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Methods The external surface of the coronary artery in the open-chest dogs were stimulated by micro-electric current stimulator for inducing the coronary arterial thrombosis.Another,pathological and biological-chemical examinations were performed.

采用自制的微电流刺激仪刺激犬冠状动脉血管外膜导致冠脉内急性血栓形成,并予生化和病理检测。

More attention should be paid to the risk of valve malfunction by thrombosis or tissue ingrowth.

但要重视因血栓形成或内膜组织长入导致机械瓣功能障碍的危险性。

We recently reported a high prevalence of intracardiac thrombus in cardiac amyloid patients at autopsy.

我们最近报道了尸检心脏淀粉样变病人心内血栓形成的高发生率。

Methods: Mutations of FX Leiden in 103 samples of DVT and 106 samples of control were examined with PCR-RFLP.

利用聚合酶链反应和限制性片段长度多态性方法,检测103例深静脉血栓形成患者与106例正常对照的FV Leiden突变,并进行对比分析。

Objective To investigate the effect and mechanism of lipoprotein[Lp] on platelet thrombosis.

目的研究脂蛋白[Lp]对血小板血栓形成的作用及其机理。

The median time to achieve a neutrophile count of 0.5×109/L was 10 days after the last dose of chemotherapy in regimen A,and the time was 16 days in regimen B.The average SLEDAI decreased from 9.2 to 4.4,and the proteinuria decreased from to (0~+) in 3 weeks after the treatment.Two cases with complication of hemolytic anemia and 1 with thrombocytopenia before the treatment recovered to normal or nearly normal hemogram respectively.Among these 5 cases,1 patient had a short time improvement during the therapy,but died 50 days later because of refractory thrombosis of renal vein; 4 other patients achieved complete or partial remission within 5~16 months follow-up.

结果方案1从CTX结束算起,中性粒细胞恢复到0.5×109/L平均需10d,方案2从Ara-C结束起,中性粒细胞恢复到0.5×109/L需16d;治疗3周时 SLEDAI平均从9.2降至4.4,尿蛋白从降至(0~+),合并有重度难治性贫血或血小板减少者,治疗后血红蛋白或血小板分别恢复正常或接近正常;方案2治疗的1例由于肾血管血栓形成未能控制,病情短暂好转后再度恶化,1个月后死于DIC和肾功能衰竭;另4例随访5~16个月,病情基本控制。

To study the inhibitory effects of nimodipine Nim on rat platelet aggregation and arterial thrombosis in vivo.

目的 研究尼莫地平Nim对大鼠体内血小板聚集和动脉血栓形成的影响。

In treatment group, there was no progressive necrosis in stasis zone, and at 24 h post injury, capillary dilation, cell edema and inflammatory infiltration were lessened significantly. In control group, 2 wounds had progressive necrosis (accounted for 10% of the total). Cell edema, inflammatory infiltration and capillary thrombosis were serious, Until 72 hr post injury, cell edema did not subside and necrosis of the dermis worsened. 2. Pathological assessment of the stasis zone tissue: As compared with that in control group, in treatment group the dermis structure in stasis zone was intact and the collagenous fiber bundle was normal.

结果:①创面细胞形态学改变:伤后8h毛细血管扩张、细胞水肿,炎性浸润最明显;治疗组中央淤滞区无进行性坏死,伤后24h后毛细血管扩张、细胞水肿、炎性浸润减轻;对照组2个创面呈进行性坏死(占10%),中央淤滞区细胞水肿、炎性浸润明显,毛细血管血栓形成,伤后72h水肿仍明显,真皮坏死加重;②淤滞区组织病理学评分:治疗组与对照组相比,治疗侧淤滞区的表皮结构相对完整、胶原纤维束相对正常,粒细胞浸润小于5个/400倍视野。

AIM: To report a rare case of antiphospholipid syndrome presenting as papilledema and sixth nerve palsy in right eye due to superior sagittal sinus thrombosis, and regression of papilledema following anticoagulation and acetazolamide therapy.

目的:报告1例罕见抗磷脂综合征的患者,由于上矢状窦血栓形成而表现为双眼视乳头水肿及右眼第六颅神经麻痹,经抗凝和乙酰唑胺治疗后视乳头水肿恢复。

Objective To investigate the cause, prevention and treatment of portal vein thrombosis following pericardial devascularization with splenectomy.

目的 探讨门静脉高压症患者行贲门周围血管离断术后门静脉系统血栓形成的原因、预防和治疗方法。

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