冠状动脉再狭窄的动物模型

在冠脉支架应用的时代,再狭窄仍然制约着经皮冠脉介入治疗。许多动物模型被用于研究冠状动脉再狭窄的病理生理机制,并探讨其防治途径。现就近年来冠脉再狭窄动物模型研究的相关进展作一综述。     

治疗冠状动脉血栓形成的新起点

应用重组脱氧核糖核酸(DNA)技术,为临床医学提供了新的更有效,更特异性的治疗手段。这种方法对冠状动脉血栓形成的治疗带来了很大希望。由于急性心肌梗塞(AMI)是冠状动脉急性血栓闭塞的后果,应将主要努力集中在冠状动脉血栓形成的治疗上。动脉血栓形成及其后果是由于存在于血小板和血管细胞上正常促凝因子激活及血浆中抗凝因子抑制的结果,这种失调导致血栓闭塞。功脉粥样硬化可引起对血管细胞的损伤。近来根据动脉粥样硬化的发病机理,生产了一些新药以防止胆固醇沉积和动脉粥样硬化性血管损伤。虽然有些进展,但对伴有动脉粥样硬化血管性疾     

微量直流电刺激犬冠状动脉血栓形成模型的实验研究

采用改进后的冠脉外膜微量直流电刺激法建立犬冠状动脉血栓形成模型。结果提示，形成的血栓构成与人类冠脉血栓相似，方法简便可靠，血栓形成耗时短。是理想的科研实验模型。     

狗冠状动脉血栓形成模型的建立

用改良电刺激法建立狗冠状动脉血栓形成模型,结果提示所形成的血栓构成与人类动脉血栓有较好的相似性。     

冠状动脉支架内血栓形成

冠状动脉内支架是致血栓物质,主要是因为支架金属表面的阳离子电荷作用.支架的材料、形状、大小都会影响支架血栓的形成.根据支架内血栓发生的时间分为三类.(1)急性支架内血栓:24 h内进行冠状动脉造影显示支架部位血栓.(2)亚急性支架内血栓:1～30天进行冠状动脉造影见支架部位血栓形成.(3)后期支架内血栓形成:其定义为支架置入30天以上发生在支架置入部位急性血栓形成[1].     

冠状动脉支架内血栓形成(附5例报告)

目的分析冠状动脉支架内血栓形成的临床相关因素。方法回顾性分析571例冠状动脉支架治疗中的5例支架内血栓形成患者的临床资料、冠状动脉造影结果以及围手术期的抗血栓治疗等相关因素。结果5例急性冠状动脉综合征患者6处靶病变支架内血栓形成,其中3处为C型病变,4处置入药物洗脱支架。支架内血栓形成的原因:1处为支架不完全贴壁,2处支架不能完全覆盖病变,2例为患者抗血栓治疗不充分。结论冠状动脉支架内血栓形成可能与下列因素相关:(1)急性冠状动脉综合征;(2)长病变,支架贴壁不好,支架没有完全覆盖病变,使用药物涂层支架;(3)不充分的抗血栓治疗。     

冠状动脉微循环障碍实验动物模型的研究进展

<正>阻塞性冠状动脉疾病是心肌缺血的主要原因,但越来越多的研究证据表明,冠状动脉微循环障碍同样会导致心肌缺血^[1]。冠状动脉微循环障碍不仅存在于阻塞性冠状动脉疾病患者中,而且在非阻塞性冠状动脉心肌缺血患者中同样存在^[2]。在人群中进行冠状动脉微循环障碍相关研究非常困难,因此冠状动脉微循环障碍动物模型显得特别重要。我们将重点介绍作为非阻塞性冠状动脉心肌缺血重要标志的冠状动脉微循环障碍动物模型。鉴于每种冠状动脉微循环障碍动物模型都有其各自优缺点,     

不稳定型心绞痛病人冠状动脉血栓形成的机制

本文论述不稳定型心绞痛病人的冠脉粥样硬化斑破裂后血栓形成的发生机制,影响血栓形成的局部因素和全身性因素,凝血酶的作用,血栓与血管收缩的关系,残留血栓的重要性和抗血栓治疗方案。     

冠状动脉支架术后支架内亚急性血栓形成(附5例报告)

目的评价和探讨支架内亚急性血栓（SAT）的发生机制和预防。方法随访和分析2004-2007年5例冠心病患者支架置入术后发生SAT患者的临床和冠脉造影特点。结果（1）在529例冠心病支架置入患者中有5例（0.94%）发生SAT,多于术后2～5d出现。其中3例冠脉造影证实SAT,积极治疗后6个月冠脉造影随访支架内无再狭窄;2例可能为SAT;死亡2例,1例在院外死亡,均为未及时介入治疗。（2）上述5例患者中3例表现为ST抬高型心肌梗死,1例表现为急性左心衰,心源性休克,1例表现为不稳定性心绞痛。4例患者为药物洗脱支架后SAT,1例为裸支架后SAT。结论支架内SAT可能与C型病变,术中支架贴壁不良,急性心肌梗死有关,及时介入治疗可以减少不良后果的发生。     

冠状动脉支架内血栓形成原因分析

目的探讨冠状动脉支架内血栓形成（ST）的相关因素、预后及预防措施。方法对我院1999年1月-2006年8月1028例行冠状动脉支架治疗中6例ST病人的临床特征、冠状动脉造影及支架置入情况、预后及预防措施等进行分析。结果1028例病人行冠状动脉支架治疗,6例病人发生ST（0.6%）,均为急性冠脉综合征病人。其中急性ST2例,亚急性ST4例。6例ST中5例有血栓形成的高危因素。6根靶血管5根为前降支。6处靶病变均为近段病变,共置入7枚支架（4枚裸支架,3枚药物支架）,其中2枚长支架,2枚小直径支架。6例ST病人4例发生急性或再次心肌梗死,同时合并左心室收缩功能不全;1例死亡。结论ST发生可能与急性冠脉综合征、前降支病变、近段病变及置入长支架、小直径支架等因素有关。ST病人预后差。对于高危病人宜加强抗血小板、抗凝治疗及术中使用高压球囊后扩张等措施防治支架内血栓形成。     

中国小型猪冠状动脉慢性完全闭塞病变模型的建立

目的探讨采用铜丝缠绕型支架置入中国小型猪冠状动脉内的方法制作慢性完全闭塞病变（CTO）模型的可行性,建立一种新的CTO模型方法。方法 56头中国小型猪经股动脉穿刺,在前降支置入自制的铜丝缠绕型支架。分别在术前和术后1周、2周、4周、3个月、6个月时观察心电图、心脏超声和冠状动脉造影（CAG）,然后处死取出心脏,取目标冠状动脉和梗死区域心肌,做病理学检查。结果 56头猪中共8头死亡,总的死亡率14.3%（8/56）。1周、2周时目标冠状动脉均为100%闭塞;4周、3月、6月时部分动物冠状动脉未完全闭塞（血栓机化再通）,前向血流TIMI2～3级;完全闭塞的冠状动脉包括了绝对性闭塞（TIMI0级）和功能性闭塞（TIMI1级）,并出现同侧的桥侧枝循环。以4周为CTO时间点,CTO模型的成功率为66.7%（28/42）。心肌病理学和心脏超声结果显示所有存活动物均发生了心肌梗死。冠状动脉病理学发现1、2周时闭塞病变处主要为血栓和炎症细胞浸润,4周、3个月、6个月时组血栓逐渐机化,发生纤维化,病变两端形成纤维帽,中间有微血管和孔道形成,与人体CTO病变极为相似。结论该CTO模型与人体CTO病变较为相似,而且有操作简单、创伤小、成本低、死亡率低、成功率高等诸多优点,可作为实验研究较好的动物模型。     

可逆性上矢状窦血栓大鼠模型的建立

目的建立可逆性上矢状窦血栓（SSST）大鼠模型，观察模型的稳定性和成功率。方法取雄性SD大鼠90只，随机分为模型组和对照组，每组45只；模型组采用上矢状窦局部置管并注射活化部分凝血活酶试剂建立大鼠SSST模型；对照组采用上矢状窦三氯化铁滤纸贴敷法建立SSST模型。两组于手术后24h行MRI及MR静脉造影（MRV），确定造模是否成功。模型成功后，分别于1、2、3、4周行MRI、MRV，观察上矢状窦再通情况及脑组织改变；取大鼠上矢状窦顶叶皮质脑组织标本行病理学观察。结果模型组模型成功41只，成功率为91％；总再通率为10％；对照组模型成功34只，成功率为75％，总再通率为45％。两组比较差异有统计学意义，P〈0．05。模型组大鼠脑组织水肿及梗死较对照组明显，而内皮细胞损伤较对照组轻微。结论改良法建立的大鼠可逆性上矢状窦血栓模型成功率高、稳定和重复性好。     

介入法置入栓塞弹簧圈制作猪急性心肌梗死模型

目的探讨介入法在猪冠状动脉内置入栓塞弹簧圈制作急性心肌梗死模型的可行性,建立一种新的急性心肌梗死模型方法。方法 26头中国实验用小型猪经股动脉穿刺,在前降支远段置入栓塞用弹簧圈(Cook公司产,型号:35-3-3),1周内观察心肌肌钙蛋白Ⅰ、心电图和冠状动脉造影,然后处死取出心脏,取目标冠状动脉和心肌,做病理学检查。结果术中2只死于造模过程中室颤,1只死于造模过程中出现麻醉意外,23头小型猪均发生了心肌梗死,且存活在1周以上,完成复查,总的成功率为88.5%。结论该模型制作具有操作简单、创伤小、死亡率低、成功率高等诸多优点,可作为较好的实验研究动物模型。     

Thrombolytic effects of intracoronary streptokinase on canine coronary artery thrombosis

Summary The thrombolytic and hemodynamic properties of intracoronary streptokinase (SK) application were studied in anin-vivo canine model with left circumflex coronary artery thrombosis, initiated by electrical stimulation (150 A, DC for 6 h) of the artery's intima via an implanted silver wire. In pentobarbitalanesthetized, open-chest dogs acute myocardial ischemia was determined by a dehydrogenase-dependent staining of the coronary artery perfusion area. Thrombus weight was determinedpost-mortem.Saline-treated control animals developed coronary thrombosis after 3.1±0.4 h of stimulation. Thrombus weight was 64±3.1 mg. Acute infarct volume was 32±3.1% of total left ventricle, and 53±6.2% of the coronary artery risk region for infarction. At occlusive thrombosis, blood pressure, ventricular pressure and the LV dP/dt_max fell significantly, whereas heart rate and the end-diastolic filling pressure increased. Severe ST-segment elevation and loss of R wave voltage indicated myocardial ischemia. At 20 min into thrombotic vessel occlusion, 2,000 IU/min SK were infused by way of a Sonescatheter advanced to the thrombus. Coronary thrombosis consistently lysed after 12±0.7 min of SK infusion, and coronary blood flow as well as hemodynamics were restored. Only minor acute infarction was found indicating viability of ischemic jcopardized myocardium. In another group, the continuous SK-infusion (20 IU/kg/min) concomitant with electrical vessel stimulation prevented coronary thrombosis and acute ischemia, and no significant hemodynamic alterations were noted.These results indicate that intracoronary SK-infusion can lyse acute thrombosis as sequel of electrical stimulation. This prevents development of acute myocardial infarction. Continuous SK-infusion can completely prevent coronary thrombosis in response to intimal injury.Professor Dr. Otto Bayer in memoriam     

Aurintricarboxylic acid in a canine model of coronary artery thrombosis

Platelet thrombus formation occurs at sites of severe arterial narrowing where shear stress is elevated. Shear stress appears to induce platelet aggregation in vitro by means of initiation of von Willebrand factor binding to platelet glycoprotein Ib. Recent in vitro studies have demonstrated that aurintricarboxylic acid can inhibit shear stress-induced platelet aggregation. This effect is mediated by aurintricarboxylic acid binding to von Willebrand factor; this binding results in inhibition of von Willebrand factor interaction with glycoprotein Ib. In this study, we examined the effect of aurintricarboxylic acid on platelet-dependent cyclic flow reductions (CFRs) in a canine coronary stenosis model. In dose-response experiments, six animals received 4 mg/kg aurintricarboxylic acid by bolus infusion, followed by 1 mg/kg every 10 minutes. Total inhibition of CFRs was observed in all animals after 6.7 mg/kg aurintricarboxylic acid; CFRs could not be reinitiated by the thromboxane A2 analogue U46619. Continuous infusion of epinephrine (0.4 micrograms/kg/min) caused CFRs to return; however, 3.7 mg/kg additional aurintricarboxylic acid again induced total inhibition of CFRs. In addition, five animals received a bolus infusion of 10 mg/kg aurintricarboxylic acid, which caused total inhibition of CFRs. The average area of stenosis in the constricted vessels was 83%, and shear stress at the site of constriction averaged 350 dynes/cm2. Aurintricarboxylic acid did not alter hemodynamics, thrombin time, platelet count, or ADP/epinephrine-induced platelet aggregation. These data indicate that platelet glycoprotein Ib-von Willebrand factor interactions are important during coronary occlusion and that aurintricarboxylic acid can inhibit coronary thrombosis associated with coronary constriction.     

Cannabis-induced coronary artery thrombosis and acute anterior myocardial infarction in a young man

Information concerning acute myocardial infarction after cannabis usage is limited and the actual mechanism of cannabis-induced myocardial infarction is not well known. In the report, we described a young man with an acute myocardial infarction and cannabis-induced coronary thrombosis.     

葡聚糖硫酸钠致大鼠急性溃疡性结肠炎模型建立与评价

目的探讨葡聚糖硫酸钠（dextran sulfate sodium,DSS）诱导大鼠溃疡性结肠炎（ulcerative colitis,UC）急性期模型的建立。 方法60只SD大鼠,雌雄各半,随机分成空白组（n=12）、模型组（n=48）,空白组给予自由饮食,模型组给予3%DSS溶液自由饮用7天。应用疾病活动指数（DAI）及组织学评分（HI）对各组进行对比。 结果模型组DAI及HI评分与空白组比较均有统计学意义（P<0.01）。模型组均不同程度的出现腹泻、隐血试验阳性、脓血便,病理可见炎症主要累及黏膜和黏膜下层,上皮内杯状细胞减少,隐窝破坏。 结论DSS诱导的UC急性期模型的临床和病理表现与人类UC相似,是理想的UC模型之一。     

Bilateral coronary fistulae to pulmonic valve in presence of severe three-vessel coronary artery disease

A 62-year-old man was admitted to the coronary care unit due to anginal pain and palpitations--coronary angiography revealed three-vessel coronary artery disease. The unexpected finding was the presence of coronary to pulmonary artery fistulae bilaterally, from both the proximal RCA and the proximal LAD. Right heart catheterization revealed normal right ventricular and pulmonary artery pressure and absence of hemodynamically significant left to right shunt. The patient underwent a triple coronary bypass including the closure of bilateral fistulae, which were draining into the left sinus of the pulmonary valve. One month after the operation he was in good health and had no complaints. Bilateral coronary artery fistulae is a rare anomaly diagnosed in 0.002-0.0013% of adult coronary angiograms. (Int J Cardiovasc Intervent 1999; 2: 249-251).