Kadletz M, Mullen P G, Ding M, Wolfe L G, Wechsler A S
Division of Cardiothoracic Surgery, Medical College of Virginia-Virginia Commonwealth University, Richmond.
Ann Thorac Surg. 1994 Mar;57(3):657-62. doi: 10.1016/0003-4975(94)90563-0.
Thyroid dysfunction has been shown to have a significant impact on hemodynamic status and cardiac function. The purpose of this study was to determine the influence of triiodothyronine (T3) on cardiac functional recovery after ischemia in a dose-dependent manner. Postischemic functional recovery was assessed in isolated rabbit hearts mounted in a modified Langendorff preparation. Left ventricular systolic, diastolic, and peak developed pressures were measured before and after ischemia, and calculated as a percentage of preischemic function. Two cohorts of hearts were studied: the first was exposed to warm ischemia until a myocardial contracture of 4 mmHg was produced; the second cohort was exposed to warm ischemia until a contracture of 15 mm Hg was observed. In each cohort, T3 was added to the perfusion solution after ischemia in a physiologic concentration (2.5 x 10(-9) g/mL; 1 x T3), as well as ten times (2.5 x 10(-8) g/mL; 10 x T3) and a hundred times (2.5 x 10(-7) g/mL; 100 x T3) the physiologic concentration. One group, given the carrier only but without T3, served as the control. Rabbit hearts exposed to a short period of ischemia (4-mmHg diastolic contracture) showed increased recovery with 1 x T3 and 10 x T3. 100 x T3 did not bring about improved left ventricular recovery versus that in the control group. Rabbit hearts in the 15 mm Hg-diastolic contracture cohort showed increased recovery with 10 x T3 but not with 1 x T3. 100 x T3 led to decreased recovery in this cohort versus that in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
甲状腺功能障碍已被证明对血流动力学状态和心脏功能有重大影响。本研究的目的是以剂量依赖的方式确定三碘甲状腺原氨酸（T3）对缺血后心脏功能恢复的影响。在改良的Langendorff装置中安装的离体兔心脏上评估缺血后的功能恢复情况。在缺血前后测量左心室收缩压、舒张压和最大发展压力，并计算为缺血前功能的百分比。研究了两组心脏：第一组暴露于热缺血，直到产生4 mmHg的心肌挛缩；第二组暴露于热缺血，直到观察到15 mmHg的挛缩。在每个组中，缺血后将生理浓度（2.5×10⁻⁹ g/mL；1×T3）、生理浓度的十倍（2.5×10⁻⁸ g/mL；10×T3）和生理浓度的一百倍（2.5×10⁻⁷ g/mL；100×T3）的T3添加到灌注溶液中。一组只给予载体但不给予T3作为对照。暴露于短时间缺血（4 mmHg舒张期挛缩）的兔心脏在给予1×T3和10×T3时恢复增加。与对照组相比，100×T3并未改善左心室恢复情况。舒张期挛缩为15 mmHg组的兔心脏在给予10×T3时恢复增加，但给予1×T3时未增加。与对照组相比，该组给予100×T3导致恢复下降。（摘要截断于250字）
