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目的探讨冠脉原位血栓大鼠血浆血管性假血友病因子(vWF)水平的变化及意义。方法将雄性SPF级SD大鼠78只,随机分为模型组(n=36)、假手术组(n=36)和正常对照组(n=6),模型组与假手术组按术后1 h,1,7,14,21,28 d各分6只。模型组经主动脉根部注入月桂酸钠,假手术组注入生理盐水,正常对照组不做任何处理。将心肌切片经HE与纤维素快速染色后,观察冠脉微血管原位血栓的形成。用ELISA检测血浆中vWF的水平。用超声心动图检查心脏的结构与功能。结果模型组大鼠心肌微血管中,可见血小板纤维蛋白血栓,有原位血栓形成的微血管数量显著增加(P<0.01);血浆中vWF的水平明显升高(P<0.05);心脏扩大,心功能降低;而假手术组和正常对照组未见明显变化。结论冠脉微血管内皮细胞损伤释放的vWF可介导冠脉微血管内以血小板纤维蛋白沉积为主的原位血栓形成。
Objective To investigate the changes of plasma von Willebrand factor (vWF) in coronary artery thrombosis rats and its significance. Methods Seventy eight Sprague-Dawley male Sprague-Dawley rats were randomly divided into model group (n = 36), sham operation group (n = 36) and normal control group (n = 6) h, 1,7,14,21,28 d each 6. Sodium laurate was injected into the model group via the aortic root, saline was injected into the sham-operated group, and no treatment was given to the normal control group. After myocardial sections were rapidly stained with HE and cellulose, the formation of coronary microvascular in situ thrombosis was observed. Plasma levels of vWF were measured by ELISA. Echocardiography was used to examine the structure and function of the heart. Results The number of microvessels in situ thrombosis increased significantly (P <0.01), the level of vWF in plasma increased significantly (P <0.05), and the cardiac enlargement, cardiac function Reduced; while sham-operated group and normal control group no significant changes. Conclusion The vWF released from the injury of coronary microvascular endothelial cells can mediate the in situ thrombosis of platelet fibrin deposition in coronary microvascular.