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目的 研究不同甲状腺功能状态下，三碘甲腺原氨酸（T3）对大鼠缺血再灌注（I/R）心肌细胞能量代谢的影响，探讨T3在心肌保护中的作用。方法 将实验大鼠分为甲状腺功能正常（A组）和甲状腺功能减退（甲减，B组）组，两组又随机分成空白缺血组、单纯灌注液组、T3灌注液组；建立离体心工作模型；利用反相高效液相色谱法测定各组心肌细胞ATP、ADP、AMP含量。结果 甲减状态心肌细胞ATP、ADP、AMP含量均明显降低（P<0.01）；I/R过程中，A、B两组ATP、ADP、AMP含量均大幅度下降，然而，T3灌注液组ATP含量显著高于单纯灌注液组：A组（1.03±0.02）vs（0.62±0.02）(mol/g，B组（0.85±0.02）vs（0.40±0.01）(mol/g，P<0.01。结论 甲减或I/R损伤使心肌细胞的能量合成及利用受到严重损害，T3可明显增加心肌细胞ATP的合成量与储备量，具有良好的心肌保护作用。
Objective To investigate the effect of triiodothyronine (T3) on the energy metabolism of myocardial cells during ischemia / reperfusion (I / R) in rats with different thyroid function and to explore the role of T3 in myocardial protection. Methods The experimental rats were divided into three groups: normal thyroid function (group A) and hypothyroidism (hypothyroidism group B). The two groups were randomly divided into blank ischemia group, perfusion group and T3 perfusion group. Heart model; Determination of ATP, ADP, AMP in each group by reverse-phase high-performance liquid chromatography. Results The levels of ATP, ADP and AMP in cardiomyocytes in hypothyroidism were significantly decreased (P <0.01). During I / R, ATP, ADP and AMP in groups A and B decreased significantly. However, (1.03 ± 0.02) vs (0.62 ± 0.02) (mol / g) in group B (0.85 ± 0.02) vs (0.40 ± 0.01) (mol / g, P <0.01) Hypothyroidism or I / R injury in myocardial cell energy synthesis and utilization of severely damaged, T3 can significantly increase myocardial ATP synthesis and reserve, has a good myocardial protection.