<0.05) and the positive expression rate of Bax protein was lower in group G than in group C (P<0.05). Histological and ultrastructural changes of liver tissue were inhibited in group C compared to group G. CONCLUSION: Our results suggest that Ala-Gln pre-treatment provides the rat liver with significant tolerance to warm ischemia-reperfusion injury, which may be mediated partially by enhancing GSH content and regulating the expression of Bcl-2 and Bax proteins in the liver tissue.     

Administration of the Rho-Kinase Inhibitor Fasudil Before Ischemia or just After Reperfusion,but not 30 min After Reperfusion,Protects the Stunned Myocardium in Swine

OBJECTIVES: We assessed the effect of administration time for fasudil treatment of the stunned myocardium in 40 anesthetized open chest swine. MATERIALS AND METHODS: All swine were subjected to 12 min ischemia followed by reperfusion to generate stunned myocardium. Group A (n = 11) received saline in place of fasudil both before ischemia and after reperfusion. Group B (n = 10) received 30 min intravenous fasudil at a rate of 13 mug/kg/min starting 45 min before ischemia and received saline after reperfusion. Groups C (n = 10) and D (n = 9) received saline before ischemia, and received fasudil at a rate of 13 mug kg(-1) min(-1) starting just before reperfusion in group C and 30 min after reperfusion in group D. In both groups, treatment lasted 30 min. Myocardial contractility was assessed by percent segment shortening (%SS). RESULTS AND DISCUSSION: Three swine in group A, 2 swine in each of groups B and C, and one swine in group D had ventricular fibrillation or tachycardia after reperfusion and were excluded from further analysis. The changes of %SS from baseline at 90 min after reperfusion in groups B and C were 68 +/- 8% and 75 +/- 8%, respectively, which were significantly higher than in group A or D (47 +/- 10% or 43 +/- 8%). CONCLUSION: We conclude that fasudil administered before ischemia or just after reperfusion, but not 30 min after reperfusion, protects the stunned myocardium.     

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。