中文摘要：

背景：既往心力衰竭模型制作方法主要通过开胸结扎不同部位冠状动脉建立急性心肌梗死模型,该方法创伤大、开胸手术复杂,动物死亡率高、术后恢复较慢。目的：应用选择性冠状动脉前降支微血栓微球混悬液灌注方法造成心肌缺血坏死,探索建立稳定存活的小型猪急性心肌梗死后心力衰竭动物模型。方法：对小型猪行冠状动脉造影监测心电图及应用漂浮导管监测有创血流动力学参数,并行pigtail导管测量左室舒张末压的变化,以4F导管超选左前降支行微血栓微球混悬液分次注入,心肌梗死溶栓实验心肌灌注分级〈2级和左室舒张末压力〉15mmHg（1mmHg=0.133kPa）时停止注射,间隔10min重复注射,待左室舒张末压稳定在15~18mmHg后结扎血管,并加压包扎。监测心肌坏死标志物心肌肌钙蛋白Ⅰ和肌酸激酶同工酶变化。造模后1,7,14,30d行心脏超声检查,造模30d复查有创血流动力学检查,并行心脏病理检查,认定和评价模型的成功率、稳定性和可重复性。结果与结论：造模30d后共有14头小型猪成活,心电图、心肌坏死标记物、病理检查均符合急性心肌梗死病生理过程。其中13头小型猪达到动物模型标准,肺毛细血管楔压明显升高（P〈0.01）,心输出量和左室射血分数明显降低（P〈0.01）,模型成功率为76.47%;病理检查显示心肌梗死面积占左心室面积的（33.85±4.43）%。微血栓微球混悬液灌注构建小型猪急性心肌梗死后心力衰竭模型更接近急性心肌梗死-心力衰竭临床病理生理学特点。

英文摘要：

BACKGROUND： Previous acute myocardial infarction （AMI） models are prepared via opening chest and ligating coronary artery, which result in great trauma and death. OBJECTIVE： To evaluate minipig models of ischemic heart failure caused by AMI by perfusing microsphere suspension into the left anterior descending branch . METHODS： After coronary angiography, 4F judkins angiographic catheter was inserted into the left anterior descending branch and 3 mL microsphere suspension was injected repeatedly at 10 minutes interval until TIMI myocardial perfusion grade （TMPG） 2 and left ventricular end-diastolic pressure maintaining from 15 to 18 mm Hg steadily. Electrocardiography, hemodynamic parameters, ultrasonic cardiogram, cardiac troponin I and CK-MB were measured. Myocardial infarct area was determined by pathologic examination. At 1, 7, 14, and 30 days after model preparation, cardiac ultrasound inspection was performed. At 30 days, hemodynamic parameters and pathological examination were used to evaluate the stability and repeatability of models. RESULTS AND CONCLUSION： A total of 14 minipigs survived at 30 days after model preparation, which were consistent with AMI criteria. There were 13 minipigs consistent with the models criteria with notably increased pulmonary capillary wedge pressure （P 0.01） and decreased cardiac output and left ventricular ejection fraction （P 0.01）. The success rate was 76.47%. The pathological examination demonstrated that the infarct size accounted for （33.85±4.43）% of the left ventricle. The model prepared by this method is more close to pathophysiological characteristics of ischemic heart failure caused by AMI.