在氯化钡（BaCl2），氯仿-肾上腺素，毒毛花苷G，乌头碱，乙酰胆碱-氯化钙（ACh-CaCl2）5种实验性心律失常模型上观察了3，6-（二甲氨基）二苯并碘杂六环葡萄糖酸盐（IHC-93）对抗心律失常的作用。结果表明IHC-930.25和0.50mg·kg-1均可对抗ACh-CaCl2诱发的小鼠房颤（扑）；明显缩短BaCl2诱发的大鼠室性心律失常持续时间；对氯仿肾上腺素诱发家兔的心律失常有预防及缓解作用；能提高毒毛花苷G致豚鼠室性早搏，室性心动过速，室颤和心搏停止的用量；能提高乌头碱导致室性早搏用量，对室性心律失常有部分对抗作用。

1 Administration of bovine thrombin (100ukg-1) into the carotid artery of rabbits induces a sustained accumulation of Indium-labelled platelets within the cranial vasculature over the subsequent 3h. 2 Intracarotid (i.c.) administration of defibrotide (64mg kg-1 bolus plus 64mg kg-1h-1 for 1h) prior to i.c. thrombin (100ukg-1) significantly reduces the ability of thrombin to induce cranial thromboembolism in rabbits. 3 Intravenous (i.v.) administration of thrombin (20ukg-1) in rabbits induces a reversible accumulation of radiolabelled platelets into the thoracic circulation which is significantly reduced by i.v. administration of defibrotide (64mg kg-1 bolus plus 64mg kg-1h-1 for 1h) prior to i.v. thrombin. In contrast, platelet accumulation in response to adenosine diphosphate (ADP; 20pg kg-1, i.v.) or platelet activating factor (PAF; 50ng kg1, i.v.) is not significantly affected by this treatment. 4 Intravenous administration of the nitric oxide (NO)-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10mgkg-1) potentiates platelet accumulation induced by low dose thrombin (10ukg-1, i.v.) within the pulmonary vasculature of rabbits. The potentiated response is significantly abrogated following pretreatment with defibrotide (64mg kg-1 bolus plus 64 mg kg-1 h-for 1h, i.v.). 5 Intravenous injection of human thrombin (1250u kg-1) to mice induces death within the majority of animals which is significantly reduced by pretreatment with defibrotide (150-175mg kg1, i.v.). In contrast, death induced by i.v. collagen (1.25mg kg-1) plus adrenaline (75gg kg-1) is not significantly affected by defibrotide pretreatment. 6 The inhibitory effect of defibrotide in mice is abolished following concomitant treatment with the inhibitor of fribrinolysis, tranexamic acid (100mg kg-1, i.v.), but is unaffected following treatment with the cyclo-oxygenase inhibitor, aspirin (300mg kg-1, i.p.). 7 The protective effect of defibrotide against thrombin-induced thromboembolism in the mouse is potentiated by recombinant tissue-plasminogen activator (rt-PA; 1 mg kg-1, i.v.) or unfractionated heparin (10ukg-1, i.v.) administration. 8 The results suggest that defibrotide may possess antithrombotic activity on thrombin-induced thromboembolism which, at least in the mouse, may be partially mediated via induction of the fibrinolytic pathway.

目的：观察缺氧缺糖条件下血管内皮细胞（ECV2304）释放乳酸脱氢酶（LDH）、一氧化氮（NO）、丙二醛（MDA）水平和细胞膜流动性的变化及川芎嗪对它们的影响。方法：缺氧缺糖诱导血管内皮细胞损伤，自动生化分析仪测定培养液和细胞层中LDH活性；用比色法测定细胞培养液中NO水平；用荧光法检测细胞内脂质过氧化产物MDA以评价脂质过氧化程度；荧光偏振法测定内皮细胞膜流动性。结果：缺氧缺糖引起的血管内皮细胞LDH释放增加、MDA生成增多和膜流动性增高，NO水平降低。而川芎嗪可抑制缺氧缺糖引起的血管内皮细胞释放LDH，MDA生成和降低细胞膜流动性，提高NO水平。结论：川芎嗪可保护缺氧缺糖诱导血管内皮细胞的损伤，其作用机制有待进一步研究。

Inflammation plays a pivotal role in the formation of atherosclerosis. In addition to being a risk marker for cardiovascular diseases, the role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. CD40-CD40L system is proven to be an important mediator of several auto-immune and chronic inflammation diseases. Interruption of CD40–CD40L signaling pathway not only reduces the initiation and progression of atherosclerotic lesions, but also modulates plaque architecture. By using a flow cytometry and western blotting, we found that incubation of human umbilical vein endothelial cells (HUVECs) with CRP resulted in a timeand dose-dependent increase in the cell-surface expression of CD40 and CD40L. In addition, CRP (25mg/ml) increased gelatinolytic activities of MMP-2 and MMP-9. Anti-CD40 antibody significantly reversed the upregulated activities of MMP-2 and MMP-9 induced by CRP with gelatin zymography. Furthermore, lovastatin (10-7, 10-6, 10-5mol/l) and fenofibrate (5×10-5, 10-4, 2×10-4mol/l) significantly diminished the expression of CD40, CD40L and gelatinase activities (MMP-2, MMP-9) induced by CRP in HUVECs. In conclusion, our data provide evidence to support the direct pro-inflammatory effects of CRP via CD40-CD40L signaling pathway involved in the pathogenesis of atherosclerosis, and lovastatin and fenofibrate possess anti-inflammatory effects independent of their lipid-lowering action.

目的 观察红毛七的提取物（HMO4）对H202损伤内皮细胞核转录因子-KB的表达和一氧化氮（NO）、一氧化氮合酶（NOs）的影响。方法 用H2O2造成血管内皮细胞损伤模型，采用MTT法观察HMO-4对血管内皮细胞活性的影响；用比色法测定细胞培养液中NO，NOs含量；免疫细胞化学法观察内皮细胞核转录因子-kB的表达。结果 H2O2对血管内皮细胞具有损伤作用，HMO4在一定剂量内减少细胞的死亡；HMO-4还可促进H2O2损伤的血管内皮细胞内No，Nos释放的增加和抑制核转录因子-kB的表达的加强。结论 HMO-4对H2O2损伤的血管内皮细胞具有保护作用，其机制可能与其增加NO，N0s释放和转录因子-KB的表达有关。