蝮蛇抗栓酶对家兔DIC肠系膜微循环障碍的影响

本实验结果表明,蝮蛇抗栓酶可明显改善微循环障碍,增快血流速度,解除RBC聚集,促进毛细血管血流再通,减少白细胞贴壁粘附(P<0.01)。证明蝮蛇抗栓酶对实验性家兔DIC有显著治疗作用。     

蝮蛇抗栓酶对脑血栓患者血液流变学影响的观察(附52例)

应用蝮蛇抗栓酶治疗脑血栓52例,治疗前后分别测定血液流变学各项指标。结果表明,脑血栓患者的血液流变学各项指标均高于健康组;应用蝮蛇抗栓酶治疗后,随症状、体征的好转血液流变的各项指标均有显著下降(P<0.01)。     

蝮蛇抗栓酶对心脑血管疾病治疗机理及其对微循环作用的研究

本文应用蝮蛇抗栓酶治疗124例缺血性心脑血管疾病,取得满意疗效,总有效率为87.90％。用药剂量为0.008u/kg,加生理盐水250ml静滴,每日一次,15天为一疗程,共二个疗程。治疗前后血液流变学及甲襞微循环测定结果表明,蝮蛇抗栓酶具有降低血粘度(以还原粘度最为明显),改善RBC变形性,降低血小板粘附性,抑制血栓形成(P<0.05和P<0.01)。其改善微循环主要以改善流态为主,解除RBC聚集,增快血流速度,亦具有某种程度扩张微血管口径和增加毛细血管开放数的作用。 值得提出的是,蝮蛇抗栓酶对缺血性心脑血管疾病的疗效,急性期优于慢性期,以血液流态改变为主型优于以微血管痉挛为主型。     

蝮蛇抗栓酶治疗高粘滞血症939例血液流变性临床分析

高粘滞血症939例使用蝮蛇抗栓酶0.5U/天、静滴15天一疗程。一般2疗程。治疗后除血小板不下降外(P>0.05),血液流变学各项指标均下降至正常或接近正常。治疗前后有非常显著性差异(P<0.01)。其中以降低纤维蛋白原及红细胞电泳时间作用最明显;其他依次为血浆粘度、血小板粘附率、全血粘度、全血还原粘度、体外血栓形成试验、血沉方程K值、血沉、红细胞比积。对高血脂患者,蝮蛇抗栓酶也能降低总胆固醇及甘油三酯。治疗前后比较二者有显著性差异(0.05>P>0.01)。     

蝮蛇抗栓酶治疗糖尿病及其对血液流变性的影响

本文对糖尿病患病者应用蝮蛇抗栓酶进行对比观察。其中107例做了血液流变性检查。结果表明糖尿病患者存在高粘血症。62例应用蝮蛇抗栓酶治疗者,观察检测治疗前后血液流变性指标。结果提示该药有明显改善血液流变性的作用,特别是纤维蛋白原下降更为明显(P<0.01)。故该药可能对糖尿病血管并发症的治疗有积极意义。     

蝮蛇抗栓酶对家兔DIC肠系膜微循环障碍的影响

健康家兔20只,随机分为生理盐水对照组和蝮蛇抗栓酶治疗组。静注2%兔脑粉诱发DIC,剂量60 mg/kg。10分钟后,颈动脉平均压显著降低(8.1±0.37kPa),P<0.01,血流速度显著减慢,RBC重度聚集,毛细     

蝮蛇抗栓酶对冠心病心绞痛血液流变性的影响

为 验证蛇毒类抗栓药物的作用机制、提高心血管病的治疗效果 ,我院自 1992年以来应用蝮蛇抗栓酶治疗冠心病心绞痛并观察其用药前后血液流变性的变化 ,现报告如下。1　资料与方法1.1　资料本组病例均我院住院患者 ,共 35例 ,男 30例、女 5例 ,年龄 5 0～ 79岁 ,平均 6 4.5岁 ,诊断标准依据ＷＨＯ/ＩＣＨ1979年制定的“缺血性心脏病”的命名和诊断标准。其中稳定型心绞痛 8例、不稳定型心绞痛 2 6例、变异性心绞痛1例。1.2　治疗方法用蝮蛇抗栓酶 (辽宁省沈阳市康复医学研究所实验药厂生产 ,批号 92 10 0 2 ) ,皮试阴性后 ,将蝮蛇抗栓酶 0 .75…     

蝮蛇抗栓酶对失血性休克动物肾微循环血液灌流量的影响

在40只失血性休克大鼠中静脉注射不同剂量的蝮蛇抗栓酶(0.05U,0.025U/100g B.W.)后用激光多普勒微循环血流量计测定肝、脾、肾、小肠及尾部微循环血流量,结果发现肾微循环血流量在用药后5～20分均有显著增加(P<0.05),在15只家兔的类似实验中同时测定肾表面微循环血流量与肾动脉血流量(电磁血流量计),结果发现静脉注射蝮蛇抗栓酶后(0.05U/ml/kg),肾动脉血流量并无明显增加,而肾皮质微循环血液灌流量显著增加,并与尿量增加一致。作者认为蝮蛇抗栓酶具有降低肾微循环血流阻力,加快流速,增加肾皮质微循环血液灌流量的作用。     

精制蝮蛇抗栓酶治疗肺源性心脏病

精制蝮蛇抗栓酶治疗肺源性心脏病肖旭，贾振喜，周世喜我院１９９３年３月至８月共收治肺源性心脏病人５８例，用精制蝮蛇抗栓酶大剂量冲击治疗取得较好疗效，治愈率达７５％，同时测定病人外周血中凝血酶原时间（ＰＴ）、凝血酶时间（ＴＴ）、部分凝血活酶时间（ＫＰＴＴ...     

山莨菪硷、蝮蛇抗栓酶佐治狼疮性肾炎临床研究

目的观察山莨菪硷、蝮蛇抗栓酶改善狼疮性肾炎(LN)患者的肾脏微循环及高凝、高粘状态,促进患者对激素发挥良好作用的疗效.方法 70例 LN患者随机分为 A、B两组.A组常规治疗加用山莨菪硷、蝮蛇抗栓酶共 38例;B组常规治疗共 32例.两组病人治疗前后检测尿蛋白质定量、BUN、Cr,观察临床症状,对比两组疗效.结果两组临床疗效差异显著(P<0.05);两组尿蛋白、BUN、Cr变化差异显著(P<0.01). 结论山莨菪硷、蝮蛇抗栓酶佐治 LN具有一定疗效.     

蝮蛇抗栓酶治疗缺血性脑血管病的甲襞微循环及血液流变性观察

对使用蝮蛇抗栓酶、维脑路通的缺血性脑血管病患者各５０例进行甲襞微循环和血液流变指标的检测。结果表明：蝮蛇抗栓酶组用药后，微循环和血液流变各项异常指标显著下降（Ｐ＜０．０１～０．０５）。而维脑路通对脑血栓的微循环障碍、血液粘度、β－脂蛋白、甘油三酯、血小板聚集等异常指标改善不大（Ｐ＞０．０５）。提示：蝮蛇抗栓酶是优于维脑路通的降粘药物。     

缺血性心脏病患者运动引发T波交替作为危险因素价值的探讨

目的:探讨微伏T波交替(TWA)可否作为一项缺血性心脏病患者伴室性心律失常危险因素的预测指标。方法:选择经Holter心电图监测检出阵发性室速及/或有室速病史的23例缺血性心脏病患者、30例无室速的缺血性心脏病患者和39例正常人进行运动中TWA检测。TWA采用微机化6353心电图检测系统,在受检者运动至心率95~110bpm时,波间T波变异差超过1.9微伏并在心率阈值内持续出现即为阳性。结果:23例缺血性心脏病室速组中,TWA阳性14例,占60.7%,非室速缺血组阳性出现率为10%(3/30),正常对照组0%(0/39);TWA电压三组分别是2.3±1.1uV、1.1±0.6uV和0.8±0.3uV,组间差异非常显著(P<0.05或P<0.01)。结论:运动微伏TWA测定可作为缺血性心脏病室性心律失常危险因素的参考指标之一。     

Plasma brain natriuretic peptide levels in coronary heart disease with preserved systolic function

We evaluated the circulating levels of brain natriuretic peptide (BNP) in stable angina, unstable angina, and myocardial infarction relating hormone levels to extension of coronary disease and number of vessels involved after angiographic examination. We studied 86 patients consecutively undergoing angiographic coronary examination and echocardiographic evaluation for coronary heart disease. These included 15 control subjects (group 0), 21 with stable angina (group I), 26 with unstable angina (group II), and 24 with non-Q myocardial infarction (group III). Patients with heart failure, a history of myocardial infarction, or recent myocardial damage with electrocardiographic S-T elevation were excluded. BNP levels in patients with unstable angina and myocardial infarction were significantly increased with respect to the group with stable angina (P<0.01). There were no differences between the groups with unstable angina and myocardial infarction. Analysis of peptide levels in relation to the number of involved vessels demonstrated a significant increase in patients with three-vessel disease compared with subjects with one or two vessels involved (P<0.03); among subjects with mono-vessel disease, patients with left descendent anterior stenosis had a more-marked BNP elevation than subjects with stenosis in other regions (P<0.01). Hence, BNP levels appear to be elevated in coronary disease, especially in acute coronary syndromes, even in the absence of systolic dysfunction. BNP levels also seem to be related to the severity of coronary atherosclerosis and number of vessels involved. BNP could prove a novel marker for risk stratification, not only in heart failure but also in coronary heart disease.     

Plasma brain natriuretic peptide levels in coronary heart disease with preserved systolic function

Abstract. We evaluated the circulating levels of brain natriuretic peptide (BNP) in stable angina, unstable angina, and myocardial infarction relating hormone levels to extension of coronary disease and number of vessels involved after angiographic examination. We studied 86 patients consecutively undergoing angiographic coronary examination and echocardiographic evaluation for coronary heart disease. These included 15 control subjects (group 0), 21 with stable angina (group I), 26 with unstable angina (group II), and 24 with non-Q myocardial infarction (group III). Patients with heart failure, a history of myocardial infarction, or recent myocardial damage with electrocardiographic S-T elevation were excluded. BNP levels in patients with unstable angina and myocardial infarction were significantly increased with respect to the group with stable angina (P<0.01). There were no differences between the groups with unstable angina and myocardial infarction. Analysis of peptide levels in relation to the number of involved vessels demonstrated a significant increase in patients with three-vessel disease compared with subjects with one or two vessels involved (P<0.03); among subjects with mono-vessel disease, patients with left descendent anterior stenosis had a moremarked BNP elevation than subjects with stenosis in other regions (P<0.01). Hence, BNP levels appear to be elevated in coronary disease, especially in acute coronary syndromes, even in the absence of systolic dysfunction. BNP levels also seem to be related to the severity of coronary atherosclerosis and number of vessels involved. BNP could prove a novel marker for risk stratification, not only in heart failure but also in coronary heart disease.     

Soluble Antiapoptotic Molecules and Immune Activation in Chronic Heart Failure and Unstable Angina Pectoris

Programmed myocyte cell death and activation of the immune system have been shown to occur in patients with congestive heart failure. Besides, unstable angina episodes are likely to be associated with immune activation. Our aim was to evaluate the role of changes in circulating levels of soluble Fas (sFas), suggestive of an enhanced inhibitory response to ongoing apoptosis, and soluble IL2 receptor (sIL2-R), indicative of T-lymphocyte activation, in chronic heart failure and unstable angina pectoris. Thirty patients affected by chronic heart failure (20 idiopathic and 10 ischemic cardiomyopathy) and 13 patients with unstable angina were evaluated. Twenty healthy individuals matched for age and gender were used as controls. A complete biochemical determination of indexes of myocardial damage including cardiac troponin I (cTnI) and creatine kinase (MB/CK) was performed. The results demonstrated that mean levels of sFas and sIL2-R were significantly increased in patients affected by chronic heart failure and unstable angina and were not associated with changes in renal function or with serum levels of cTnI. Highest values of sFas were found in NYHA class IV patients (IV NYHA class = 7.39 ± 0.52 vs. controls = 1.34 ± 0.12 ng/ml; P < 0.01) and more elevated in idiopathic than in ischemic cardiomyopathy (3.64 ± 0.40 vs. 1.82 ± 0.37 ng/ml; P < 0.01). Moreover, in chronic heart failure patients sFas and ejection fraction were negatively correlated (P = 0.01), whereas sFas and sIL2-R were positively correlated (P < 0.01). In unstable angina patients too, sFas and sIL2-R appeared to be correlated (P = 0.03); whereas sFas (angina group = 3.18 ± 0.39 vs. controls = 1.34 ± 0.12 ng/ml; P < 0.01) and sIL2-R (angina group = 0.46 ± 0.11 vs. controls = 0.00 UI/ml; P < 0.01) were higher in angina group than in controls. In most of the cases, the increase of sFas was associated with comparable changes in sIL2-R serum levels, indicating that the activation of Fas system is strictly associated with autoimmune–inflammatory reactions. This phenomenon, both in chronic heart failure and in unstable angina, occurs in the absence of biochemical evidences of myocardial damage and seems to parallel the activation of T cell. Soluble Fas could have a role in sustaining inflammatory response and in prolonging the detrimental effects correlated with it in chronic heart failure and angina pectoris.     

The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes

BACKGROUND: Brain (B-type) natriuretic peptide is a neurohormone synthesized predominantly in ventricular myocardium. Although the circulating level of this neurohormone has been shown to provide independent prognostic information in patients with transmural myocardial infarction, few data are available for patients with acute coronary syndromes in the absence of ST-segment elevation. METHODS: We measured B-type natriuretic peptide in plasma specimens obtained a mean (+/-SD) of 40+/-20 hours after the onset of ischemic symptoms in 2525 patients from the Orbofiban in Patients with Unstable Coronary Syndromes-Thrombolysis in Myocardial Infarction 16 study. RESULTS: The base-line level of B-type natriuretic peptide was correlated with the risk of death, heart failure, and myocardial infarction at 30 days and 10 months. The unadjusted rate of death increased in a stepwise fashion among patients in increasing quartiles of base-line B-type natriuretic peptide levels (P< 0.001). This association remained significant in subgroups of patients who had myocardial infarction with ST-segment elevation (P=0.02), patients who had myocardial infarction without ST-segment elevation (P<0.001), and patients who had unstable angina (P<0.001). After adjustment for independent predictors of the long-term risk of death, the odds ratios for death at 10 months in the second, third, and fourth quartiles of B-type natriuretic peptide were 3.8 (95 percent confidence interval, 1.1 to 13.3), 4.0 (95 percent confidence interval, 1.2 to 13.7), and 5.8 (95 percent confidence interval, 1.7 to 19.7). The level of B-type natriuretic peptide was also associated with the risk of new or recurrent myocardial infarction (P=0.01) and new or worsening heart failure (P<0.001) at 10 months. CONCLUSIONS: A single measurement of B-type natriuretic peptide, obtained in the first few days after the onset of ischemic symptoms, provides powerful information for use in risk stratification across the spectrum of acute coronary syndromes. This finding suggests that cardiac neurohormonal activation may be a unifying feature among patients at high risk for death after acute coronary syndromes.     

复方缬芎提取物对心、脑组织微循环影响的实验研究

目的 :研究复方缬草 川芎提取物对心、脑组织微循环的影响。方法 :68Rb、99mTC摄入示踪法观察复方缬 芎对正常及缺血心肌和脑组织微循环的影响 ;以细胞培养法考察复方缬 芎对心肌细胞缺氧 /再给氧损伤的防护作用。结果 :复方缬 芎组的心肌组织摄取的68Rb量明显高于溶剂对照组 ,组间具有显著或极显著性差异 (P <0 .0 5或 0 .0 1) ;复方缬 芎组的脑组织摄取的99mTC量明显高于溶剂对照组 ,组间具显著或极显著性差异 (P <0 .0 5或 0 .0 1) ;复方缬 芎组缺氧 /再给氧损伤试验的心肌细胞LHD活性高于溶剂对照组 ,组间具显著性差异 (P <0 .0 5 )。结论 :复方缬草 川芎提取物可以显著增加心、脑组织微循环灌流量 ;对垂体后叶素引起的心、脑缺血有良好的防护作用 ;对心肌细胞缺氧 /再给氧损伤具有明显的保护作用     

冠心病患者血浆OLAB、BNP和CRP水平变化分析

检测冠心病患者血浆OLAB、BNP和CRP水平变化, 探讨冠心病发病机制及不稳定性心绞痛(UAP)治疗前后对其影响.用RIA和ELISA法对124例冠心病患者和30名对照者血浆中的OLAB、BNP和CRP水平变化及相关性进行研究, 同时对48例UAP经皮冠状动脉形成术(PTCA)治疗前、后对上述三项指标的变化进行分析; 结果表明冠心病患者与对照组比较BNP水平有显著性差异(P＜0.01),尤其是AMI和UAP组比SAP组升高更明显; CRP水平比对照组明显增高(P＜0.05),特别是不稳定性心绞痛和AMI组升高明显(P＜0.05);AMI组血浆OLAB水平明显高于正常和其他两组, OLAB、BNP和CRP三项在UAP组中治疗前后比较差异显著(P＜0.01).总之,OLAB、BNP和CRP参与了冠心病的发病过程, 并可预测心肌梗死患者远期心功能恢复的情况, UAP组经PTCA支架术后, 三项指标均明显降低, 可作为疗效观察的一个重要参数, OLAB参与了冠状动脉粥样硬化的全过程及AMI的发病始末.     

冷刺激对实验性心肌缺血家兔血浆内ET和血液流变学的影响

本文测定了冷刺激条件下，正常家兔和心肌缺血家兔内皮素（ＥＴ）和血液流变学各指标，结果发现冷刺激组ＥＴ高于非冷刺激组，心肌缺血组ＥＴ高于非冷刺激组，且心肌缺血二组间差值是非心肌缺血二组间差值的二倍多，说明冷刺激促进正常机体和心肌缺血机体ＥＴ分泌释放，心肌缺血机体对冷刺激反应更为敏感，同时，冷刺激下，正常机体血液流变学异常，心肌缺血家兔也在原异常基础之上呈加重趋势，提示：ＥＴ升高和血液流变异常可以作为     

家兔实验性心肌缺血损伤机制的研究

目的　研究左室前壁缺血不同时间琥珀酸脱氢酶 (SDH)和酸性磷酸酶 (ACP)活性的改变 ,探讨心肌缺血损伤的机制。方法　结扎 2 2只家兔的左冠状动脉主干建立实验性心肌缺血动物模型 ,利用硝基四氮唑蓝法和硝酸铅法研究结扎后 0 5、1、2、4、8、12h后左室前壁SDH、ACP活性的动态变化 ,并用Meta Morph/CoolSnapfx/AX70显微图像分析系统进行分析。结果　①结扎后 1hSDH平均灰度值为 97 85±8 13,缺血 2、4、8、12h平均灰度值分别为 10 5 37± 6 0 7、112 5 8± 5 18、12 4 88± 12 12和 14 4 6 0± 13 99,与对照组比较显著升高 (P<0 0 1) ;②结扎后 4hACP平均灰度值为 186 4 9± 15 70 ,缺血 8、12h平均灰度值分别为 173 16± 12 6 4和 16 2 5 1± 11 5 2 ,与对照组比较显著下降 (P <0 0 1)。结论　线粒体损伤引起的SDH活性减低和溶酶体破坏造成的ACP激活在心肌缺血损伤的发生和发展过程中可能起重要作用