小剂量阿司匹林对缺血性脑血管病患者血小板聚集功能的影响

目的 :观察小剂量阿司匹林 (ASA)对ICVD患者血小板聚集功能的影响。方法 :用花生四烯酸 (AA ,5 0 0 μmol·L-1)、二磷酸腺苷 (ADP ,5 μmol·L-1)、肾上腺素 (EPN ,5 μmol·L-1)和胶原 (COL ,2 μg·mL-1)做诱导剂检测ICVD患者服用不同剂量ASA组 ( 2 5、5 0和10 0mg·d-1)的血小板聚集率。结果 :各ASA组对AA、COL诱导聚集的变异系数较大。对AA诱导聚集无显著抑制者的比例分别为2 5mg·d-1组 44 4%、5 0mg·d-1组 2 9 6%、10 0mg·d-1组 2 9% ,其中 5 0mg·d-1组中合并糖尿病的例数较显著抑制者中多。结论 :ICVD患者中小剂量ASA作用个体差异较大 ,部分与自身危险因素有关。提示临床中ASA的效果需要实验室检测并应个体化     

A multiparametric index of platelet in vitro aggregation in cerebrovascular disease

148 patients with various forms of cerebrovascular disease (CVD) were studied by means of a multiparametric analysis ofin vitro platelet aggregation, based on the following six parameters: ADP and epinephrine primary and secondary aggregation thresholds and percent maximum aggregation induced by optimal concentrations of ADP and epinephrine. These patients were assigned to four study groups, according to clinical diagnosis supported by CT scan, of transient ischemic attack and reversible neurological deficit (TIA-RIND), or completed stroke, in the presence or absence respectively of antiplatelet medical treatment at the time of the study. A statistically significant increase of thein vitro platelet aggregation was found in 44.4% of the untreated TIA-RIND patients and in 33.9% of the untreated stroke patients. However this last group showed a higher percentage of very marked hyperaggregation. Differences between the two treated study groups and controls were not signicant. No difference was found in collagen-and ristocetin-induced aggregation between the patient groups and the controls.

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Sommario 148 pazienti con varie forme di malattia cerebrovascolare, sono stati studiati con analisi multiparametriche dell'aggregazione piastrinica in vitro sulla base dei seguenti sei parametri: le soglie di aggregazione primaria e secondaria e l'aggregazione massima percentuale indotta da ADP ed Epinefrina. Questi pazienti sono stati suddivisi in 4 gruppi di studio in accordo con la diagnosi clinica confortata dai dati della TAC e cioè: TIA, RIND, o rammollimento in presenza o in assenza rispettivamente di un trattamento antiaggregante nel momento dello studio. è stato trovato un aumento statisticamente significativo dell'aggregazione in vitro delle piastrine nel 44.4% dei casi TIA, RIND non trattati e nel 33,9% dei casi di rammollimento non trattati. Quest'ultimo gruppo, però, ha dimostrato una più alta percentuale di iperaggregazione molto marcata. Le differenze tra i 2 gruppi di studio trattati con antiaggreganti e i controlli non erano significative. Inoltre nessuna differenza è stata riscontrata tra i gruppi e i controlli nell'aggregazione indotta da collageno e ristocetina.

     

高脂血症患者血小板体积及有关参数的研究

本文报道242例高脂血症患者血小板(PLT)、平均血小板数(MPLT)及平均血小板体积(MPV)等参数的测定结果,其中高胆固醇并高甘油三酯患者,PLT、MPLT及巨大血小板比例(Macro-PLT)高于正常,MPV正常;而单纯高胆固醇或高甘油三酯患者,上述指标与正常人无显著性差异。提示高胆固醇并高甘油三酯患者,存在血小板生成动力学异常,其血小板的破坏增加,生成率加速、但处于一种高水平的动态平衡之中。这可能是高脂血症出现高凝状态的原因之一。同时表明此类患者使用抗血小板疗法具有一定的合理性和必要性。     

特异性血小板抗体检测的实验研究

目的　建立一种简易、特异性强的血小板抗体检测方法。方法　利用磷酸氯喹溶液对血小板进行处理 ,去掉血小板相关抗原 (HLA抗原 ) ,用只含特异性抗原的血小板包被聚乙烯板来捕获血小板抗体。结果　与常用的SEPSA和淋巴细胞毒实验 (LCT)比较 ,该方法只表现血小板特异性抗体反应。结论　本方法能够鉴别血小板相关抗原的抗体和血小板特异性抗原的抗体 ,为临床血小板减少疾病的鉴别诊断、非溶血性发热反应和血小板输注无效的原因提供有用的参考依据     

脊柱化脓性骨髓炎的诊断及治疗

目的探讨脊柱化脓性骨髓炎的诊断及治疗方法.方法1999年7月～2003年8月,收治以腰痛伴发热为主要临床表现的患者12例,男7例,女5例;年龄13～61岁,平均36.6岁.患者先有胸、腰背部疼痛,11例出现剧烈疼痛,伴有体温升高(超过39℃),局部无红肿,有深压痛及叩击痛,脊柱活动受限,但无脊髓及马尾神经压迫症状,二便正常.对患者行白细胞计数、血沉和MR等检查.12例患者中,10例血沉超过60 mm/1 h,1例血沉为28mm/1 h,1例血沉为50mm/1 h.2例患者白细胞计数超过1.0×109/L.4例患者经椎弓根穿刺活检,阳性率为75%.入院后即给予静脉滴注抗生素治疗至少6周,继而口服抗生素治疗6周,11例患者血沉于治疗后1个月下降50%以上,约91.7%的患者保守治疗有效.结果12例患者9例获得随访,随访时间6个月～4年,平均2年2个月.获得随访的9例患者中,7例无临床症状,1例有轻微背痛,1例有慢性严重背痛的患者,经保守治疗无效后,行手术治疗;7例行MR检查,2例显示局部椎体及椎间盘仍有破坏,T1加权像示低信号范围缩小,T2加权像示仍为高信号,但无腰背痛等临床症状.结论脊柱化脓性骨髓炎患者血沉较白细胞计数敏感;MR及病理检查对明确诊断有重要意义.采用静脉滴注抗生素及口服抗生素序贯疗法治疗1个月后血沉下降是保守治疗成功的标志,保守治疗无效者可手术治疗.     

血细胞彩色图像的微机自动计数方法探讨

目的　探讨血细胞自动计数的方法。方法　采用微机彩色图像处理技术对血液细胞图像进行图像分割和细胞计数。结果　与人工计数相平行 ,相关系数r =0 .96 1～ 0 .997,P >0 .0 5。结论　该方法可行且计数相对精确、迅速、客观     

Thrombosis triggered by severe arterial lesions is inhibited by oral administration of a glycoprotein IIb/IIIa antagonist

Platelet aggregation and thrombosis play an important role in the onset of acute coronary events. Regardless of the stimulus for activation, platelet thrombus formation is ultimately regulated through the IIb/IIIa receptor complex. The effects of oral administration of xemilofiban, a non-peptide mimetic of the RGDF sequence of the IIb/IIIa receptor complex, on thrombus formation were evaluated in a canine model. Xemilofiban significantly reduced platelet deposition on severely damaged arterial wall. Platelet deposition was reduced at both low (13 ± 1 from 56 ± 18 × 10⁶ platelets cm⁻²; P  < 0.05) and high (23 ± 2 from 111 ± 21 × 10⁶ platelets cm⁻²; P  < 0.01) shear rates. Platelet deposition was reduced to a monolayer as seen by electron microscopy (platelet–vessel wall interaction). Therefore, the availability of an orally active IIb/IIIa antagonist for chronic use may have significant value in preventing thrombus formation in those clinical situations associated with severe arterial injury, such as atherosclerotic plaque disruption.     

The assembly of the factor X-activating complex on activated human platelets

Summary.  Platelet membranes provide procoagulant surfaces for the assembly and expression of the factor X-activating complex and promote the proteolytic activation and assembly of the prothrombinase complex resulting in normal hemostasis. Recent studies from our laboratory and others indicate that platelets possess specific, high-affinity, saturable, receptors for factors XI, XIa, IX, IXa, X, VIII, VIIIa, V, Va and Xa, prothrombin, and thrombin. Studies described in this review support the hypothesis that the factor X-activating complex on the platelet surface consists of three receptors (for the enzyme, factor IXa; the substrate, factor X; and the cofactor, factor VIIIa), the colocalization of which results in a 24 million-fold acceleration of the rate of factor X activation. Whether the procoagulant surface of platelets is defined exclusively by procoagulant phospholipids, or whether specific protein receptors exist for the coagulant factors and proteases, is currently unresolved. The interaction between coagulation proteins and platelets is critical to the maintenance of normal hemostasis and is pathogenetically important in human disease.