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目的 探讨Ｔ３ 增补于停搏液中的心肌保护作用。方法 离体鼠心（ ｎ ＝ １６） 在改良的ＬａｎｇｅｎｄｏｒｆｆＮｅｅｌｙ 灌注模型上、３７ ℃下经历２０ 分钟预灌注、２０ 分钟停搏、３０ 分钟再灌注。结果 再灌注３０ 分钟时，左室功能指标（ＬＶＤＰｄｐ／ｄｔ）百分恢复率治疗组显著高于对照组（ Ｐ ＜０ ．０１），心肌超氧化物歧化酶（ＳＯＤ） 治疗组显著高于对照组（ Ｐ＜ ０．０１），过氧化脂质（ＬＰＯ） 治疗组显著低于对照组（ Ｐ ＜０．０５）；心肌酶（ＨＢＤＨ．ＬＤＨ）释放量再灌注期对应时点组间比较，治疗组显著低于对照组（ Ｐ＜ ０ ．０１） ；电镜观察心肌超微结构，治疗组显著优于对照组。结论 Ｔ３ 增补于心脏停搏液中可以显著地促进缺血后左室功能的恢复，显著减轻心肌缺血再灌注损伤，具有良好的心肌保护作用。
Objective To investigate the cardioprotective effects of T3 supplement on cardioplegic solution. Methods Isolated rat heart (n = 16) was subjected to 20 min pre-priming, 20 min arrest and 30 min reperfusion at 37 ° C on a modified Langendorff-Neely perfusion model. Results At 30 minutes after reperfusion, the percent recovery of LVDPdp / dt in treatment group was significantly higher than that in control group (P <0.01), and the level of myocardial SOD in treatment group was significantly higher than that in control group (P <0.01), LPO treatment group was significantly lower than the control group (P <0.05); myocardial enzyme (HBDH.LDH) The treatment group was significantly lower than the control group (P <0.01); electron microscopy myocardial ultrastructure, the treatment group was significantly better than the control group. Conclusion T3 supplementation in cardioplegic solution can significantly promote the recovery of left ventricular function after ischemia, significantly reduce myocardial ischemia-reperfusion injury and have good myocardial protective effect.