球囊拉伤致家兔动脉粥样硬化斑块破裂及血栓形成

为建立动脉粥样硬化的兔模型并用药物触发造成斑块破裂及血栓形成，将60只雄性纯种新西兰兔随机平均分成三组：球囊损伤 高脂(1％胆固醇)组、高脂喂养组及普通饲料喂养组．喂养3个月后分别给予鲁塞尔蝰蛇毒和组胺药物触发以造成斑块破裂及血栓形成。结果发现，球囊损伤 高脂组与高脂喂养组均形成动脉粥样硬化斑块，其中球囊损伤 高脂组所形成的粥样斑块为具有较大脂质核的软斑块；药物触发后球囊损伤 高脂组存活的18只中有11只共15处发生斑块破裂及血栓形成；高脂喂养组中的19只经药物触发后仅5只共7处发生斑块破裂及血栓形成；普通饲料喂养组中未见斑块破裂及血栓形成。结果提示，在构建的动脉粥样硬化斑块的动物模型基础上，应用药物触发后能够造成斑块破裂及血栓形成。

Research on Triggering Plaque Disruption and Arterial Thrombosis in Vivo

Aim To build an animal model of plaque disruption and arterial thrombosis by pharmacological triggering atherosclerotic rabbits. Methods Sixty New Zealand White rabbits were equally divided into 3 groups at random: balloon-injury +high lipid diet group, high lipid diet group and regular diet group. Rabbits in balloon-injury +high lipid diet group underwent balloon-induced arterial wall injury and then were fed on a diet of 1% cholesterol; rabbits in high lipid diet group were only given 1% cholesterol; rabbits in regular diet group were fed on a regular diet. They were all fed for 3 months. Then the three groups underwent pharmacological triggering with Russell's viper venom (RVV) and histamine. Results Atherosclerotic plaques were found in balloon-injury +high lipid diet group and high lipid diet group; the lipid cores in the first group were larger than those in the second group. In balloon-injury +high lipid diet group, it was found that plaques disruption and thrombosis occurred in 11 out of the 18 rabbits and in total 15 lesions occurred plaque disruption and thrombi after triggering. In high lipid diet group, only 5 rabbits demonstrated plaques disruption and thrombosis and there were in all 7 thrombi. However, rabbits in the regular diet group did not have plaques disruption and thrombosis. Conclusions With atherosclerotic plaque animal models, we could pharmacologically trigger plaque disruption and arterial thrombosis.