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目的：观察温血停搏液中加入０．６ｍｇ／ＬＴ３对停搏心肌能量代谢、左心收缩及舒张功能、心肌酶谱及冠状动脉内皮细胞功能的影响。方法：观察离体鼠心停搏前后左室收缩压（ＬＶＳＰ）、左室收缩压力微分（ＬＶ＋ｄｐ／ｄｔｍａｘ）、左室舒张压力微分（ＬＶ－ｄｐ／ｄｔｍａｘ）及心肌氧耗量（ＭＶＯ２），测定鼠心复跳后１ｍｉｎ冠状静脉窦流出液中乳酸脱氢酶（ＬＤＨ）、肌酸磷酸激酶（ＣＰＫ）含量。观察乙酰胆碱（Ａｃｈ）和硝普钠灌注冠状动脉后的血管阻力变化。结果：实验组ＬＶＳＰ、ＬＶ＋ｄｐ／ｄｔｍａｘ及ＬＶ－ｄｐ／ｄｔｍａｘ的恢复均优于对照组（Ｐ＜０．０５），ＭＶＯ２、ＬＤＨ及ＣＰＫ含量无差别（Ｐ＞０．０５），实验组因Ａｃｈ所致的冠脉血管阻力下降较对照组明显。结论：Ｔ３具有促进停搏心肌功能恢复、降低冠状血管阻力的作用而不影响心肌氧耗量。
Objective: To observe the effect of adding 0.6 mg / L T 3 in warm blood cardioplegia on cardiac energy metabolism, left ventricular systolic and diastolic function, myocardial zymogram and coronary endothelial cell function. Methods: The left ventricular systolic pressure (LVSP), left ventricular systolic pressure (LV + dp / dtmax), left ventricular diastolic pressure (LV-dp / dtmax) and myocardial oxygen consumption (MVO2) The concentrations of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) in the coronary sinus effluent were determined at 1 minute after resuscitation. To observe the changes of vascular resistance after perfusion of coronary artery with acetylcholine (Ach) and sodium nitroprusside. Results: The recovery of LVSP, LV + dp / dtmax and LV-dp / dtmax in the experimental group were better than those in the control group (P <0.05), but there was no difference in the contents of MVO2, LDH and CPK (P> 0.05) Resulting coronary artery resistance decreased significantly compared with the control group. Conclusion: T3 can promote myocardial function recovery and reduce coronary vascular resistance without affecting myocardial oxygen consumption.