盐酸替罗非班对急性心肌梗死急诊经皮冠状动脉介入治疗中TIMI血流影响的临床研究

目的分析Ⅱb/Ⅲa受体拮抗剂盐酸替罗非班对ST段抬高急性心肌梗死(STEMI)患者急诊经皮冠状动脉介入治疗(PCI)治疗中TIMI血流的影响。方法选择急诊入院STEMI患者48名,分为试验组(盐酸替罗非班+PCI)27例和对照组(直接PCI)21例。收集所有病例的临床和冠状动脉造影资料,观察PCI术前、术后TIMI血流情况。结果试验组于术前应用盐酸替罗非班使PCI前梗死相关血管TIMI血流分级提高,试验组达1级血流者比例高于对照组(37%比9.5%,P<0.05);对照组完全闭塞者比例明显高于试验组(38.1%比7.4%,P<0.01);两组患者PCI术后TIMI3级血流比例差异无统计学意义,TIMI2级血流比例试验组低于对照组。结论Ⅱb/Ⅲa受体拮抗剂盐酸替罗非班可改善STEMI患者梗死相关血管的TIMI血流。  

中国成人血脂异常诊断和危险分层方案的研究

目的为配合制订《中国成人血脂异常防治指南》，提出适合我国人群疾病和危险因素特点的血脂异常诊断界值和以血脂异常为基础的危险分层方案建议，以期更好地指导我国的血脂异常防治工作。方法汇总“中美心肺疾病流行病学合作研究”和“中国多省市心血管病队列研究”资料（基线入组共计40719人，年龄35—64岁，男女约各半，随访总计345140．5人年），用统一的分析方案分析血脂异常与缺血性心血管病发病（ICVD，包括冠心病事件和缺血性脑卒中事件）的关系。相对危险的估计采用多元Cox比例风险模型，并控制其他危险因素。采用该模型计算不同危险因素组合时一个50岁的人今后10年发生缺血性心血管病的绝对危险，用于确定危险分层方案。结果两队列均呈现如下规律：（1）TC和LDL-C水平与ICVD发病危险的关系是连续性的，并无明显的拐点；（2）LDL—C〈3．37mmol／L（130mg／dl）与TC〈5．18mmol／L（200mg／dl）的发病率（绝对危险）基本接近，而LDL—C〈4．14mmol／L（160mg／dl）与TC〈6．22mmol／L（240mg／dl）的发病率基本接近；（3）TC〈5．18mmol／L（200mg／dl）时的绝对危险略高于理想血压[〈120／80mmHg（1mmHg=0．133kPa）]时的绝对危险，TC≥6．22mmol／L（240mg／dl）时的绝对危险略低于高血压1级的绝对危险；（4）随着HDL—C水平的降低，ICVD发病危险增加；（5）TG与ICVD发病危险间未见显著关联；（6）在任一TC水平，仅合并高血压时ICVD发病的绝对危险已高于合并3个其他危险因素时ICVD发病的绝对危险。结论我国人群血脂异常诊断标准可准确定为：TC〈5．18mmol／L（200mg／dl）或LDL—C〈3．37mmol／L（130mg／dl）为合适范围，TC5．18—6．19mmol／L（200～239mg／dl）或LDL．C3．37～4．12mmol／L（130～159mg／dl）为边缘升高，TC≥6．22mmol／L（240mg／dl）或LDL-C≥4．14mmol／L（160ms／dl）为升高。HDL—C〈1．04mmol／L（40mg／dl）为减低，1．04～1．53mmol／L（40～59mg／dl）为正常，≥1．55mmol／L（60mg／dl）为理想水平。此标准与国际相关标准一致。在危险分层方案中高血压的作用相当于其他任意3个危险因素的作用之和。  

细胞间粘附分子—1表达水平对心肌再灌注损伤的影响及N—乙 …

探讨细胞间粘附分子表达与中性粒细胞浸润与心肌血再灌注损伤的关系并观察Ｎ－乙酰半胱氨酸对ＩＲＩ的保护效果。方法大鼠１１６只，分设：（１）缺血再灌注（ＩＲ）组；（２）ＩＲ＋ＮＡＣ组；（３）假手术对照组，并分庙再灌注１、３、６、１２、２４ｈ时相点。取缺血心肌用原位杂交和免疫组织检测ＩＣＡＭ－１ｍＲＮＡ及其蛋白表达水平，用酶法测定ＰＭＮｓ浸润数，ＴＴＣ染色法测心肌梗死范围，结果心肌再灌注时，ＩＣＡＭ－１表  

Transient increase in plasma brain (B-type) natriuretic peptide after percutaneous transluminal coronary angioplasty

BACKGROUND: Brain (B-type) natriuretic peptide (BNP) is known to be secreted predominantly from the myocardium. Brain natriuretic peptide plasma concentrations have been shown to be markedly increased in patients with acute myocardial infarction; however, plasma BNP response during episodes of myocardial ischemia has not been established. HYPOTHESIS: This study was designed to examine plasma BNP in patients with transient myocardial ischemia induced by inflation of a percutaneous transluminal coronary angioplasty (PTCA) balloon. METHODS: Thirty consecutive patients (26 men and 4 women; mean age 61 years) who underwent PTCA, and another 49 patients (39 men and 10 women; mean age 63 years) who underwent diagnostic coronary angiography were enrolled in this study. Serum BNP concentrations were assayed in all patients. RESULTS: Plasma BNP was increased significantly with a peak concentration of 66.1 +/- 65.2 pg/ml 24 h after PTCA. Coronary angiography did not cause plasma BNP increase (immediately before 30.4 +/- 29.0 pg/ml, 24 h after 33.7 +/- 30.6 pg/ml). No significant differences were present in hemodynamic parameters measured immediately before and 24 h after PTCA. CONCLUSION: Plasma BNP is increased by transient myocardial ischemia induced by PTCA.  

实验性家兔缺血预适应减轻心肌细胞凋亡

为探讨缺血预适应在预防或减轻心肌损伤和心肌细胞凋亡中的作用，制备了家兔缺血预适应、缺血－再灌注损伤和持续缺血模型，并采用末端脱氧核苷酸转换酶介导的生物素平移缺口末端标记技术检测心肌细胞凋亡情况；同时观察外周血心肌酶、氧自由基等水平。结果发现，再灌注损伤组和持续缺血组血清心肌酶含量明显高于正常组和无显著差异（Ｐ〉０．０５）；同时，前两组的血浆过氧化物歧化酶活性明显降低（Ｐ〈０．０１），而在正常组和缺  

极化液对缺血/再灌大鼠心肌细胞死亡及心脏功能的影响:胰岛素的关键作用

目的　探讨葡萄糖 胰岛素 钾极化液 (GIK)对心肌缺血 /再灌 (MI/R)后心肌细胞死亡(坏死和凋亡 )及心脏功能的影响 ,并比较和分析GIK各组分在其中的作用。方法　制备大鼠MI/R模型 ,分别用生理盐水、GIK、葡萄糖 钾液 (GK)或胰岛素干预分组。观察动脉血压、血糖、左室压等的变化 ,再灌注结束后检测心肌梗死或提取DNA检测心肌细胞凋亡。结果　MI/R造成明显的心脏功能障碍、心肌梗死和缺血区细胞凋亡。GIK与胰岛素 (而非GK)具有相似的减轻再灌注心肌损伤作用 ,包括减少心肌梗死范围 [(41 3± 8 3) %和 (39 6± 8 6) %比对照组 (54 4± 1 0 4) % ,q =4 34和q=4 90 ,P值均 <0 0 5]、减弱DNA梯带形成及促进再灌后心脏收缩 /舒张功能恢复。结论　GIK可减少心肌梗死、促进缺血心脏功能恢复 ,胰岛素可能通过抑制缺血心肌细胞凋亡在GIK心肌保护中发挥关键作用。  

Production of free radicals and lipid peroxides in early experimental myocardial ischemia

Free radicals and lipid peroxides have recently been identified by us [1, 2, 3] as metabolic intermediates during acute myocardial ischemia. The mechanisms by which evolving myocardial ischemia initiates free radical production are not clear. Based on studies in vitro, it is feasible to consider the following possibilities: (a) dissociation of intramitochondrial electron support system and altered phospholipid integrity with inactivation of cytochrome oxidase, which results in release of ubisemiquinone, flavoprotein and superoxide radicals; (b) accumulation and increased release of intra/extracellular metabolites like NADH, lactate flavoproteins and catecholamines which react either with themselves or with O2 and ascorbic acid; (c) interaction of the metabolic product hypoxanthine with O2 in the presence of xanthine oxidase and (d) activation of phospholipase by calcium influx with enhanced arachidonic acid metabolism and superoxide radical production. Detailed in vitro radiobiological studies [4] have demonstrated that free radical reactions occur even at very low O2 tensions (83% of maximum rate of PO2 approximately 6 mmHg and 50% at PO2 approximately 1 mmHg), and Smith [5] has demonstrated that free radical peroxidation takes place quite rapidly in rat brain homogenates incubated in gas mixtures containing only 5% O2. Thus, the low oxygen tensions in ischemic tissue are adequate to support free radical reactions. The free radicals thus produced may initiate and enhance lipid peroxidation by attacking polyunsaturated membrane lipids.  

大鼠心肌缺血/再灌注损伤心肌细胞凋亡与Fas、FasL基因表达的变化

目的：探讨大鼠实验性心肌缺血再灌注时心肌细胞凋亡与Fas及Fas蛋白配体（Fas Ligand,FasL）基因表达的变化及与心肌组织损伤的关系。方法：以穿线结扎或松扎左冠状动脉制备大鼠心肌缺血再灌注模型。64只大鼠随机分成假手术组（假手术24h）、缺血再灌注I组（缺血30min、再灌注24h）、缺血再灌注Ⅱ组（缺备30min、再灌注72h）及缺血再灌注Ⅲ组（缺血3h、再灌注24h）。以缺口末端标记法检测心肌细胞凋亡的变化，S－P免疫组化法分别检测Fas与FasL蛋白水平变化，采用逆转录聚合酶链反应法检测Fas基因mRNA的表达改变，并分析心肌组织病理学损伤程度。结果：心肌缺血再灌注后心肌细胞凋亡指数Fas蛋白阳性染色指数与炎性细胞FasL蛋白阳性染色指数均增加，且均随缺血或再灌注时间延长而进一步增高； Fas基因的mRNA表达也上调，但以再灌注24h时达高峰；心肌缺血再灌注后心肌组织呈大小不一的灶性坏死，坏死周围有爆炸性一细胞浸润。结论：心肌缺血再灌注时心肌细胞凋亡、Fas基因的蛋白与mRNA表达水平及炎性细胞的FasL蛋白表达量均增加，心肌细胞凋亡与Fas/FasL系统参与了心肌缺血再灌注损伤过程。  

Erythropoietin in cardiovascular diseases.

Several studies showed that anaemia is commonly observed in patients with Chronic Heart Failure (CHF) and is associated with worsened symptoms and survival. When anaemia in these patients is treated with erythropoietin (EPO), a significant improvement in cardiac function and symptoms was observed. Although it was originally believed that EPO specifically acted on haematopoietical cells, recent evidence demonstrated several non-haematopoietical effects. Ischaemia/reperfusion experiments in rat heart and brain showed large infarct reduction when treated with EPO. Other effects of EPO are related to its pro-angiogenic effects on endothelial cells, which could be of potential value in patients with ischaemic heart disease. These preclinical findings suggest that EPO may have potential effects in cardiovascular disease beyond correction of haemoglobin levels.  

低分子肝素对无症状心肌缺血的治疗

目的 :探讨低分子肝素 (L MWH)在治疗无症状心肌缺血 (SMI)中的临床疗效。方法 :将 6 6例 SMI患者随机分成 A组和 B组 ,每组各 33例 ,均服用抗心肌缺血基础药物 ,A组加用 L MWH0 .4ml(410 0抗 Xa IU) ,每日 1次 ,腹壁皮下注射 ,连续 15 d。B组阿司匹林 75 mg每晚顿服。观察用药前后动态心电图 (DCG)、血液粘稠度、红细胞聚集指数、血小板聚集率、血总胆固醇、甘油三酯等变化。结果 :A组 DCG心肌缺血改善总有效率93.9% ,明显优于 B组 (P <0 .0 0 1)。 A组全血粘度、血浆粘度、全血还原粘度均显著降低 (P <0 .0 1～ 0 .0 0 5 ) ;血小板聚集率显著降低 (P <0 .0 1) ;血总胆固醇、甘油三酯降低显著 (P <0 .0 5 ) ;A组疗效明显优于 B组 (P <0 .0 5～ 0 .0 1)。结论 :L MWH能改善 SMI