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.     

用模型方法研究灌注压对缺血区心肌血流时相分布的影响

为了研究在舒张期提高冠脉灌注压对缺血区血流时相分布的影响,建立了一个左心室壁血流灌注仿真模型。模型中正常心肌和缺血心肌中血管网都用３个支路来代表,各个支路由符合生理实际的非线性时变阻容元件组成。以６条雄性犬的左心室压和主动脉压的实测数据作为输入进行仿真,得出了符合已有实验观察的结论。结果表明：舒张期提高灌注压对缺血心肌的血流灌注有明显改善。     

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。     

刺五加对大鼠脑缺血损伤修复作用的研究

采用双侧颈总动脉结扎制作SD大鼠暂时性全脑缺血模型,手术后尾静脉分别注射药物刺五加注射液或生理盐水进行观察和神经行为学评分,制片作常规HE染色和Nestin免疫组化染色检测缺血损伤后的修复情况.神经行为学评分显示刺五加组神经功能恢复明显好于生理盐水组.脑缺血再灌注后3d时海马、室管膜和室管膜下区神经干细胞有少量Nestin阳性表达;脑缺血再灌注后5d和7d时海马、室管膜、室管膜下区和缺血区神经干细胞阳性Nestin阳性细胞数明显增加,尤其在缺血区,刺五加组Nestin阳性表达细胞数显著多于生理盐水对照组.     

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.     

灯盏花素葡萄糖注射液的药效学研究

目的验证灯盏花素葡萄糖注射液的临床前药效学作用;方法选择不同的药理学指标对灯盏花素葡萄糖注射液的药效学作用进行评价;结果灯盏花素葡萄糖注射液对实验性大鼠急性脑缺血具有显著的保护作用,可使大鼠血液中纤维蛋白溶解酶活性明显增加,对大鼠血液血栓形成具有明显的抑制作用,可使小鼠血液凝血时间显著性延长,对小鼠肠系膜微循环具有明显的改善作用,具有明显抑制血小板聚集的功能,亦可显著性降低家兔脑血管阻力,改善脑循环;结论试验结果证明了灯盏花素葡萄糖注射液具有良好的活血化瘀作用,对改善脑血循环、增加脑血流量、降低脑血管阻力、急性脑缺血改善、增加血液纤溶酶活性、防治血液血栓形成等功效显著;讨论研究结果与文献相关报道基本一致,为其临床广泛应用提供了有力的科学依据.     

体外反搏对犬动脉剪切应力参数的影响

为研究体外反搏对不同情况下剪切应力参数的影响，对18条开胸犬实时测量颈主动脉，头臂干和胸主动脉等处的血流量，计算出各处剪切应力的变化，结果表明，急性心肌缺血和体外反搏可以使剪切应力的平均值，变化范围和变化速率发生变化，即改变了剪切应力的脉动性。     

大鼠不完全性视网膜缺血的组织学变化

采用双侧颈总动脉阻断血流（２ＶＯ）的方法，造成大鼠不完全性视网膜缺血，用组织学方法观察了不同缺血时间（３０、９０ｍｉｎ，４、７、３０ｄ）的缺血后再灌注与不再灌流对视网膜变化的影响。结果显示：缺血３０和９０ｍｉｎ再灌流４ｄ后，内炕网膜（包括外网层、内核层、内网层、节细胞层、神经纤维怪和内界膜）明显增厚；其他不再灌流的缺血组，厚度趋向减少。节细胞计数随缺血时间延长逐渐减少；缺血４ｄ后明显减少。提示不完     

Cerebral ischemia revisited: New insights as revealed using in vitro brain slice preparations

Summary The elucidation of the pathophysiological mechanisms of cerebral ischemia/hypoxia dictates the use of experimental models which mimic this disabling brain condition. In vivo experimental models have been available for many decades and are responsible for the bulk of, though incomplete, knowledge we have about these mechanisms. Since study in isolation of each postulated mechanism is impossible in vivo, the need for an in vitro experimental model has intensified in recent years. Consequently, rat and guinea pig hippocampal slice preparations have emerged as the models of choice. This review attempts to highlight some of the results obtained using brain slices in the study of cerebral ischemia/hypoxia and compare them to those obtained in vivo. Both the biochemical and the physiological correlates of energy metabolism, ion homeostasis, neurotransmission and neuromodulation of this brain condition are reviewed. The agreements, and especially the disagreements, between the in vivo and in vitro findings are emphasized. Details are given of the possible roles of both lactic acid, Ca²⁺ and excitotoxins in the neuronal damage inflicted by cerebral ischemia/hypoxia. Recent attempts to protect brain slices against experimental cerebral ischemic/hypoxic damage are also reviewed here briefly.