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本实验采用大鼠离体心脏模型，探讨激活粒细胞对大鼠离体心脏再灌注损伤的作用机制。实验过程观察冠状动脉流量，冠状动脉阻力，冠状动脉流出液中乳酸脱氢酶的活性及丙二醛的含量。实验完毕后对心肌进行组织学检查及超微结构观察。实验结果表明：激活组与对照组相比较冠状动脉流量明显减少，阻力明显增加（Ｐ＜０．０１）。冠状动脉流出液中乳酸脱氢酶的活性及丙二醛的含量明显增加（Ｐ＜０．０１）。在光镜及电镜下可见明显的组织损伤。资料提示激活粒细胞可导致大鼠离体心脏再灌注损伤。激活粒细胞是通过释放氧自由基及对心肌微循环的阻塞引起心肌再灌注损伤。
In this study, isolated rat heart model was used to investigate the mechanism of activated granulocytes on isolated rat heart reperfusion injury. The experimental course was observed coronary flow, coronary resistance, lactate dehydrogenase activity in coronary effusion and the content of malondialdehyde. Myocardial histology and ultrastructure were observed after the experiment. The experimental results showed that compared with the control group, the coronary artery flow rate was significantly decreased and the resistance was significantly increased (P <0.01). Lactate dehydrogenase activity and MDA content in coronary effluent increased significantly (P <0.01). In light microscope and electron microscopy visible obvious tissue damage. Data suggest that activation of granulocytes can lead to isolated rat heart reperfusion injury. Activation of granulocytes is caused by the release of oxygen free radicals and obstruction of myocardial microcirculation caused by myocardial reperfusion injury.