白花前胡甲素对心肌缺血再灌注大鼠血清IL-6水平的影响

目的　探讨白花前胡甲素 (Pd Ia)抗缺血再灌注损伤的机制 ,为寻找高效、低毒及安全的防治缺血再灌注损伤的药物提供理论基础。方法　采用放射免疫分析测定血清IL— 6水平 ,并通过常规HE染色比较中性粒细胞等炎性细胞的心肌浸润情况。结果　Pd Ia低、中、高三个剂量组IL— 6水平分别由对照组的 (15 2 88±15 2 5 ) pg/ml降至 (12 8 45± 18 37)pg/ml、 (119 6 6± 15 72 ) pg/ml和 (116 13± 10 45 )pg/ml (P <0 0 1) ,其作用强度与硝苯地平相近 (12 3 5 5± 18 6 2 )pg/ml。 结论　Pd Ia明显抑制缺血再灌注大鼠血清IL— 6水平 ,提示Pd Ia可能通过抑制NF—kB途径实现再灌注性损伤的防治     

表没食子儿茶素没食子酸酯对缺血再灌注损伤大鼠心肌脂质过氧化及心肌酶活性的影响

目的：观察表没食子儿茶表没食子酸酯（EGCG）对缺血再灌注损伤大鼠心肌脂质过氧化及心肌酶活性的影响。方法：雄性Wistar大鼠50只分为5组，假手术组、缺血再灌注组（IR），丹参（SM，100mg/kg）组，EGCG1（10mg/kg)组和EGCG2（20mg/kg）组，每组10只动物，采用结扎大鼠左冠状动脉前降支30min后再灌注60min的方法建立在体缺血再灌注损伤模型，分别测定心肌丙二醛（MDA）含量，超氧化物歧化酶（SOD）及ATP酶活性和血浆乳酸脱氢酶（LDH）水平。结果：与假手术组比，IR组大鼠心肌MDA及血浆LDH明显升高，SOD及ATP酶活性则显著降低（P＜0．01）；EGCG和SM均能显著，降低MDA与LDH，明显增加SOD与ATP酶活性（与IR组比，P＜0．01），并且EGCG（20mg/kg)，降低MDA与LDH的作用较SM（100mg/kg)更明显（P＜0．05）。结论：EGCG通过抑制脂过氧化反应和提高心肌SOD与ATP酶活性，对大鼠缺血再灌注损伤心肌有显著的保护作用。     

蛋白激酶C激活调控FOS表达参与缺血诱导神经元凋亡的研究

目的：探讨蛋白激酶C（PKC）与神经元凋亡的可能机制，方法：采用大鼠全脑缺血模型，观察脑缺血／再灌流后PKC活性，FOS表达及神经元凋亡的变化。结果：脑缺血／再灌流可以导致PKC的移位激活伴FOS表达及神经元凋亡的增加；用蛋白激酶C抑制剂灯盏花可以阻止上述变化。结论：蛋白激酶C的激活可能通过促进FOS表达参与了脑缺血／再灌流诱导的神经元凋亡。     

黄连素对缺血再灌注心肌细胞损伤的保护作用

目的　研究黄连素对新生大鼠心肌细胞缺血再灌注损伤的保护作用。方法　取体外培养的新生大鼠心肌细胞于缺氧 2 4h复氧 1h造成缺血再灌注 ( I/ R)模型 ,观察细胞损伤情况 ;并将黄连素以 1.5× 10 - 6 m ol/ L、1.5× 10 - 5m ol/ L、1.5× 10 - 4 mol/ L 三种浓度分别加入培养基中 ,预处理 2 4h后 ,再置于上述缺氧复氧环境中培养 ,检测以上不同条件下细胞上清液中的乳酸脱氢酶 ( L DH)、丙二醛 ( MDA)、超氧化物歧化酶 ( SOD)含量 ,并检测各组细胞的凋亡率。结果　与正常对照组相比 ,缺血及再灌组细胞上清液中 L DH、MDA含量明显升高 ( P<0 .0 1) ,SOD活力则显著降低 ( P<0 .0 1) ,缺血组和再灌组凋亡率均升高明显 ( P<0 .0 1)。而用黄连素预处理后缺血及再灌组的 L DH、MDA显著低于用药前 ( P<0 .0 1) ,SOD则高于单纯缺血和再灌组 ( P<0 .0 1) ,上述作用在本实验黄连素浓度为 1.5× 10 - 6 m ol/ L～ 1.5× 10 - 4 mol/ L 范围内 ,随浓度升高而更加明显。特别是用黄连素 1.5× 10 - 5mol/ L 浓度预处理后 ,缺血组和再灌组的细胞凋亡率分别是 14.4%和 2 0 % ,分别与用药前 ( 17.4%和 41% )比较有显著性差异 ( P<0 .0 1)。结论　黄连素对缺血再灌心肌细胞有保护作用 ,其作用与浓度有一定依赖关系     

硒对沙土鼠脑缺血再灌注的保护作用及其作用机制研究

目的 研究亚硒酸钠对沙土鼠脑缺血再灌注损伤的保护作用及其机制。方法 将50只沙土鼠随机分为5组，Ⅰ组：假手术组；Ⅱ组：缺血灌注1天处死组；Ⅲ组：缺血再灌注4天处死组；Ⅳ组：硒处理、缺血再灌1天处死组；Ⅴ组：硒处理、缺血再灌注4天处死组。采用夹闭双侧颈动脉法制备沙土鼠脑缺血再灌注模型，焦油紫染色，光镜下观察各组海马CAl区神经细胞的形态变化，电镜下超微结构变化。同时测定脑组织中丙二醛(MDA)、谷胱甘肽过氧化酶(GSH-PX)、超氧化物歧化酶(SOD)的含量。结果 硒处理组沙土鼠脑缺血再灌注后，神经细胞病理形态损伤较轻，SOD、GSH-PX含量较高，MDA含量较低。结论 硒对沙土鼠脑缺血再灌注损伤具有保护作用，其机制可能和增强脑缺血再灌注早期脑组织中SOD、GSH-PX的活性，抑制氧自由基损伤，减轻脂质过氧化反应有关。     

Compartment syndrome. Exclusively the result of increased pressure in the muscular compartment?

Summary The compartment syndrome (cs) is characterized by an increased tissue pressure in a limited space. Pathophysiologically, it is a multifactorial disease that is potentially induced by an initial trauma and develops according to the existence of cofactors. Cofactors are, for instance, the circulation of the patient and the initial treatment of the impending cs. In particular, the microcirculation is altered with endothelial destruction, development of a capillary leak, protein loss from intravasal space and the development of an interstitial and intracellular third space. An impaired drainage of the lymphatic and venous system causes a venous infarction. An arterial infarction results if the tissue pressure exceeds the arteriolar pressure. An accompanying ischemia reperfusion mechanism increases the trauma load. In disadvantageous cases, the patients are in danger of developing a multi-organ deficiency syndrome (MODS) by an uncontrolled inflammatory reaction, by intravasal volume loss and by a myonephropathic systemic reaction. Clinically, the patients suffer a disproportionate amount of pain, followed by neurological signs. Especially in noncompliant patients, tissue pressure measurement is useful. Resuscitation of the circulation as well as splitting of casts is important. In case of a manifest cs, dermatofasciotomy has to be performed as an emergency operation. Even if cs is diagnosed early and fasciotomy is carried out early, the development of sequellae cannot be avoided in every single case.      

急性心肌梗塞静脉溶栓治疗冠脉再通者早期ST段再抬高的临床意义

急性心肌梗塞早期静脉溶栓治疗后，一些溶栓再通患者中，可见早期降低的ＳＴ段再度出现抬高现象。本文回顾溶栓成功者８１例，其中早期出现ＳＴ段再度抬高者２１例（占３５％），与ＳＴ段非再度抬高者相比，ＣＰＫ、ＣＰＫ－ＭＢ峰值，心功能及院内死亡率等无显著差异。笔者认为，此现象也为再通的标志之一。因此，急性心肌梗塞溶栓治疗的早期连续监测心电图对确认再通与否非常重要     

高压氧对大鼠局灶性脑缺血再灌注时神经元特异性烯醇化酶的影响

目的研究高压氧(HBO)对大鼠局灶性脑缺血再灌注(IR)时．大鼠脑梗塞体积．脑组织病理改变及神经元特异性烯醇化酶(NSE)含量的影响。方法用线栓法制备阻断大脑中动脉(MCA)的局灶性脑IR模型。Wistar大鼠30只，随机分为5组：正常对照组(N组n=-6)，缺血再灌注2h 常压空气组(Rt组,n=-6)，缺血再灌注24h 常压空气组(R2组，n=-6)，缺血再灌注2h HBO组(H1组，n=-6)，缺血再灌注24h HBO组(H2组，n=-6)。R1、R2、H1、H2组缺血时间均为2h。R1、R2组暴露于常压空气，H1、H2组暴露于2．5MPa氧气。病理切片用HE染色，用Swanson方法测定脑梗塞体积，用酶联免疫法测定NSE含量。结果H1、H2组与R1、R2组相比，神经元缺血性损害较轻，脑梗塞体积缩小，NSE含量明显下降，差异有统计学意义。结论HBO能减轻缺血性脑损害，保护脑组织。     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .