股骨多段闭合骨折病人术前凝血功能的变化

目的 探讨股骨多段闭合骨折病人术前凝血功能的变化。方法 选择创伤股骨多段闭合骨折后当天入院的病人20例,年龄19-45岁,ASA Ⅰ级,为试验组(Ⅰ组);选择健康成年人15人,年龄21-39岁,作为对照组(Ⅱ组);Ⅱ组于清晨空腹采上肢静脉血标本,Ⅰ组病人入院后于骨折的第2天、第6天(手术当天清晨)空腹采上肢静脉血样本,检测血栓弹力图(TEG)指标[R时间、K时间、α角、血栓最大幅度(MA)、血栓硬度(G)]、D-二聚体浓度(D-Di)、血小板计数(PLC)及血小板聚集率(PAgR)的变化。结果 Ⅱ组TEG指标、D-Di、PLC及PAgR均在正常范围。与Ⅱ组比较,Ⅰ组骨折后第2天,K时间缩短(P<0.05),α角、MA、G及D-Di增高(P<0.01);骨折后第6天,R时间缩短(P<0.05),α角、MA、G、D-Di、PLC及PagR增高(P<0.01)。与骨折后第2天比较,Ⅰ组骨折后第6天MA、G、PLT及PAgR增高(P<0.05或0.01)。结论 病人创伤骨折后凝血功能24 h内增强,随时间的延长至术日呈高凝状态,应加强术中管理,并采取相应措施预防术中静脉血栓的发生。     

卡介苗配用腺苷接种提高巨噬细胞抗结核杆菌效能的研究

目的　通过腺苷 (ADO)改善卡介苗 (BCG)初次免疫接种效果 ,提高巨噬细胞抗结核杆菌毒力株效能。方法　将BALB/C小鼠随机分BCG组、ADO组和对照组。对BCG、ADO两组分别一次性皮内注射卡介苗 0 1ml。对ADO组腹腔注射ADO 30mg/(kg·d) ,对BCG组、对照组腹腔注射生理盐水 0 1ml/d ,共 5d。 6周后 ,三组均经血管接种人型结核分枝杆菌标准毒力株 1× 10 6CFU ,BCG组、ADO组于结核杆菌感染后第 10、2 0天和 30天分批取材 ,对照组于第 30天取材。将肺、脾用多聚甲醛固定 ,石蜡包埋 ,HE染色与抗酸染色 ,进行原位细胞凋亡检测。结果　对照组结核杆菌感染后第30天 ,肺组织大部分实变 ,以中性粒细胞浸润为主 ,结核结节多 ,肺实变与肺泡隔重度增宽处弥漫分布大量菌体 ;BCG组于感染后第 10～ 30天肺泡隔增宽 ,逐渐加重至肺大部分实变 ,间质内以淋巴细胞浸润为主 ,结核结节较少 ,肺内大量菌体 ;而ADO组肺实变和肺泡隔重度增宽的面积较小 ,间质内以单核细胞浸润为主 ,结核结节很少 ,肺内菌体明显减少。结论　ADO促进BCG诱导的免疫记忆性反应中能引起单核 巨噬细胞的数量增多和杀菌能力的增强     

Prostaglandin E1 and dibutyryl cyclic AMP enhance platelet resistance to deformation

The effect of prostaglandin E₁ (PGE₁) on platelets is mediated through the PGE₁ receptor and the consequent maintenance of the platelet's discoid shape. The effects of PGE₁ and dibutyryl cAMP (dbcAMP) on the deformability of human platelets were studied. Deformability tests based upon the micropipette aspiration on the platelets were performed by using pipettes with radii (Rp) of 0.26-0.36 gm. The time course of the extension length (Dp, in μg) of the platelets in response to aspiration with a negative pressure (ΔP) of 5 cm H₂ O (ΔP × Rp = 0.15 dynes/cm) was analyzed. PGE₁ treatment (0.1 μM) resulted in a decrease of platelet deformability as compared with results obtained for apparently non-activated, control platelets. The deformation index, i.e., Dp/Rp (PGE₁ -treated) / Dp/Rp (control), was significantly reduced to 0.90 ± 0.04. DbcAMP treatment also significantly decreased the deformability of platelets and this decrease was dbcAMP dose dependent. In contrast, colchicine- or cytochalasin D-treated platelets increased deformability. PGE₁ -treated platelets had a higher [cAMP]_i than controls. Platelets treated with PGE₁ or dbcAMP showed a reduced [Ca²⁺]i increment induced by thrombin as compared to non-treated controls. These results indicate that PGE₁ and dbcAMP treatment of platelets is accompanied by an enhancement of platelet resistance to deformation. The increased [cAMP]_i and low [Ca²⁺]_i after PGE₁ treatment may limit the rearrangement of cytoskeleton and thus enhance platelet resistance to deformation.     

4-芳杂环胺甲基酚衍生物的体外抗血小板聚集活性

血小板体内聚集可使心肌微循环功能产生障碍,导致心律失常或心肌梗塞,血小板聚集在心脑血管疾病的发病机理中起着重要作用,因而对抗血小板聚集药物的研究日益引起人们     

A double-blind cross-over study of nifedipine retard in patients with Raynaud's phenomenon

Summary The effectiveness of nifedipine retard as a treatment for Raynaud's phenomenon was assessed in 15 patients in a placebo controlled double blind study. An associated connective tissue disease was evident in 7 patients. Changes in finger and forearm blood flow (venous occlusion plethysmography), digital skin temperature and digital systolic pressure were measured acutely before and after a 2-week treatment period. Subjective assessment of efficacy was based on patient diary data. In addition alpha₂-adrenoceptor density on platelets was measured before and after chronic nifedipine therapy in both the patient group and in an age-and-sex-matched control group. No significant haemodynamic changes were observed. Nifedipine retard significantly reduced the frequency (p<0.05) with no change in either the duration or severity of vasospastic attacks. Side effects were commono following nifedipine retard. A reduction in alpha₂-adrenoceptor density on platelets was observed in patients compared to a control group (p<0.05). Alpha₂-adrenoceptor density was unchanged following a 2-week treatment period with nifedipine retard. This study concludes that nifedipine retard is not effective in the treatment of Raynaud's phenomenon over a short time course. Patients with Raynaud's phenomenon have reduced alpha₂-adrenoceptor densities on their platelets.     

Epileptogenic actions of xanthines in relation to their affinities for adenosine A1 receptors in CA3 neurons of hippocampal slices (guinea pig)

In order to analyze the epileptogenic mechanisms of caffaine and related xanthines, putative effects of these drugs were studied on adenosine receptors of CA3 neurons in hippocampal slices. Epileptogenic concentrations of different xanthine derivatives strongly correlated with their affinities for the inhibitory A₁ adenosine receptor subtype. The A₁ receptor agonists adenosine and R-PIA reversibly depressed xanthine-induced epileptic activity without effects on the resting membrane potential or on spontaneously occuring action potentials. These findings suggest that the epileptogenic potency of xanthines is primarily due to the blockade of the A₁ receptors through an abnormal rise of intracellular cAMP and to the excessive transmembrane calcium fluxes underlying paroxysmal depolarization shifts.     

粉防己碱与牛磺酸合用对血小板聚集与血栓形成的影响

粉防己碱（Ｔｅｔ）和牛磺酸（Ｔａｕ）均能抑制ＡＤＰ、胶原和凝血酶诱导的大鼠血小板聚集及血栓形成。Ｔｅｔ抑制ＡＤＰ诱导聚集较强，Ｔａｕ则对胶原作用最明显，二药减半量合并应用时，较各药单用强     

人参总甙对正常家兔血液流变学的影响

本实验采用小剂量、长期给药的方法观察了人参总甙对正常家兔血液流变学的影响。结果表明人参总甙具有降低正常家兔血液粘度和血小板聚集性的作用,这可能是人参增加组织血流量、防治心血管疾患的重要依据。     

Triflavin, an Arg-Gly-Asp containing snake venom peptide, inhibits aggregation of human platelets induced by human hepatoma cell line

Triflavin, an Arg-Gly-Asp (RGD)-containing peptide, purified from snake venom of Trimeresurus flavoviridis, inhibits human platelet aggregation through the blockade of fibrinogen binding to fibrinogen receptors associated with glycoprotein IIb/IIIa complex. In this report, we examined the effect of triflavin on tumor cells (human hepatoma J-5)-induced platelet aggregation (TCIPA) of heparinized platelet-rich plasma (PRP). ADP-scavenger agents, apyrase (10 U/ml) and creatine phosphate (5 mM)/creatine phosphokinase (5 U/ml) did not inhibit TCIPA while hirudin (5u/ml) completely inhibited it. J-5 cells initially induced platelet aggregation, then blood coagulation occurred. J-5 cells concentration-dependently shortened the recalcification time of normal as well as Factor VIII, IX-deficient human plasmas, while it was inactive at shortening the recalcification time of Factor VII-deficient plasma, suggesting J-5 cells induced platelet aggregation through activation of extrinsic pathway, leading to thrombin formation as evidenced by the amidolytic activity on S-2238 by expressing tissue factor-like activity. Triflavin inhibited TCIPA in a dose-dependent manner (IC₅₀, 0.02 μM). When compared on molar ratio, triflavin was approximately 30,000 times more potent than GRGDS (IC₅₀,0.58 mM). On the other hand, GRGES showed no significant effect on TCIPA, even its concentration was raised to 4 mM. Additionally, the monoclonal antibodies, raised against glycoprotein IIb/IIIa complex (i.e., 7E₃ and 10 E₅) inhibited J-5 TCIPA. In conclusion, we suggest the inhibitory effect of triflavin on J-5 TCIPA may be chiefly mediated by the binding of triflavin to the fibrinogen receptor associated with glycoprotein IIb/IIIa complex on platelet surface membrane.