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模拟在体心脏缺血-再灌注损伤的离体心脏模型

焦博, 张琳, 余立群, 卢元明, 岳志杰, 余志斌^*

四军医大学航空航天医学教育部重点实验室,第四军医大学航空航天生理学教研室，西安 710032

摘要

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。

关键词： 大鼠; 心脏; 缺血-再灌注损伤; 相似性

分类号：R337.2

[n vitro heart models simulating in vivo cardiac ischemia-reperfusion injury.] [Article in Chinese]

Jiao Bo, ZHANG Lin, YU Li-Qun, LU Yuan-Ming, YUE Zhi-Jie, YU Zhi-Bin^*

Key Laboratory of Aerospace Medicine, Ministry of Education； Department of Aerospace Physiology, Fourth Military Medical University, Xi’an 710032, China

Abstract

The aim of this study was to compare in vivo and several in vitro cardiac ischemia-reperfusion (I-R) myocardial injury models, and choose a superior in vitro cardiac I-R model. Sprague-Dawley (SD) rats were randomly grouped into in vivo, Langendorff, Langendorff + pacing, and working heart groups. Left anterior descending (LAD) coronary artery was ligated for 60 min and then reperfused for 120 min in in vivo and in vitro rat hearts. Cardiac function and myocardial infarct size were measured by using pressure transducer and TTC/Evans blue double staining, respectively. The results showed that heart rate was greater in in vivo model than those in the three in vitro models. Coronary flows were dropped after LAD ligation and could recover at early phase of releasing LAD ligation in I-R models of the isolated working heart, Langendorff and Langendorff with 300 beats/min of electrical stimulation. Left ventricular end-systolic pressure (LVESP) decreased during ischemia, and partially restored during reperfusion in the three in vitro models. Left ventricular end-diastolic pressure (LVEDP) increased during ischemia in the three in vitro models. LVEDP was significantly higher in the isolated working heart than those in Langendorff models during ischemia, whereafter decreased slowly during reperfusion. LVEDP elevated further in the initiation of reperfusion period and then decreased, but did not recover to normal levels during reperfusion in Langendorff and Langendorff + pacing groups. Left ventricular myocardial infarct size was (60.4 ± 5.4)% in in vivo I-R model, which was significantly higher than that in Langendorff model and the isolated working heart. Notably, there was no significant difference in myocardial infarct size between in vivo model and Langendorff model with electrical stimulation. These results suggest that Langendorff I-R model with 300 beats/min of electrical stimulation can simulate the in vivo I-R myocardial injury.

Key words: Rat; heart; ischemia-reperfusion injury; similarity

收稿日期：2013-07-13　　录用日期：2013-09-17

通讯作者：余志斌　　E-mail: yuzhib@fmmu.edu.cn

引用本文：

焦博, 张琳, 余立群, 卢元明, 岳志杰, 余志斌. 模拟在体心脏缺血-再灌注损伤的离体心脏模型[J]. 生理学报 2013; 65 (6): 647-653.

Jiao Bo, ZHANG Lin, YU Li-Qun, LU Yuan-Ming, YUE Zhi-Jie, YU Zhi-Bin. [n vitro heart models simulating in vivo cardiac ischemia-reperfusion injury.] [Article in Chinese]. Acta Physiol Sin 2013; 65 (6): 647-653 (in Chinese with English abstract).