Wechsler A S, Kadletz M, Ding M, Abd-Elfattah A, Dyke C
Department of Surgery, Medical College of Virginia, Richmond 23298-0645.
J Card Surg. 1993 Mar;8(2 Suppl):338-41. doi: 10.1111/j.1540-8191.1993.tb01336.x.
Administration of thyroid hormone, triiodothyronine (T3), causes numerous cardiovascular effects such as increases in stroke volume, cardiac output, heart rate, and myocardial contractility, and decreases in systemic vascular resistance. Along with other stressors, cardiopulmonary bypass (CPB) has been associated with reduced levels of T3. We examined the effects of T3 on early postischemic myocardial recovery in rabbit hearts subjected to crystalloid perfusion to simulate a low T3 state, and in pig hearts following global ischemia due to CPB. Studies using the former system showed that T3 administration results in significantly improved developed pressure after reperfusion of mildly ischemic hearts compared to controls, without producing inotropic effects. In more severely stunned rabbit hearts, physiologic and 10 times physiologic doses of T3 produced significantly improved (p < 0.05) stroke work end-diastolic length compared to placebo treatment. T3 treated pigs undergoing CPB and subjected to 30 minutes of global normothermic ischemia experienced significantly enhanced recovery of left ventricular contractility compared to controls at 90 and 120 minutes post reperfusion. Neither placebo nor T3 affected myocardial adenosine triphosphate levels. These data show that T3 enhances recovery from myocardial stunning without producing acute inotropic effects.
给予甲状腺激素三碘甲状腺原氨酸（T3）会产生多种心血管效应，如每搏输出量增加、心输出量增加、心率加快、心肌收缩力增强，以及全身血管阻力降低。与其他应激源一样，体外循环（CPB）与T3水平降低有关。我们研究了T3对模拟低T3状态的晶体灌注兔心脏以及CPB导致全心缺血后的猪心脏缺血后早期心肌恢复的影响。使用前一种系统的研究表明，与对照组相比，给予T3可使轻度缺血心脏再灌注后的舒张末压显著改善，且无正性肌力作用。在更严重的顿抑兔心脏中，与安慰剂治疗相比，生理剂量和10倍生理剂量的T3可使每搏功舒张末期长度显著改善（p<0.05）。接受CPB并经历30分钟全心常温缺血的T3治疗猪在再灌注后90分钟和120分钟时，左心室收缩力的恢复明显优于对照组。安慰剂和T3均未影响心肌三磷酸腺苷水平。这些数据表明，T3可增强心肌顿抑后的恢复，且不产生急性正性肌力作用。
