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本研究旨在比较在体与各种离体心脏缺血-再灌注(ischemia-reperfusion,I-R)模型心肌损伤程度,以选择能够较好地模拟在体模型的离体I-R模型。Sprague-Dawley(SD)大鼠随机分为4组进行处理:在体模型组、Langendorff模型组、电刺激Langendorff模型组、工作心脏模型组,结扎各组大鼠心脏冠状动脉左前降支60 min,松开结扎行再灌注120 min,用压力传感器和TTC/Evans blue双染色法分别检测各模型心脏功能与心肌梗死面积的变化。结果显示,I-R期间Langendorff模型和工作心脏模型心率显著低于在体模型。离体工作心脏、Langendorff与电刺激(300次/min)Langendorff模型组冠脉流量在结扎后下降均大于40%,再灌注期各组冠脉流量均回升。3种离体模型左心室收缩末期压力(left ventricular end-systolic pressure,LVESP)在缺血期均降低,再灌注期部分恢复。3种离体模型左心室舒张末期压力(left ventricular end-diastolic pressure,LVEDP)在缺血期均升高,工作心脏模型明显高于Langendorff模型;在再灌注期工作心脏模型LVEDP缓慢下降,而Langendorff与电刺激Langendorff模型组LVEDP在再灌注即刻呈现短暂的升高峰,然后降低。在体心脏I-R模型左室心肌梗死面积为(60.4±5.4)%,离体工作心脏与Langendorff模型的梗死面积显著低于在体模型,而电刺激Langendorff心脏I-R模型的心肌梗死面积与在体模型无显著性差别。以上结果提示,电刺激维持心率300次/min的Langendorff心脏I-R模型可模拟在体心脏I-R模型的心肌损伤程度。
The purpose of this study was to compare the degree of myocardial damage in ischemia-reperfusion (I-R) models in vivo with various isolated hearts to select an ex vivo I-R model that can better model in vivo models. Sprague-Dawley rats were randomly divided into 4 groups: model group, Langendorff model group, Langendorff model group and working heart model group. The left anterior descending coronary artery was ligated for 60 min, Ligation was performed for 120 min after reperfusion, and the changes of cardiac function and myocardial infarct size in each model were detected by pressure sensor and TTC / Evans blue double staining. The results showed that heart rate of Langendorff model and working heart model during I-R was significantly lower than that of in-vivo model. In isolated heart, Langendorff and electrical stimulation (300 beats / min), Langendorff model group coronary flow decreased more than 40% after ligation, coronary flow rose in each group during reperfusion. Left ventricular end-systolic pressure (LVESP) decreased in both ischemia and reperfusion phases in 3 in vitro models. The left ventricular end-diastolic pressure (LVEDP) of three kinds of isolated models increased during ischemia, and the working heart model was significantly higher than that of Langendorff model. The LVEDP of working heart model decreased slowly during reperfusion, while Langendorff In the Langendorff model group, the LVEDP peaked immediately after reperfusion and then decreased. The myocardial infarct size in left ventricular myocardium was (60.4 ± 5.4)% in IR and Langendorff models were significantly lower than those in Langendorff model, while the myocardial infarct size in Langendorff IR model was significantly higher than that in in vivo model No significant difference. These results suggest that Langendorff’s cardiac I-R model, which is electrically stimulated to maintain a heart rate of 300 beats / min, can simulate the degree of myocardial damage in the I-R model in vivo.