哑型急性肺栓塞的临床研究

目的 探讨哑型急性肺栓塞（APE）患者的临床特点和预后。方法 51 例经肺动脉增强CT确诊，但无明显肺栓塞常见临床特征的哑型APE患者予以低分子肝素钠、华法林抗凝治疗。分析患者D- 二聚体、血管彩超、心脏彩超、心电图检查结果，并观察治疗后情况，了解哑型APE患者的临床特点及预后。结果 51 例患者均痊愈出院，4 例患者因出现活动性出血停止抗凝治疗。31 例患者在3个月后复查肺动脉增强CT 未见明显栓塞征象，其余16 例患者在4~6 月后肺栓塞征象消失。结论 哑型APE患者临床表现不典型，肺动脉增强CT 检查是明确诊断的金标准，D-二聚体、心电图等可作为相应的补充，经过恰当及时的治疗，患者预后良好。     

阿司匹林与低分子肝素钠联合治疗进展性脑梗死的临床疗效

目的探讨阿司匹林与低分子肝素钠联合治疗进展性脑梗死的临床疗效。方法收集2012-10—2014-08我院就诊的155例进展性脑梗死患者,随机分为对照组77例,研究组78例,对照组口服阿司匹林肠溶片治疗,研究组采用阿司匹林肠溶片及低分子肝素钠联合治疗,比较2组临床疗效、NIHSS评分、ADL评分。结果研究组总有效率89.74%,对照组75.32%,2组疗效差异有统计学意义(P0.05)。治疗后2组NIHSS评分明显降低,ADL评分明显升高,研究组治疗后NIHSS评分较对照组明显较低,ADL评分明显较高,差异有统计学意义(P0.05)。研究组治疗后PLT、Fg较治疗前及对照组治疗后显著降低,PT、APTT明显延长,差异有统计学意义(P0.05)。且2组均未见不良反应。结论阿司匹林与低分子肝素钠联合治疗进展性脑梗死临床疗效好,可改善患者NIHSS评分及ADL评分,可以在临床推广应用。     

低分子肝素钙联合血液净化治疗重症脓毒血症的临床研究

目的探讨低分子肝素钙联合血液净化治疗重症脓毒血症的临床效果。方法用随机数字分表法将该院收治的80例重症脓毒血症患者分为对照组与观察组各40例,其中对照组采用普通肝素(HP)联合血液净化治疗,观察组采用低分子肝素钙(LMWHC)联合血液净化治疗。比较治疗前后两组患者凝血功能指标[凝血酶原时间(PT)、凝血酶时间(TT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fbg)、血小板含量(PLT)]、血清炎症因子指标[白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、C-反应蛋白(CRP)、血浆降钙素原(PCT)、血栓前体蛋白(TpP)]、肾功能指标[血肌酐(SCr)、血尿素氮(BUN)]及不良反应发生率(滤器凝血、管路凝血)的结果变化。结果治疗1周后,两组患者PT、TT、APTT水平均高于治疗前(P<0.05),且观察组均高于对照组(P<0.05);Fbg、PLT、IL-6、TNF-α、CRP、PCT、TpP、SCr、BUN水平均低于治疗前(P<0.05),且观察组均低于对照组(P<0.05);观察组不良反应发生率低于对照组(P<0.05)。结论LMWHC联合血液净化治疗重症脓毒血症可有效改善患者凝血功能与炎症反应,促进器官功能恢复。     

Effects of low molecular weight heparin in obstructed kidneys: decrease of collagen, fibronectin and TGF-beta, and increase of chondroitin/dermatan sulfate proteoglycans and macrophage infiltration.

BACKGROUND: Heparin exerts beneficial effects in different experimental models of nephropathy, as observed by the preservation of the structural morphology of the kidney after heparin therapy. Here we investigate molecular and cellular events involved in the protective effects of heparin in the progression of renal disease after unilateral ureteral obstruction. METHODS: Thirty-six rats were divided into six groups: group C (control) was not subjected to any surgical manipulation; group S (sham) was subjected to surgical manipulation but without ureteral ligation; group UUO was subjected to ureteral obstruction and received no treatment; group UUO + S was subjected to ureteral obstruction and received saline subcutaneously (s.c.) once daily; group UUO + H was subjected to ureteral obstruction and received low molecular weight heparin (LMW-Hep; 4 mg/kg) s.c. once daily; and group C + H was not subjected to any surgical manipulation and received LMW-Hep (4 mg/kg) s.c. once daily. After 14 days, the content of collagen, fibronectin, total glycosaminoglycans (GAGS), chondroitin sulfate/dermatan sulfate proteoglycans (CS/DSPGs), transforming growth factor-beta (TGF-beta) and cellular infiltration were determined in the kidneys by immunohistochemical and biochemical techniques. RESULTS: Collagen, fibronectin, total GAGS, CS/DSPGs, TGF-beta and cellular infiltration increased significantly in group UUO. LMW-Hep treatment reduced collagen, fibronectin and TGF-beta, but induced an increase in the content of total GAGS, CS/DSPGs and macrophage infiltration in group UUO + H when compared with group UUO. CONCLUSIONS: LMW-Hep diminishes fibrosis in obstructed kidneys by downregulating the synthesis of collagen, fibronectin and TGF-beta. The mechanisms underlying the overproduction of CS/DSPGs and the increase in cellular infiltration upon LMW-Hep administration remain to be elucidated.     

体外循环术后鱼精蛋白中和肝素对肺循环一氧化氮含量的影响

目的　探讨体外循环术后鱼精蛋白中和肝素对肺循环一氧化氮含量变化及体、肺循环血流动力学的影响。方法　测定 2 4例体外循环下行房间隔缺损、室间隔缺损修补术的儿童患者注射鱼精蛋白前后左、右心房血NO的终代谢产物亚硝基(NO2 -)和硝基 (NO3 -)含量。测定注射前后心率、平均动脉压、平均肺动脉压、左房压和中心静脉压。结果　注射鱼精蛋白前右房和左房NO2 -含量分别为 (3 85± 0 73) μmol/L和 (4 12± 0 85 ) μmol/L(P >0 0 5 ) ,注射后左房NO2 -含量 [(4 5 7± 0 90 )μmol/L]明显高于右房 [(4 0± 0 81) μmol/L](P <0 0 5 ) ,NO3 -含量呈类似的改变 (P <0 0 5 )。注射鱼精蛋白后平均动脉压和中心静脉压较注射前显著性降低 (P <0 0 5 ,P <0 0 1) ,其他血流动力学参数无显著性变化。结论　鱼精蛋白可以刺激体、肺循环系统合成释放一氧化氮 ,前者导致动脉压下降 ,后者可预防注射鱼精蛋白后可能出现的肺血管收缩反应     

急性肾炎贫血发病机制:神经氨酸酶致溶血作用的实验研究

为进一步确定神经氨酸酶(NM)的致急性肾炎贫血作用,本文在体外将纯化NM加入人外周血红细胞(RBC)悬液中进行培养。结果RBC逐渐出现变形和溶血;并发现该溶血过程需血清补体系统参与;肝素具有抑制和减缓NM诱导RBC溶血作用。     

Platelets of patients with peripheral arterial disease are hypersensitive to heparin

We sought to verify earlier reports of increased platelet reactivity in patients with peripheral arterial disease (PAD) during perioperative heparin administration, and to test the hypothesis of platelet hypersensitivity to heparin in these patients. Before and after incubation of platelet rich plasma with unfractionated (UH), low molecular weight heparin (LMWH), and a low molecular weight heparinoid, real-time quantitative assessment of platelet function was performed by stagnation point flow adhesio-aggregometry (SPAA) in 21 patients with PAD and 14 healthy volunteers. With SPAA the occurrence of spontaneous aggregation is pathological. In the 15 patients requiring operation, platelet function and count were measured at regular intervals. To detect heparin dependent antibodies, the heparin induced platelet activation assay (HIPA) was performed preoperatively and after 10 days of heparin therapy. Mean baseline platelet adhesion in patients was double that observed in controls (p < 0.001). Spontaneous aggregation was seen in 9 (43%) patients and no controls (p < 0.001). In controls heparinoid reduced, whereas UH and LMWH slightly increased adhesion. Spontaneous aggregation was observed once with UH. Platelets from patients showed significantly enhanced adhesiveness and aggregability (p < 0.05) with UH and LMWH when compared to controls. Effects with the heparinoid were less pronounced and non-significant. In patients requiring operation, postoperative increases in platelet function and reductions in count were significant (p < 0.001). Ten (67%) experienced a fall in platelet count of > 50%. Preoperatively the HIPA assay showed no evidence of antibodies, whereas after heparin administration antibodies were verified in 4 (32%) patients and could not be ruled out in 6 (40%). Three developed postoperative thrombosis, in one case fatal. A hypersensitive in vitro and in vivo platelet response to heparin was verified in patients with PAD and a large number developed the immunological type of heparin-associated thrombocytopenia. Our findings suggest that a thrombin antagonist which does not interact with platelets may give the best perioperative protection in these patients.     

Role of heparin and tissue type plasminogen activator in high altitude adaptation of the hemostasis system

All-Union Hematology Research Center, Ministry of Health of the USSR. Department of Human and Animal Physiology, Faculty of Biology, M. V. Lomonosov State University, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. I. Vorob'ev.) Translated from Byulletin Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 11, pp. 494–497, November, 1991.     

Heparin induces fibroblast proliferation, cell-matrix interaction and epidermal growth inhibition

Abstract We have examined the effect of heparin on fibroblasts cultivated in monolayer or in a 3-dimensional culture system: the so-called collagen lattices. Thereafter, we have investigated the effect of heparin on the kinetics of epidermal growth on the collagen lattices. In monolayer culture, heparin stimulated the fibroblast growth with an optimal response at 0.01 mg/ml. The volume of treated fibroblasts was smaller than that of untreated controls. In the collagen lattices, heparin stimulated the fibroblast growth with an optimal respone at 0.1 mg/ml. The volume of treated fibroblasts was greater than that of untreated controls, the opposite to the result observed in monolayer culture. The beginning of the contraction of the collagen lattices was inhibited by heparin. Heparin inhibited epidermal growth on the immersion as well as on the emersion collagen lattices. These effects of heparin should be the consequences of heparin-induced modifications of cell-matrix interactions.