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目的：本研究旨在探讨心肌再灌注损伤（ＲＩ）的机制并评价费乐地平（Ｆｅｌｏｄｉｐｉｎｅ，Ｆｅｌ）对ＲＩ的保护作用及其机制。方法：用家兔心肌缺血再灌注模型，分别设对照组、单纯缺血再灌注组及再灌注＋Ｆｅｌ治疗组，设再灌注０．５、１．５和６．０小时３个时相点，测定心肌Ｃａ２＋、丙二醛（ＭＤＡ）含量、中性粒细胞（ＰＭＮ）浸润数、Ｎａ＋Ｋ＋ＡＴＰ酶及Ｃａ２＋Ｍｇ２＋ＡＴＰ酶活性，并观察心肌超微结构改变及测定心肌梗塞范围。结果：心肌再灌注后Ｃａ２＋、ＭＤＡ含量及ＰＭＮ浸润数明显增高，Ｎａ＋Ｋ＋ＡＴＰ酶和Ｃａ２＋Ｍｇ２＋ＡＴＰ酶活性明显降低，其改变以Ｃａ２＋升高发生最快；Ｆｅｌ可使上述指标改变的程度明显减轻（Ｐ＜０．０５～０．０１），并可缩小心肌梗塞范围，改善其超微结构的变化。结论：心肌ＲＩ是多种因素于不同时间所致的一种复合性损伤，Ｆｅｌ对心肌ＲＩ有保护作用，其保护机制可能与其对心肌能量依赖性酶活性的改善有关。
Objective: This study aimed to investigate the mechanism of myocardial reperfusion injury (RI) and evaluate the protective effect of Felodipine (Fel) on RI and its mechanism. Methods: Rabbit model of myocardial ischemia-reperfusion was set up control group, ischemia-reperfusion group and reperfusion + Fel treatment group respectively. At 0.5, 1.5 and 6.0 hours after reperfusion, The content of Ca2 +, malondialdehyde (MDA), the number of neutrophil (PMN) infiltration, the activity of Na + K + ATPase and Ca2 + Mg2 + ATPase in myocardium were measured. The myocardial ultrastructure was observed and the extent of myocardial infarction was determined. Results: After myocardial reperfusion, the content of Ca2 +, MDA and the number of PMN infiltration were significantly increased, while the activities of Na + K + ATPase and Ca2 + Mg2 + ATPase were significantly decreased. The change of Ca2 + .05 ~ 0.01), and can narrow the scope of myocardial infarction, improve its ultrastructure changes. CONCLUSION: RI is a complex injury caused by multiple factors at different time points. Fel may have protective effect on RI. The protective mechanism may be related to the improvement of myocardial energy-dependent enzyme activity.