Dyke C M, Yeh T, Lehman J D, Abd-Elfattah A, Ding M, Wechsler A S, Salter D R
Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond.
Ann Thorac Surg. 1991 Jul;52(1):14-9. doi: 10.1016/0003-4975(91)91410-w.
Hypothyroidism is associated with profound left ventricular dysfunction. Brain-dead organ donors and patients undergoing cardiopulmonary bypass are chemically hypothyroid with significantly reduced circulating free triiodothyronine (T3). To test the hypothesis that T3 enhances left ventricular function in a hormonally deficient environment, a total of 36 healthy New Zealand White rabbit hearts were studied using a modified Langendorff preparation with Krebs-Henseleit perfusate and intra-ventricular balloon. In 9 normal rabbit hearts a cumulative dose-response curve with logarithmically increasing doses of T3 was obtained. The vehicle solution for T3 dissolution served as control (n = 9). Left ventricular function was assessed from peak developed pressure at baseline and after T3 administration. Triiodothyronine had no effect in normal hearts on peak developed pressure or end-diastolic pressure. In 18 rabbits, the acute effect of T3 administration after ischemia was investigated. Preischemic left ventricular function was measured to serve as baseline, and hearts were subjected to 37 degrees C global ischemia. Triiodothyronine (n = 9) or vehicle (n = 9) was infused during reperfusion, and left ventricular peak developed pressure was measured at 30 and 60 minutes of reperfusion. Recovery of function (expressed as percent return of left ventricular peak developed pressure) was significantly improved within 15 minutes of reperfusion (65.0% +/- 2.1% versus 80.2% +/- 4.1%) and remained significantly improved throughout the reperfusion period (p less than 0.05 by analysis of variance). These data suggest that although T3 possesses no inotropic properties, it significantly improves postischemic left ventricular function. The rapidity of the functional improvement suggests that these effects may be due to plasma membrane-mediated mechanisms.
甲状腺功能减退与严重的左心室功能障碍有关。脑死亡器官供体和接受体外循环的患者处于化学性甲状腺功能减退状态，循环游离三碘甲状腺原氨酸（T3）显著降低。为了验证T3在激素缺乏环境中增强左心室功能的假说，使用改良的Langendorff装置，以Krebs-Henseleit灌注液和心室内球囊，对总共36只健康的新西兰白兔心脏进行了研究。在9只正常兔心脏中，获得了T3剂量呈对数增加的累积剂量-反应曲线。用于溶解T3的溶媒溶液作为对照（n = 9）。根据基线和给予T3后的最大发展压力评估左心室功能。三碘甲状腺原氨酸对正常心脏的最大发展压力或舒张末期压力没有影响。在18只兔子中，研究了缺血后给予T3的急性效应。测量缺血前的左心室功能作为基线，心脏接受37℃全心缺血。在再灌注期间输注三碘甲状腺原氨酸（n = 9）或溶媒（n = 9），并在再灌注30分钟和60分钟时测量左心室最大发展压力。功能恢复（以左心室最大发展压力恢复的百分比表示）在再灌注15分钟内显著改善（65.0%±2.1%对80.2%±4.1%），并且在整个再灌注期间仍显著改善（方差分析p<0.05）。这些数据表明，尽管T3不具有正性肌力特性，但它能显著改善缺血后左心室功能。功能改善的快速性表明这些效应可能是由于质膜介导的机制。
