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目的：观察冷晶体停搏液中加入生理浓度Ｔ３对大鼠停搏心肌收缩及舒张功能恢复、心肌酶谱、氧耗量及冠脉内皮细胞功能的影响。方法：运用离体鼠心作功模型，实验组（ｎ＝６）含０．６ｍｇ／ＬＴ３，比较停搏９０ｍｉｎ前后左室收缩压力（ＬＶＳＰ）、左室收缩压力微分（ＬＶ＋ｄｐ／ｄｔｍａｘ）、左室舒张压力微分（ＬＶ－ｄｐ／ｄｔｍａｘ）、肌酸磷酸激酶（ＣＰＫ）、乳酸脱氢酶（ＬＤＨ）的变化。同时评价乙酰胆碱（Ａｃｈ）和硝普钠（ＳＮＰ）所致的冠脉血管舒张功能的改变。结果：实验组ＬＶＳＰ恢复率为（９０．１±３．７）％，ＬＶ＋ｄｐ／ｄｔｍａｘ为（７９．２±５４）％，优于对照组；而ＬＶ－ｄｐ／ｄｔｍａｘ、ＬＤＨ、ＣＰＫ、Ｖｍｏ２（即ＭＶＯ２）两组无显著差异。Ａｃｈ所致的冠状血管阻力（ＣＶＲ）降低两组都不明显，ＳＮＰ所致ＣＶＲ下降程度基本一致。结论：含Ｔ３冷晶体停搏液仅能促进大鼠左室收缩功能恢复，而对舒张功能、心肌氧耗量、心肌酶谱影响不大，Ｔ３由于内皮细胞功能降低而不能明显扩张冠状血管。
OBJECTIVE: To observe the effects of physiological concentration of T3 in cold crystalloid cardioplegia on contractile and diastolic function recovery, myocardial zymogram, oxygen consumption and coronary endothelial cell function in isolated cardioplegia rats. Methods: The left ventricular systolic pressure (LVSP), left ventricular systolic pressure differential (LV + dp / dtmax), left ventricular systolic pressure (LV-dp / dtmax), creatine phosphokinase (CPK), and lactate dehydrogenase (LDH) were measured. The changes of coronary vasodilation function induced by acetylcholine (Ach) and sodium nitroprusside (SNP) were also evaluated. Results: The recovery rate of LVSP in experimental group was (90.1 ± 3.7)%, and LV + dp / dtmax was (79.2 ± 5.4)%, which was better than that in control group. LV-dp / dtmax, Vmo2 (MVO2) no significant difference between the two groups. Ach-induced coronary vascular resistance (CVR) decreased in both groups were not obvious, SNP caused by the degree of CVR decreased basically the same. CONCLUSION: The T3 cold crystalloid cardioplegia can only promote the recovery of left ventricular systolic function in rats, but has little effect on the diastolic function, myocardial oxygen consumption and myocardial zymogram. T3 can not obviously dilate coronary vessels due to the decrease of endothelial function.