Detecting myocardial ischemia with 2-D CVIB imaging method--an in vivo animal experiment study

A 2-D cyclic variation of integrated backscatter (CVIB) imaging method was established for detecting myocardial ischemia. To demonstrate the feasibility and validity of this method, animal experiments were conducted. Acute myocardial ischemia was induced by occluding left anterior descending coronary artery in 10 anesthetized open-chest dogs. While scanning the normal hearts and the ischemic hearts with a B scanner, digital radiofrequency data were acquired by a real-time acquisition system in synchronism. The offline analysis to the radio-frequency signal with the 2-D CVIB imaging method was performed to verify the consistency between the imaging result and the design of the experiment. In addition, 4 dogs in experiment were treated with the heart pacemaker in order to investigate the influence of changing in heart rate on the detection of ischemic myocardium with the proposed method. The experimental result showed that the 2-D CVIB imaging method succeeded in detecting the ischemic myocardium and is a new non-invasive way for the cardiologists to both quantitatively and visually evaluate the contractile performance of the myocardium.     

硝酸酯类药物临床应用

硝酸酯类药物,在临床上广泛用于治疗心绞痛,其对血管平滑肌有舒张作用。小剂量时可扩张静脉,使静脉回流减少,左室舒末压下降,使心脏前负荷降低,降低心肌耗氧量。较大剂量时,也能舒张外周阻力血管和心肌阻力血管从而降低血压,还可以间接地增强心肌收缩力。硝酸酯类药物可增加冠脉缺血区的血流量,增强缺血区的节段收缩,从而达到抗心肌缺血、抗心绞痛的作用。临床医生只有了解了硝酸酯类药物的药理性质、作用机制、用量、用法及副作用,在临床工作中,才能更好地治疗疾病。     

血管紧张素与一氧化氮的调节平衡对缺血心肌的作用

在心血管系统中,肾素 血管紧张素系统是重要的体液调节系统,一氧化氮是具有多种作用的重要的细胞信使。本文就这二者之间的联系对于缺血心肌的影响及血管内皮生长因子表达的机制作一综述。     

二十二碳六烯酸乙酯对沙土鼠缺血再灌注脑损伤及水肿作用的研究

研究二十二碳六烯酸乙酯(E-DHA)对沙土鼠缺血再灌注脑损伤及其脑水肿的影响.选用雄性断奶沙土鼠灌胃给予二十二碳六烯酸乙酯(150 mg/(kg·d))或等体积溶媒10周,阻断沙土鼠双侧颈总动脉血流10 min,造成缺血再灌注模型;测定再灌注后脑组织中丙二醛(MDA)水平,还原型谷胱甘肽(GSH)含量,超歧化氧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和钾、钠-ATP酶(Na ,K -ATPase)活性,脑水含量,钠、钾离子浓度及海马CA1区神经细胞存活百分数.结果表明:E-DHA预处理显著降低缺血再灌注沙土鼠脑组织MDA水平,阻止GSH含量、GSH-PX和Na ,K -ATPase活性下降,而对SOD的活性未表现出明显作用;E-DHA亦调节缺血再灌注沙土鼠脑组织钠、钾离子浓度,减轻缺血再灌注所致的脑水肿和神经细胞死亡.提示E-DHA对脑缺血再灌注脑损伤有显著保护作用,机制可能其与抗氧化作用有关.     

脑缺血损伤的研究进展

缺血性脑血管疾病是一种致死致残的常见病、多发病. 近年来,对脑缺血再灌注损伤的研究越来越深入. 大量的实验研究表明,脑缺血再灌注损伤对脑损害的机制是非常复杂的,在缺血性损伤过程中除缺氧和能量代谢衰竭外,由缺血诱导的一系列瀑布样效应是导致缺血性神经元死亡的重要机制. 同时脑缺血损伤的研究受到很多因素的影响,诸如血糖浓度、脑温、脑血流量、血压、鼠种以及大鼠的性别等. 本文就脑缺血损伤的相关病理生理机制、影响因素及治疗等方面的进展进行综述,以期对缺血后神经元的死亡机制作进一步的探索.     

rAAV1载体介导外源性VEGF-165和Angiopoietin-1基因治疗大鼠脑缺血的疗效评价及其机制研究

为研究经脑室途径联合应用血管内皮生长因子（VEGF）和血管生成素（Angiopoietin-1,Ang-1）,治疗大鼠急性脑梗塞的效果,并探讨治疗的机制。采用脑立体定向输注的方法,将rAAV1-VEGF治疗载体或者rAAV1-VEGF和rAAV1-Ang-1的混合治疗载体,通过侧脑室转染途径对大鼠大脑中动脉阻塞缺血再灌注模型进行基因治疗。观测VEGF和Ang-1蛋白表达、血脑屏障通透性、脑微血管密度等指标,并对大鼠进行神经功能行为评分等。结果显示,联合应用VEGF和Ang-1治疗急性脑梗塞可降低血脑屏障通透性,减轻脑水肿。增加缺血灶周围脑区的微血管密度,改善大鼠的神经功能。由此得出结论：联合应用VEGF和Ang-1基因治疗大鼠急性脑缺血。可保护脑细胞,促进新生血管生成,减轻脑水肿。改善大鼠的神经功能。     

瑞替普酶溶栓治疗急性心肌梗死的疗效观察

目的:研究ST段抬高的急性心肌梗死(STEMI)发病后不同时间溶栓的疗效和不良反应.方法:对86例住院的STEMI患者用瑞替普酶行溶栓治疗,依据发病到溶栓开始的时间将86例患者分为三组:A组≤lh (n=28),B组>lh,但<6h(n=36),C组>6h,但≤12h(n=22),观察梗塞相关动脉(IRA)的开通率、5周病死率和溶栓副作用.结果:IRA开通率:A组92.9%(26/28),B组86.1%(31/36),C组45.5%(10/22),C组与A、B两组差异性显著(P<0.01),A、B两组间无显著性差异(P>0.05).病死率:A组、B组和C组的5周病死率分别为0%(0/28),2.77%(1/36)和4.54%(1/22).A、B两组间无显著性差异[0%(0/28)vs 2.77%(1/36),P>0.05],A组与C组有显著性差异[0%(0/28)VS 4.54%(1/22),P<0.01],B组与c组有显著性差异[2.77%(1/36)V8 4.54%(1/22),P<0.01],三组中均无包括脑出血在内的重大出血并发症.结论:瑞替普酶溶栓治疗STEMI疗效好、安全性高.     

连续生产精品肝素钠的新工艺

本文首次报道连续生产精品肝素钠的新工艺。猪小肠粘膜的提取液在用离子交换树脂吸附之前,先经过氧化除杂蛋白和脱色过程,既提高了树脂对肝素钠的吸附率,同时也减轻提取液中杂质对树脂的竞争和毒害。肝素钠从树脂上被洗脱后,再连续地进行再氧化、除酸、碱性蛋白和核酸、酒精反复沉淀等工艺过程,生产出精品肝素钠,效价为156±5u/mg,得率为1.092±0.035亿单位/1000kg粘膜,本工艺具有较大的应用价值。     

Pyruvate dehydrogenase kinase regulatory mechanisms and inhibition in treating diabetes, heart ischemia, and cancer

The fraction of pyruvate dehydrogenase complex (PDC) in the active form is reduced by the activities of dedicated PD kinase isozymes (PDK1, PDK2, PDK3 and PDK4). Via binding to the inner lipoyl domain (L2) of the dihydrolipoyl acetyltransferase (E2 60mer), PDK rapidly access their E2-bound PD substrate. The E2-enhanced activity of the widely distributed PDK2 is limited by dissociation of ADP from its C-terminal catalytic domain, and this is further slowed by pyruvate binding to the N-terminal regulatory (R) domain. Via the reverse of the PDC reaction, NADH and acetyl-CoA reductively acetylate lipoyl group of L2, which binds to the R domain and stimulates PDK2 activity by speeding up ADP dissociation. Activation of PDC by synthetic PDK inhibitors binding at the pyruvate or lipoyl binding sites decreased damage during heart ischemia and lowered blood glucose in insulin-resistant animals. PDC activation also triggers apoptosis in cancer cells that selectively convert glucose to lactate. Received 25 August 2006; received after revision 20 November 2006; accepted 20 December 2006     

胰岛素预处理对心肌缺血性损伤的延迟相保护

探讨胰岛素预处理对大鼠心肌缺血／再灌注（I／R）的延迟相保护作用．健康Wistar大鼠,随机分成假手术组（Sham）、缺血／再灌注组（I／R）、雷米普利组（RMP）、胰岛素低剂量组（INSL）和高剂量组（INSH）．结扎冠状动脉左前降支建立大鼠在体心肌I／R模型,Sham组大鼠穿线不结扎．TTC法观察心肌梗死面积,比色法检测血清乳酸脱氢酶（LDH）和肌酸激酶（CK）的活力．结果显示,I／R组心肌梗死面积大于Sham组（P〈0．01）,而RMP、INSL和1NSH组心肌梗死面积低于I／R组（P〈0．01）;I／R组血清LDH活力高于Sham组（P〈0．01）,而RMP和INSL组血清LDH活力均低于L／R组（P〈0．01,P〈0．05）;各组血清CK活力无显著性差异．结果表明,胰岛素预处理对大鼠心肌I／R损伤有延迟相保护作用．